Antibodies against extracellular tau block seeding, diminish brain pathology, and may improve cognition in a mouse model.
A new study finds that the cancer drug imatinib does not lower Aβ in humans, casting doubt on a previously described relationship between imatinib, γ-secretase activating protein (GSAP), and Aβ.
Changing ApoE levels in midlife influences Aβ pathology in mice, supporting an ApoE-oriented therapeutic strategy in Alzheimer’s disease.
Neural activity sends amyloid precursor proteins into endosomes where β-secretase drives Alzheimer pathology.
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.
Tau and amyloid PET tracers demonstrate potential to sharpen the diagnosis of Alzheimer’s disease and frontotemporal dementias.
In mouse models, the Alzheimer’s risk gene TREM2 affects microglial behavior but does not lead to more amyloid deposition.
A study suggests that genes involved in Aβ production and endocytosis mediate ApoE4’s role in Alzheimer’s disease.
A new study proposes microtubule-chopping enzymes as the missing link in the cascade of pathology leading from Aβ to tau to neuronal death.
The latest data on TREM2 confirm that a variant in the gene associates with AD, and link it to Parkinson’s, brain degeneration, and γ-secretase.
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.
Known for his contributions to the fundamental understanding of the tau protein, Skip Binder leaves his mark on the Alzheimer's field.