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30 results
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amyloid status. This two-pathway model explains regional dissociation of amyloid
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amyloid production, resulting in 70-80% amyloid reduction compared to 40-50% with
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amyloid plaques. Enhancing TREM2 signaling may restore neuroprotective microglial functions
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amyloid-β antibodies achieved remarkable therapeutic efficacy, with quantitative analysis
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amyloid pathology, single-cell RNA sequencing has revealed distinct microglial
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This hypothesis proposes that CYP46A1 overexpression gene therapy prevents neurodegeneration
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amyloid burden by 40% and improves cognitive performance in multiple
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amyloid proteins may interact with tau, amyloid-β, and huntingtin
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amyloid-β (Aβ), tissue plasminogen activator (tPA), and lactoferrin. The transcytotic
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Alpha-theta entrainment therapy targets somatostatin (SST) interneurons to restore
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amyloid cascade hypothesis predicts a long asymptomatic amyloid phase (10–20 years
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amyloid plaques compared to wild-type controls, with corresponding increases
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amyloid (positive amyloid PET scans) but preserved cognitive function or mild
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- Hypothesis LRP1/NLRP3/IL-1β Cascade Links Aβ Endocytosis to Inflammasome Activation and SPP1 Induction
amyloid-beta (Aβ) oligomer clearance and neuroinflammatory responses in neurodegenerative
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amyloid oligomers results in 3-4 fold higher complement gene
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amyloid clearance. Early-stage studies combining anti-amyloid antibodies with
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amyloid phagocytosis via MEGF10/MERTK. This preserves essential astrocyte homeostatic functions
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amyloid-beta oligomers and hyperphosphorylated tau proteins triggers a cascade
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amyloid-β (Aβ) peptides, particularly Aβ42, forming stable complexes that
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amyloid-beta oligomers (via anti-Aβ antibodies), tau aggregates (via anti
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- Hypothesis TFEB-mediated transcriptional upregulation of lysosomal genes as a therapeutic strategy for AD
amyloid-β (Aβ) peptides and hyperphosphorylated tau proteins overwhelms the cellular
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amyloid-beta oligomers preferentially impair PV interneurons by disrupting Nav1.1
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amyloid-beta oligomers directly impair PV interneuron function, SST interneurons
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amyloid plaque burden in APOE4 carriers treated with cholesterol efflux
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amyloid PET reaches cessation thresholds because p-tau217 reflects active
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amyloid pathology, SPP1 knockout results in 40-50% reduction in TREM2
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amyloid accumulation. [PMID:24806824]. 3. Astrocyte-secreted APOE3 clears amyloid
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amyloid-β aggregates. The accumulation of neutral lipids within cytoplasmic
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amyloid antibodies fused to LA repeats achieve 8-12 fold
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amyloid angiopathy (CAA) maintains a reservoir of vascular amyloid that
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