A small molecule inhibitor kills all microglia in the brain, but the cells rapidly repopulate from a previously unidentified progenitor cell.
A new study charges that, contrary to previous studies, seeding the mouse brain with aggregated α-synuclein does not trigger a toxic spread of PD-like inclusions in wild-type mice.
Sleeping in an MRI scanner, babies with ApoE4 genotype reveal myelination and structural differences in brain areas affected in people with Alzheimer’s disease.
A single dose of a commonly prescribed antidepressant suppresses Aβ production in the human central nervous system.
Researchers identify a transcription factor that protects neurons during normal aging but goes AWOL in Alzheimer’s brains.
It’s a scenario familiar to many clinicians: A patient diagnosed with mild cognitive impairment asks if he or she will eventually develop Alzheimer’s disease.
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.