Much like people with Alzheimer's, mice modelling the disease experience seizures. New research suggests that APP, and not Aβ, makes their neurons hyperexcitable.
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.
An antibody against ApoE helps clear plaques and improves cognition in AD model mice.
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.
Hardening of the arteries correlated with greater amyloid deposition in a longitudinal study, strengthening ties between cardiovascular disease and Alzheimer’s.
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.
Astrocytes kindle neuronal hyperexcitability in mouse models of Huntington’s.
If new results hold up, enhanced phosphorylation of a ribosomal protein may explain the toxicity of mutations that cause Parkinson's.
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.
A small longitudinal study suggests that atrophy begins in the frontoparietal cortex, not the hippocampus, in early Alzheimer's.
A single dose of a commonly prescribed antidepressant suppresses Aβ production in the human central nervous system.