A drug candidate for Alzheimer’s aims to make cell trafficking more efficient, reduce Aβ production.
An antibody against ApoE helps clear plaques and improves cognition in AD model mice.
IMAGINE that: Amyloid deposition shrinks in both treatment and placebo groups, dealing a blow to the anti-aggregation drug PBT2.
Tau and amyloid PET tracers demonstrate potential to sharpen the diagnosis of Alzheimer’s disease and frontotemporal dementias.
Conformations of misfolded tau survive injection from one mouse to the next, a property shared by prions.
Researchers identify a transcription factor that protects neurons during normal aging but goes AWOL in Alzheimer’s brains.
A single dose of a commonly prescribed antidepressant suppresses Aβ production in the human central nervous system.
Hardening of the arteries correlated with greater amyloid deposition in a longitudinal study, strengthening ties between cardiovascular disease and Alzheimer’s.
Scientists had the good fortune to study the exceedingly rare instance of a pair of identical twins, only one of whom had Trisomy 21. It turned out that gene regulation was altered across the entire genome in the twin with Down’s syndrome.
Deep-brain stimulation of the nucleus basalis of Meynert appeared safe and tolerable for Alzheimer’s patients.
Death receptor role in Alzheimer's disease looks less likely than was originally thought following a high-profile paper in 2009.
People with Alzheimer’s disease and other dementias may benefit from creative activities, but hard studies are still lacking.
The first longitudinal data from DIAN conflict with some cross-sectional findings, revealing a small drop in CSF injury markers after the first appearance of symptoms of disease.
The scientific spotlight often shines on excitatory neurons as the brain’s main Aβ factories. What about other cell types?
Low levels of 10 phospholipids in blood plasma correlated with future cognitive decline in older adults, hinting at diagnostic potential.