Researchers identify a transcription factor that protects neurons during normal aging but goes AWOL in Alzheimer’s brains.
Despite ample evidence implicating Aβ in Alzheimer’s pathology, scientists still struggle to understand how the peptide harms the brain.
Neural activity sends amyloid precursor proteins into endosomes where β-secretase drives Alzheimer pathology.
A new study proposes microtubule-chopping enzymes as the missing link in the cascade of pathology leading from Aβ to tau to neuronal death.
Functional neuroimaging scans can pick up stark neural abnormalities in football players with repeated head injuries before their cognition drops much in executive function tests.
An astrocyte protein stymies toxic interplay between Aβ oligomers and prion proteins.
Changing ApoE levels in midlife influences Aβ pathology in mice, supporting an ApoE-oriented therapeutic strategy in Alzheimer’s disease.
Allegations of falsified data embroil Japanese ADNI; project leaders respond that data corrections followed quality-control procedures.
People with neurodegeneration but not brain amyloid surface in two new studies of preclinical AD, suggesting this odd population is both legitimate and potentially large.
Studies support the idea that mitochondrial changes drive aging and AD pathogenesis.
New research proposes a neuroimmune receptor as the latest Aβ binding partner.
The first report on PBB3, the latest tau ligand for brain imaging under development, suggests it binds all types of tau aggregate.
Rare mutations in the ADAM10 gene make a genetic case for the amyloid cascade as a cause of late onset Alzheimer's disease.
A single dose of a commonly prescribed antidepressant suppresses Aβ production in the human central nervous system.
Protein strains may underlie different tauopathies, according to researchers presented at this year's AAIC meeting in Boston.