At AAIC 2013, researchers present the latest genetic risk factors for Alzheimer's disease.
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.
As NIH researchers are preparing to return to their laboratories, Alzheimer's researchers warn about the greater consequences of cutting already limited resources.
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.
Sleeping in an MRI scanner, babies with ApoE4 genotype reveal myelination and structural differences in brain areas affected in people with Alzheimer’s disease.
Researchers identify a transcription factor that protects neurons during normal aging but goes AWOL in Alzheimer’s brains.
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.
Studies support the idea that mitochondrial changes drive aging and AD pathogenesis.
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.
Allegations of falsified data embroil Japanese ADNI; project leaders respond that data corrections followed quality-control procedures.