Much like people with Alzheimer's, mice modelling the disease experience seizures. New research suggests that APP, and not Aβ, makes their neurons hyperexcitable.
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.
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 Phase 2 trial suggests that the drug PBT2 is generally safe for Huntington’s patients. The drug's sponsor says it may have improved cognition, though experts remain unconvinced.
Neurons in mice spit out monomeric tau when electrically stimulated, hinting that neural activity may help drive the spread of pathological forms of tau in the brain.
Superficial siderosis, a leakage of blood matter onto the outer surface of the cerebral cortex, may be linked to AD and other dementias.
Hardening of the arteries correlated with greater amyloid deposition in a longitudinal study, strengthening ties between cardiovascular disease and Alzheimer’s.
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.
Researchers identify a transcription factor that protects neurons during normal aging but goes AWOL in Alzheimer’s brains.