Species Differences and Human Disease
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1CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference If region matters, species and disease matter more. Section{ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim_2009_jneu... -
2CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference If region matters, species and disease matter more. Section{ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim_2009_jneu... -
3CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference If region matters, species and disease matter more. Section{ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim_2009_jneu... -
4CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference If region matters, species and disease matter more. Section{ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim_2009_jneu... -
5CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference If region matters, species and disease matter more. Section{ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim_2009_jneu... -
6CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference If region matters, species and disease matter more. Section{ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim_2009_jneu... -
1CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference The morphological contrast was quantified by 1CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference, who reported that protoplasmic astrocytes in human neocortex are 2.6-fold larger in diameter and extend roughly 10-fold more GFAP+ primary processes than their rodent counterparts (Figure{ref}fig:sec12-morphometrya). 3CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference re-examined this comparison in adult human cortex and confirmed longer processes and large... -
3CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference The morphological contrast was quantified by 2CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference0, who reported that protoplasmic astrocytes in human neocortex are 2.6-fold larger in diameter and extend roughly 10-fold more GFAP+ primary processes than their rodent counterparts (Figure{ref}fig:sec12-morphometrya). 2CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference1 re-examined this comparison in adult human cortex and confirmed longer processes and large... -
2CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference2 The morphological contrast was quantified by 2CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference3, who reported that protoplasmic astrocytes in human neocortex are 2.6-fold larger in diameter and extend roughly 10-fold more GFAP+ primary processes than their rodent counterparts (Figure{ref}fig:sec12-morphometrya). 2CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference4 re-examined this comparison in adult human cortex and confirmed longer processes and large... -
2CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference5 The morphological contrast was quantified by 2CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference6, who reported that protoplasmic astrocytes in human neocortex are 2.6-fold larger in diameter and extend roughly 10-fold more GFAP+ primary processes than their rodent counterparts (Figure{ref}fig:sec12-morphometrya). 2CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference7 re-examined this comparison in adult human cortex and confirmed longer processes and large... -
2CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference8 Beyond raw size, humans and other primates possess morphological classes that are absent from rodents. 2CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference9 described interlaminar astrocytes, whose cell bodies sit in layer I and extend long processes perpendicular to the pial surface, and varicose-projection astrocytes of layers V–VI. Surveying 46 mammalian species, 3CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference0 found that typical pial interlaminar astrocy... -
3CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference1 Beyond raw size, humans and other primates possess morphological classes that are absent from rodents. 3CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference2 described interlaminar astrocytes, whose cell bodies sit in layer I and extend long processes perpendicular to the pial surface, and varicose-projection astrocytes of layers V–VI. Surveying 46 mammalian species, 3CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference3 found that typical pial interlaminar astrocy... -
3CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference4 Beyond raw size, humans and other primates possess morphological classes that are absent from rodents. 3CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference5 described interlaminar astrocytes, whose cell bodies sit in layer I and extend long processes perpendicular to the pial surface, and varicose-projection astrocytes of layers V–VI. Surveying 46 mammalian species, 3CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference6 found that typical pial interlaminar astrocy... -
3CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference7 Human / primate astrocyte morphometry, split by measurement. (a)~Human versus rodent protoplasmic cortical astrocytes, adapted from 3CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference8: soma diameter and GFAP+ primary-process count are shown as separate bars because the two features are not commensurable on a single fold axis. (b)~Primate versus marsupial interlaminar astrocytes, adapted from 3CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference9... -
4CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference0 Human / primate astrocyte morphometry, split by measurement. (a)~Human versus rodent protoplasmic cortical astrocytes, adapted from 4CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference1: soma diameter and GFAP+ primary-process count are shown as separate bars because the two features are not commensurable on a single fold axis. (b)~Primate versus marsupial interlaminar astrocytes, adapted from 4CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference2... -
4CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference3 Human / primate astrocyte morphometry, split by measurement. (a)~Human versus rodent protoplasmic cortical astrocytes, adapted from 4CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference4: soma diameter and GFAP+ primary-process count are shown as separate bars because the two features are not commensurable on a single fold axis. (b)~Primate versus marsupial interlaminar astrocytes, adapted from 4CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference5... -
4CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference6 Human / primate astrocyte morphometry, split by measurement. (a)~Human versus rodent protoplasmic cortical astrocytes, adapted from 4CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference7: soma diameter and GFAP+ primary-process count are shown as separate bars because the two features are not commensurable on a single fold axis. (b)~Primate versus marsupial interlaminar astrocytes, adapted from 4CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference8... -
4CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference9 Calcium-wave propagation speed follows the morphology. 5CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference0 used line scanning in chimeric mice to measure intracellular Ca2+ wave velocity of 15.8~±~0.7~μm s-1 in engrafted human astrocytes versus 5.7~±~0.4~μm s-1 in the same animals’ resident murine astrocytes (n~=~22–34 cells per group; Figure{ref}fig:sec12-wavespeed). Two independent measurements bracket... -
5CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference1 Calcium-wave propagation speed follows the morphology. 5CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference2 used line scanning in chimeric mice to measure intracellular Ca2+ wave velocity of 15.8~±~0.7~μm s-1 in engrafted human astrocytes versus 5.7~±~0.4~μm s-1 in the same animals’ resident murine astrocytes (n~=~22–34 cells per group; Figure{ref}fig:sec12-wavespeed). Two independent measurements bracket... -
5CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference3 Calcium-wave propagation speed follows the morphology. 5CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference4 used line scanning in chimeric mice to measure intracellular Ca2+ wave velocity of 15.8~±~0.7~μm s-1 in engrafted human astrocytes versus 5.7~±~0.4~μm s-1 in the same animals’ resident murine astrocytes (n~=~22–34 cells per group; Figure{ref}fig:sec12-wavespeed). Two independent measurements bracket... -
5CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference5 Human versus rodent astrocyte Ca2+-wave propagation speed across two preparations. (a)~Acute adult human cortical slice (5CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference6): protoplasmic astrocytes propagate Ca2+ waves at 36~μm s-1, approximately fourfold faster than rodent protoplasmic astrocytes measured in the same study with bolus-loaded multicell Ca2+ imaging. (b)~Chimeric-mouse... -
5CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference7 Human versus rodent astrocyte Ca2+-wave propagation speed across two preparations. (a)~Acute adult human cortical slice (5CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference8): protoplasmic astrocytes propagate Ca2+ waves at 36~μm s-1, approximately fourfold faster than rodent protoplasmic astrocytes measured in the same study with bolus-loaded multicell Ca2+ imaging. (b)~Chimeric-mouse... -
5CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference9 When human glial progenitor cells are engrafted neonatally into mouse forebrain, they outcompete the host glia: 6CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference0 reported that by 7–10 months most forebrain astrocytes and OPCs were of human origin, and 6CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference1 showed that the same protocol produces myelinating human oligodendrocytes in hypomyelinated hosts. 6CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference2 further observed enhanced long-term potentiation in the... -
6CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference3 When human glial progenitor cells are engrafted neonatally into mouse forebrain, they outcompete the host glia: 6CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference4 reported that by 7–10 months most forebrain astrocytes and OPCs were of human origin, and 6CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference5 showed that the same protocol produces myelinating human oligodendrocytes in hypomyelinated hosts. 6CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference6 further observed enhanced long-term potentiation in the... -
6CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference7 When human glial progenitor cells are engrafted neonatally into mouse forebrain, they outcompete the host glia: 6CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference8 reported that by 7–10 months most forebrain astrocytes and OPCs were of human origin, and 6CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference9 showed that the same protocol produces myelinating human oligodendrocytes in hypomyelinated hosts. 1CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference0 further observed enhanced long-term potentiation in the... -
1CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference1 When human glial progenitor cells are engrafted neonatally into mouse forebrain, they outcompete the host glia: 1CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference2 reported that by 7–10 months most forebrain astrocytes and OPCs were of human origin, and 1CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference3 showed that the same protocol produces myelinating human oligodendrocytes in hypomyelinated hosts. 1CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference4 further observed enhanced long-term potentiation in the... -
1CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference5 When human glial progenitor cells are engrafted neonatally into mouse forebrain, they outcompete the host glia: 1CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference6 reported that by 7–10 months most forebrain astrocytes and OPCs were of human origin, and 1CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference7 showed that the same protocol produces myelinating human oligodendrocytes in hypomyelinated hosts. 1CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference8 further observed enhanced long-term potentiation in the... -
1CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference9 When human glial progenitor cells are engrafted neonatally into mouse forebrain, they outcompete the host glia: 1CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference0 reported that by 7–10 months most forebrain astrocytes and OPCs were of human origin, and 1CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference1 showed that the same protocol produces myelinating human oligodendrocytes in hypomyelinated hosts. 1CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference2 further observed enhanced long-term potentiation in the... -
1CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference3 When human glial progenitor cells are engrafted neonatally into mouse forebrain, they outcompete the host glia: 1CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference4 reported that by 7–10 months most forebrain astrocytes and OPCs were of human origin, and 1CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference5 showed that the same protocol produces myelinating human oligodendrocytes in hypomyelinated hosts. 1CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference6 further observed enhanced long-term potentiation in the... -
1CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference7 These results consistently argue that astrocytes contribute substantively to circuit-level plasticity and behaviour; they should be interpreted with three caveats. First, engrafted human cells mature in a developmentally and environmentally non-native brain. Second, the gain-of-function readouts are generally single-laboratory. Third, in vitro human astrocyte models — hPSC monolayers 1CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference8, co... -
1CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference9 These results consistently argue that astrocytes contribute substantively to circuit-level plasticity and behaviour; they should be interpreted with three caveats. First, engrafted human cells mature in a developmentally and environmentally non-native brain. Second, the gain-of-function readouts are generally single-laboratory. Third, in vitro human astrocyte models — hPSC monolayers 3CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference0, co... -
3CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference1 These results consistently argue that astrocytes contribute substantively to circuit-level plasticity and behaviour; they should be interpreted with three caveats. First, engrafted human cells mature in a developmentally and environmentally non-native brain. Second, the gain-of-function readouts are generally single-laboratory. Third, in vitro human astrocyte models — hPSC monolayers 3CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference2, co... -
3CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference3 These results consistently argue that astrocytes contribute substantively to circuit-level plasticity and behaviour; they should be interpreted with three caveats. First, engrafted human cells mature in a developmentally and environmentally non-native brain. Second, the gain-of-function readouts are generally single-laboratory. Third, in vitro human astrocyte models — hPSC monolayers 3CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference4, co... -
3CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference5 These results consistently argue that astrocytes contribute substantively to circuit-level plasticity and behaviour; they should be interpreted with three caveats. First, engrafted human cells mature in a developmentally and environmentally non-native brain. Second, the gain-of-function readouts are generally single-laboratory. Third, in vitro human astrocyte models — hPSC monolayers 3CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference6, co... -
3CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference7 These results consistently argue that astrocytes contribute substantively to circuit-level plasticity and behaviour; they should be interpreted with three caveats. First, engrafted human cells mature in a developmentally and environmentally non-native brain. Second, the gain-of-function readouts are generally single-laboratory. Third, in vitro human astrocyte models — hPSC monolayers 3CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference8, co... -
3CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference9 These results consistently argue that astrocytes contribute substantively to circuit-level plasticity and behaviour; they should be interpreted with three caveats. First, engrafted human cells mature in a developmentally and environmentally non-native brain. Second, the gain-of-function readouts are generally single-laboratory. Third, in vitro human astrocyte models — hPSC monolayers 3CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference0, co... -
3CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference1 These results consistently argue that astrocytes contribute substantively to circuit-level plasticity and behaviour; they should be interpreted with three caveats. First, engrafted human cells mature in a developmentally and environmentally non-native brain. Second, the gain-of-function readouts are generally single-laboratory. Third, in vitro human astrocyte models — hPSC monolayers 3CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference2, co... -
3CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference3 Alzheimer’s is the best-studied disease context for astrocytes. 3CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference4 used in vivo two-photon imaging in APP/PS1 mice to show that resting cytosolic [Ca2+] in cortical astrocytes is elevated (81 versus 149 nM in controls vs APP/PS1; single-laboratory measurement) and that Ca2+ waves emanate preferentially from plaque-associated astrocytes. Related values from [shi_2017_scit... -
3CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference5 Alzheimer’s is the best-studied disease context for astrocytes. 3CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference6 used in vivo two-photon imaging in APP/PS1 mice to show that resting cytosolic [Ca2+] in cortical astrocytes is elevated (81 versus 149 nM in controls vs APP/PS1; single-laboratory measurement) and that Ca2+ waves emanate preferentially from plaque-associated astrocytes. Related values from [shi_2017_scit... -
3CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference7 Alzheimer’s is the best-studied disease context for astrocytes. 3CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference8 used in vivo two-photon imaging in APP/PS1 mice to show that resting cytosolic [Ca2+] in cortical astrocytes is elevated (81 versus 149 nM in controls vs APP/PS1; single-laboratory measurement) and that Ca2+ waves emanate preferentially from plaque-associated astrocytes. Related values from [shi_2017_scit... -
3CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference9 Complement and ApoE now sit at the centre of astrocyte–microglia disease communication. 2CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference00 showed that NFκB-activated astrocytes release C3, which acts on neuronal C3aR to disrupt dendritic morphology; 2CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference01 extended this to tauopathy, where astrocytic C3 correlates with cognitive decline and Braak staging, and C3aR1 deletion in PS19 mice rescues tau pathology. [reichenbach_2019_... -
2CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference02 Complement and ApoE now sit at the centre of astrocyte–microglia disease communication. 2CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference03 showed that NFκB-activated astrocytes release C3, which acts on neuronal C3aR to disrupt dendritic morphology; 2CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference04 extended this to tauopathy, where astrocytic C3 correlates with cognitive decline and Braak staging, and C3aR1 deletion in PS19 mice rescues tau pathology. [reichenbach_2019_... -
2CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference05 Complement and ApoE now sit at the centre of astrocyte–microglia disease communication. 2CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference06 showed that NFκB-activated astrocytes release C3, which acts on neuronal C3aR to disrupt dendritic morphology; 2CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference07 extended this to tauopathy, where astrocytic C3 correlates with cognitive decline and Braak staging, and C3aR1 deletion in PS19 mice rescues tau pathology. [reichenbach_2019_... -
2CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference08 Complement and ApoE now sit at the centre of astrocyte–microglia disease communication. 2CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference09 showed that NFκB-activated astrocytes release C3, which acts on neuronal C3aR to disrupt dendritic morphology; 2CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference10 extended this to tauopathy, where astrocytic C3 correlates with cognitive decline and Braak staging, and C3aR1 deletion in PS19 mice rescues tau pathology. [reichenbach_2019_... -
2CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference11 Complement and ApoE now sit at the centre of astrocyte–microglia disease communication. 2CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference12 showed that NFκB-activated astrocytes release C3, which acts on neuronal C3aR to disrupt dendritic morphology; 2CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference13 extended this to tauopathy, where astrocytic C3 correlates with cognitive decline and Braak staging, and C3aR1 deletion in PS19 mice rescues tau pathology. [reichenbach_2019_... -
2CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference14 Complement and ApoE now sit at the centre of astrocyte–microglia disease communication. 2CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference15 showed that NFκB-activated astrocytes release C3, which acts on neuronal C3aR to disrupt dendritic morphology; 2CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference16 extended this to tauopathy, where astrocytic C3 correlates with cognitive decline and Braak staging, and C3aR1 deletion in PS19 mice rescues tau pathology. [reichenbach_2019_... -
2CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference17 Complement and ApoE now sit at the centre of astrocyte–microglia disease communication. 2CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference18 showed that NFκB-activated astrocytes release C3, which acts on neuronal C3aR to disrupt dendritic morphology; 2CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference19 extended this to tauopathy, where astrocytic C3 correlates with cognitive decline and Braak staging, and C3aR1 deletion in PS19 mice rescues tau pathology. [reichenbach_2019_... -
2CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference20 Complement and ApoE now sit at the centre of astrocyte–microglia disease communication. 2CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference21 showed that NFκB-activated astrocytes release C3, which acts on neuronal C3aR to disrupt dendritic morphology; 2CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference22 extended this to tauopathy, where astrocytic C3 correlates with cognitive decline and Braak staging, and C3aR1 deletion in PS19 mice rescues tau pathology. [reichenbach_2019_... -
2CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference23 Complement and ApoE now sit at the centre of astrocyte–microglia disease communication. 2CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference24 showed that NFκB-activated astrocytes release C3, which acts on neuronal C3aR to disrupt dendritic morphology; 2CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference25 extended this to tauopathy, where astrocytic C3 correlates with cognitive decline and Braak staging, and C3aR1 deletion in PS19 mice rescues tau pathology. [reichenbach_2019_... -
2CitationIf region matters, species and disease matter more. Section {ref}
sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference26 Complement and ApoE now sit at the centre of astrocyte–microglia disease communication. 2CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference27 showed that NFκB-activated astrocytes release C3, which acts on neuronal C3aR to disrupt dendritic morphology; 2CitationIf region matters, species and disease matter more. Section {ref}sec:regional-diversityshowed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim2009jneu...content/12_species_human_disease.md:line 4Open reference28 extended this to tauopathy, where astrocytic C3 correlates with cognitive decline and Braak staging, and C3aR1 deletion in PS19 mice rescues tau pathology. [reichenbach_2019_... -
... 46 additional anchors in refs_json
References
- [oberheim_2009_jneurosci] “If region matters, species and disease matter more. Section {ref}`sec:regional-diversity` showed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim_2009_jneu...”
- [falcone_2019_jcomparative] “If region matters, species and disease matter more. Section {ref}`sec:regional-diversity` showed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim_2009_jneu...”
- [vasile_2017_brainstruct] “If region matters, species and disease matter more. Section {ref}`sec:regional-diversity` showed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim_2009_jneu...”
- [han_2013_cellstem] “If region matters, species and disease matter more. Section {ref}`sec:regional-diversity` showed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim_2009_jneu...”
- [goldman_2015_glia] “If region matters, species and disease matter more. Section {ref}`sec:regional-diversity` showed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim_2009_jneu...”
- [escartin_2021_natneurosci] “If region matters, species and disease matter more. Section {ref}`sec:regional-diversity` showed that cortex, hippocampus, striatum, and cerebellum are not interchangeable substrates for astrocyte function; moving from rodent to human adds a second, generally larger layer of non-transferability. Human cortical astrocytes are larger, more complex, and carry subtypes that rodents simply do not have [oberheim_2009_jneu...”
- [preman_2021_molneurodegeneration] “The morphological contrast was quantified by [oberheim_2009_jneurosci], who reported that protoplasmic astrocytes in human neocortex are 2.6-fold larger in diameter and extend roughly 10-fold more GFAP<sup>+</sup> primary processes than their rodent counterparts (Figure {ref}`fig:sec12-morphometry`a). [vasile_2017_brainstruct] re-examined this comparison in adult human cortex and confirmed longer processes and large...”
- [falcone_2021_cerebral] “Beyond raw size, humans and other primates possess morphological classes that are absent from rodents. [oberheim_2009_jneurosci] described *interlaminar* astrocytes, whose cell bodies sit in layer I and extend long processes perpendicular to the pial surface, and *varicose-projection* astrocytes of layers V–VI. Surveying 46 mammalian species, [falcone_2019_jcomparative] found that *typical* pial interlaminar astrocy...”
- [mariani_2019_methods] “When human glial progenitor cells are engrafted neonatally into mouse forebrain, they outcompete the host glia: [goldman_2015_glia] reported that by 7–10 months most forebrain astrocytes and OPCs were of human origin, and [mariani_2019_methods] showed that the same protocol produces myelinating human oligodendrocytes in hypomyelinated hosts. [goldman_2015_glia] further observed enhanced long-term potentiation in the...”
- [benraiss_2016_natcommun] “When human glial progenitor cells are engrafted neonatally into mouse forebrain, they outcompete the host glia: [goldman_2015_glia] reported that by 7–10 months most forebrain astrocytes and OPCs were of human origin, and [mariani_2019_methods] showed that the same protocol produces myelinating human oligodendrocytes in hypomyelinated hosts. [goldman_2015_glia] further observed enhanced long-term potentiation in the...”
- [park_2021_cellproliferation] “When human glial progenitor cells are engrafted neonatally into mouse forebrain, they outcompete the host glia: [goldman_2015_glia] reported that by 7–10 months most forebrain astrocytes and OPCs were of human origin, and [mariani_2019_methods] showed that the same protocol produces myelinating human oligodendrocytes in hypomyelinated hosts. [goldman_2015_glia] further observed enhanced long-term potentiation in the...”
- [windrem_2017_cellstem] “When human glial progenitor cells are engrafted neonatally into mouse forebrain, they outcompete the host glia: [goldman_2015_glia] reported that by 7–10 months most forebrain astrocytes and OPCs were of human origin, and [mariani_2019_methods] showed that the same protocol produces myelinating human oligodendrocytes in hypomyelinated hosts. [goldman_2015_glia] further observed enhanced long-term potentiation in the...”
- [krencik_2011_natbiotechnol] “These results consistently argue that astrocytes contribute substantively to circuit-level plasticity and behaviour; they should be interpreted with three caveats. First, engrafted human cells mature in a developmentally and environmentally non-native brain. Second, the gain-of-function readouts are generally single-laboratory. Third, in vitro human astrocyte models — hPSC monolayers [krencik_2011_natbiotechnol], co...”
- [pasca_2015_natmethods] “These results consistently argue that astrocytes contribute substantively to circuit-level plasticity and behaviour; they should be interpreted with three caveats. First, engrafted human cells mature in a developmentally and environmentally non-native brain. Second, the gain-of-function readouts are generally single-laboratory. Third, in vitro human astrocyte models — hPSC monolayers [krencik_2011_natbiotechnol], co...”
- [sloan_2017_neuron] “These results consistently argue that astrocytes contribute substantively to circuit-level plasticity and behaviour; they should be interpreted with three caveats. First, engrafted human cells mature in a developmentally and environmentally non-native brain. Second, the gain-of-function readouts are generally single-laboratory. Third, in vitro human astrocyte models — hPSC monolayers [krencik_2011_natbiotechnol], co...”
- [qian_2020_cellstem] “These results consistently argue that astrocytes contribute substantively to circuit-level plasticity and behaviour; they should be interpreted with three caveats. First, engrafted human cells mature in a developmentally and environmentally non-native brain. Second, the gain-of-function readouts are generally single-laboratory. Third, in vitro human astrocyte models — hPSC monolayers [krencik_2011_natbiotechnol], co...”
- [zhang_2016_neuron] “These results consistently argue that astrocytes contribute substantively to circuit-level plasticity and behaviour; they should be interpreted with three caveats. First, engrafted human cells mature in a developmentally and environmentally non-native brain. Second, the gain-of-function readouts are generally single-laboratory. Third, in vitro human astrocyte models — hPSC monolayers [krencik_2011_natbiotechnol], co...”
- [li_2020_molecularcellular] “These results consistently argue that astrocytes contribute substantively to circuit-level plasticity and behaviour; they should be interpreted with three caveats. First, engrafted human cells mature in a developmentally and environmentally non-native brain. Second, the gain-of-function readouts are generally single-laboratory. Third, in vitro human astrocyte models — hPSC monolayers [krencik_2011_natbiotechnol], co...”
- [chandrasekaran_2016_frontcell] “These results consistently argue that astrocytes contribute substantively to circuit-level plasticity and behaviour; they should be interpreted with three caveats. First, engrafted human cells mature in a developmentally and environmentally non-native brain. Second, the gain-of-function readouts are generally single-laboratory. Third, in vitro human astrocyte models — hPSC monolayers [krencik_2011_natbiotechnol], co...”
- [wang_2025_natbiotechnol] “These results consistently argue that astrocytes contribute substantively to circuit-level plasticity and behaviour; they should be interpreted with three caveats. First, engrafted human cells mature in a developmentally and environmentally non-native brain. Second, the gain-of-function readouts are generally single-laboratory. Third, in vitro human astrocyte models — hPSC monolayers [krencik_2011_natbiotechnol], co...”
- [kuchibhotla_2009_science] “Alzheimer's is the best-studied disease context for astrocytes. [kuchibhotla_2009_science] used in vivo two-photon imaging in APP/PS1 mice to show that resting cytosolic [Ca<sup>2+</sup>] in cortical astrocytes is elevated (81 versus 149 nM in controls vs APP/PS1; single-laboratory measurement) and that Ca<sup>2+</sup> waves emanate preferentially from plaque-associated astrocytes. Related values from [shi_2017_scit...”
- [shi_2017_scitransl] “Alzheimer's is the best-studied disease context for astrocytes. [kuchibhotla_2009_science] used in vivo two-photon imaging in APP/PS1 mice to show that resting cytosolic [Ca<sup>2+</sup>] in cortical astrocytes is elevated (81 versus 149 nM in controls vs APP/PS1; single-laboratory measurement) and that Ca<sup>2+</sup> waves emanate preferentially from plaque-associated astrocytes. Related values from [shi_2017_scit...”
- [fernandezcalle_2022_molneurodegeneration] “Alzheimer's is the best-studied disease context for astrocytes. [kuchibhotla_2009_science] used in vivo two-photon imaging in APP/PS1 mice to show that resting cytosolic [Ca<sup>2+</sup>] in cortical astrocytes is elevated (81 versus 149 nM in controls vs APP/PS1; single-laboratory measurement) and that Ca<sup>2+</sup> waves emanate preferentially from plaque-associated astrocytes. Related values from [shi_2017_scit...”
- [lian_2015_neuron] “Complement and ApoE now sit at the centre of astrocyte–microglia disease communication. [lian_2015_neuron] showed that NF$κ$B-activated astrocytes release C3, which acts on neuronal C3aR to disrupt dendritic morphology; [litvinchuk_2018_neuron] extended this to tauopathy, where astrocytic C3 correlates with cognitive decline and Braak staging, and C3aR1 deletion in PS19 mice rescues tau pathology. [reichenbach_2019_...”
- [litvinchuk_2018_neuron] “Complement and ApoE now sit at the centre of astrocyte–microglia disease communication. [lian_2015_neuron] showed that NF$κ$B-activated astrocytes release C3, which acts on neuronal C3aR to disrupt dendritic morphology; [litvinchuk_2018_neuron] extended this to tauopathy, where astrocytic C3 correlates with cognitive decline and Braak staging, and C3aR1 deletion in PS19 mice rescues tau pathology. [reichenbach_2019_...”
- [reichenbach_2019_embomol] “Complement and ApoE now sit at the centre of astrocyte–microglia disease communication. [lian_2015_neuron] showed that NF$κ$B-activated astrocytes release C3, which acts on neuronal C3aR to disrupt dendritic morphology; [litvinchuk_2018_neuron] extended this to tauopathy, where astrocytic C3 correlates with cognitive decline and Braak staging, and C3aR1 deletion in PS19 mice rescues tau pathology. [reichenbach_2019_...”
- [toledano_2024_brainsciences] “Complement and ApoE now sit at the centre of astrocyte–microglia disease communication. [lian_2015_neuron] showed that NF$κ$B-activated astrocytes release C3, which acts on neuronal C3aR to disrupt dendritic morphology; [litvinchuk_2018_neuron] extended this to tauopathy, where astrocytic C3 correlates with cognitive decline and Braak staging, and C3aR1 deletion in PS19 mice rescues tau pathology. [reichenbach_2019_...”
- [chiarini_2020_ijms] “Complement and ApoE now sit at the centre of astrocyte–microglia disease communication. [lian_2015_neuron] showed that NF$κ$B-activated astrocytes release C3, which acts on neuronal C3aR to disrupt dendritic morphology; [litvinchuk_2018_neuron] extended this to tauopathy, where astrocytic C3 correlates with cognitive decline and Braak staging, and C3aR1 deletion in PS19 mice rescues tau pathology. [reichenbach_2019_...”
- [gonzalezreyes_2017_frontmol] “Complement and ApoE now sit at the centre of astrocyte–microglia disease communication. [lian_2015_neuron] showed that NF$κ$B-activated astrocytes release C3, which acts on neuronal C3aR to disrupt dendritic morphology; [litvinchuk_2018_neuron] extended this to tauopathy, where astrocytic C3 correlates with cognitive decline and Braak staging, and C3aR1 deletion in PS19 mice rescues tau pathology. [reichenbach_2019_...”
- [guo_2020_molneurodegeneration] “Complement and ApoE now sit at the centre of astrocyte–microglia disease communication. [lian_2015_neuron] showed that NF$κ$B-activated astrocytes release C3, which acts on neuronal C3aR to disrupt dendritic morphology; [litvinchuk_2018_neuron] extended this to tauopathy, where astrocytic C3 correlates with cognitive decline and Braak staging, and C3aR1 deletion in PS19 mice rescues tau pathology. [reichenbach_2019_...”
- [lin_2018_neuron] “Complement and ApoE now sit at the centre of astrocyte–microglia disease communication. [lian_2015_neuron] showed that NF$κ$B-activated astrocytes release C3, which acts on neuronal C3aR to disrupt dendritic morphology; [litvinchuk_2018_neuron] extended this to tauopathy, where astrocytic C3 correlates with cognitive decline and Braak staging, and C3aR1 deletion in PS19 mice rescues tau pathology. [reichenbach_2019_...”
- [serranopozo_2021_lancetneurology] “Complement and ApoE now sit at the centre of astrocyte–microglia disease communication. [lian_2015_neuron] showed that NF$κ$B-activated astrocytes release C3, which acts on neuronal C3aR to disrupt dendritic morphology; [litvinchuk_2018_neuron] extended this to tauopathy, where astrocytic C3 correlates with cognitive decline and Braak staging, and C3aR1 deletion in PS19 mice rescues tau pathology. [reichenbach_2019_...”
- [habib_2020_natneurosci] “Complement and ApoE now sit at the centre of astrocyte–microglia disease communication. [lian_2015_neuron] showed that NF$κ$B-activated astrocytes release C3, which acts on neuronal C3aR to disrupt dendritic morphology; [litvinchuk_2018_neuron] extended this to tauopathy, where astrocytic C3 correlates with cognitive decline and Braak staging, and C3aR1 deletion in PS19 mice rescues tau pathology. [reichenbach_2019_...”
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