{
"papers": [
{
"doi": "10.1186/s40478-025-02000-4",
"value": "10%",
"method": "immunohistochemistry/in situ hybridization",
"metric": "SST neuron loss or dysfunction in neurodegeneration",
"cite_key": "Weidling2025",
"condition": "neurodegeneration",
"study_system": "rat, cortex",
"value_source_sentence": "On day 17, hiPSC-derived neural progenitor cells (hiPSC-NPCs) were collected with Accutase, resuspended in N2B27 medium (Advanced DMEM/F12, Neurobasal medium, N2 supplement, B27 supplement without vitamin A, pen/strep, GlutaMax; Thermo Fisher) + 10% DMSO at 10 million cells per mL, and frozen overni"
},
{
"doi": "10.1186/s40246-025-00875-x",
"value": "1.5%",
"method": "immunohistochemistry/in situ hybridization",
"metric": "SST neuron loss or dysfunction in neurodegeneration",
"cite_key": "Bayaraa2025",
"condition": "neurodegeneration",
"study_system": "human, cortex (Alzheimer's)",
"value_source_sentence": "Immunofluorescence staining of adjacent tissue sections The tissue sections mounted on charged slide were fixed in 1.5% paraformaldehyde (PFA) for 15 min and stained with a primary antibody solution (0.25% Triton and 4% BSA) containing mouse anti-β-amyloid antibody 6E10 at 1:10 dilution (BioLegend C"
},
{
"doi": "10.1124/pharmrev.124.001117",
"value": "95%",
"method": "immunohistochemistry/in situ hybridization",
"metric": "SST neuron loss or dysfunction in neurodegeneration",
"cite_key": "Sandoval2024",
"condition": "neurodegeneration",
"study_system": "rat, cortex",
"value_source_sentence": "AD diagnosis at age 65 or older is classified as late-onset AD (LOAD) and accounts for more than 95% of occurrences."
},
{
"doi": "10.3389/fnagi.2025.1542229",
"value": "60%",
"method": "immunohistochemistry/in situ hybridization",
"metric": "SST neuron loss or dysfunction in neurodegeneration",
"cite_key": "Futacsi2025",
"condition": "neurodegeneration",
"study_system": "rat, cortex",
"value_source_sentence": "Animals were group housed under a standard 12-h light/dark cycle at 24 ± 2°C with relative humidity of 50–60%."
},
{
"doi": "10.3389/fnins.2024.1503069",
"value": "30%",
"method": "immunohistochemistry/in situ hybridization",
"metric": "SST neuron loss or dysfunction in neurodegeneration",
"cite_key": "Elhabbari2024",
"condition": "neurodegeneration",
"study_system": "human, cortex",
"value_source_sentence": "Alzheimer’s disease (AD) is a critical public health issue and the leading cause of dementia, with an estimated 32 million persons suffering from AD dementia globally ( Gustavsson et al., 2023 ), constituting between 10 and 30% of individuals above the age of 65 ( Masters et al., 2015 ; Prince et a"
},
{
"doi": "10.1186/s13024-025-00892-3",
"value": "10%",
"method": "immunohistochemistry/in situ hybridization",
"metric": "SST neuron loss or dysfunction in neurodegeneration",
"cite_key": "Castanho2025b",
"condition": "neurodegeneration",
"study_system": "rat, cortex",
"value_source_sentence": "Given that transcriptomic changes in DLPFC are more moderate compared to other brain regions [ 36 ], DEGs were determined using FDR < 0.1 and |log2FC| > log2(1.1) cut-offs (at least 10% difference in absolute expression)."
},
{
"doi": "10.1186/s40035-022-00300-6",
"value": "70%",
"method": "immunohistochemistry/in situ hybridization",
"metric": "SST neuron loss or dysfunction in neurodegeneration",
"cite_key": "Morrone2022",
"condition": "neurodegeneration",
"study_system": "rat, cortex",
"value_source_sentence": "Notably, somatostatin (SST) and parvalbumin (PVB) cells account for ~ 70% of interneurons, and provide dendritic and somatic inhibition, respectively, to regulate excitatory activity and cognition [ 6 , 9 , 10 ]."
},
{
"doi": "10.1002/alz.14552",
"value": "significant decrease",
"method": "immunohistochemistry/in situ hybridization",
"metric": "SST neuron loss or dysfunction in neurodegeneration",
"cite_key": "Ren2025",
"condition": "neurodegeneration",
"study_system": "rat, cortex",
"value_source_sentence": "7 \n , \n 26 \n , \n 27 \n , \n 28 \n A significant decrease in PV+ neurons has been detected in the prefrontal cortex of 6‐month‐old AD animals; a preferential vulnerability of SOM+ neurons was evident in the olfactory cortex and hippocampus, but not in the prefrontal cortex."
}
],
"comparison_id": "sst-vulnerability-neurodegeneration",
"comparison_name": "SST Interneuron Vulnerability Across Neurodegenerative Conditions",
"comparison_type": "cross-study conflict",
"what_it_reveals": "SST interneurons show differential vulnerability depending on the neurodegenerative condition and brain region. This comparison reveals whether SST vulnerability is a general phenomenon or disease-specific.",
"homogeneity_check": {
"caveats": "Different diseases, different stages, different brain regions. Mouse models vs human postmortem. Detection methods affect apparent vulnerability.",
"comparable": false,
"n_definition": "postmortem brains or mouse model animals",
"scope_region": "variable (cortex, hippocampus)",
"taxonomic_level": "SST+ cell type",
"scope_population": "SST+ neurons in AD/FTD"
},
"suggested_plot_type": "grouped bar"
}