In mouse models, the Alzheimer’s risk gene TREM2 affects microglial behavior but does not lead to more amyloid deposition.
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.
New research suggests that dendritic tau may participate in synaptic plasticity, and that Aβ disrupts this function.
A drug candidate for Alzheimer’s aims to make cell trafficking more efficient, reduce Aβ production.
IMAGINE that: Amyloid deposition shrinks in both treatment and placebo groups, dealing a blow to the anti-aggregation drug PBT2.
An antibody against ApoE helps clear plaques and improves cognition in AD model mice.
Hardening of the arteries correlated with greater amyloid deposition in a longitudinal study, strengthening ties between cardiovascular disease and Alzheimer’s.
Conformations of misfolded tau survive injection from one mouse to the next, a property shared by prions.
Tau and amyloid PET tracers demonstrate potential to sharpen the diagnosis of Alzheimer’s disease and frontotemporal dementias.
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.
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.
Death receptor role in Alzheimer's disease looks less likely than was originally thought following a high-profile paper in 2009.
X-ray crystallography reveals secrets of the glutamate receptor.