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.
In mouse models, the Alzheimer’s risk gene TREM2 affects microglial behavior but does not lead to more amyloid deposition.
A newly discovered lipid modification on the amyloid precursor protein may mark it for amyloidogenic processing...
Known for his contributions to the fundamental understanding of the tau protein, Skip Binder leaves his mark on the Alzheimer's field.
IMAGINE that: Amyloid deposition shrinks in both treatment and placebo groups, dealing a blow to the anti-aggregation drug PBT2.
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.
At AAIC 2013, researchers present the latest genetic risk factors for Alzheimer's disease.
The insoluble proteome from Alzheimer’s brains points to RNA processing proteins as a novel component of aggregates.
The NIH announced $45 million in new funding to support trials in preclinical Alzheimer’s populations, as well as efforts to identify new therapeutic targets.
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.
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.
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.