Tau regulates mitochondrial reverse electron transport, producing excess reactive oxygen species and driving neurodegeneration in tauopathies.
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Tau regulates mitochondrial reverse electron transport, producing excess reactive oxygen species and driving neurodegeneration in tauopathies.
Hepatic expression of APOE3 Christchurch reduces amyloid-β burden and AD pathologies in APOE4-expressing APP/PS1 mice.
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Group II p21-activated kinases (PAKs) are identified as regulators of regional vulnerability to α-synuclein pathology in Parkinson's disease models.
Microglia in human forebrain organoids mediate amyloid-β clearance, recruit CD8+ T cells via CCL4/5 signaling, and establish a neuroinflammatory feedback loop in Alzheimer’s disease models.
A non-canonical reactive astrocyte state (Ast10) is linked to neuropathologies and cognitive decline in Alzheimer's disease across diverse human brains.
Reducing ataxin-2 activates stress-adaptive metabolic pathways in neurons and astrocytes, providing broad protection against TDP-43 toxicity in ALS models.
Amyloid clearance after aducanumab treatment is linked to reduced tau pathology and slower cortical atrophy in Alzheimer disease.
Cytoplasmic TDP-43 gain-of-function causes splicing abnormalities linked to ALS, FTLD, and AD, including APP isoform disruption, across all three diseases.
Mendelian randomization and multiomics analyses identified 19 druggable targets for Alzheimer's disease, including protective variants in EPHX2, in individuals of European and African ancestry.
Hepatic expression of APOE3 Christchurch reduces amyloid-β burden and AD pathologies in APOE4-expressing APP/PS1 mice.
A single Centiloid cutoff of 18 best distinguishes amyloid positivity in PET scans across diverse studies, with a high predictive value for visual reads.
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