Conformations of misfolded tau survive injection from one mouse to the next, a property shared by prions.
Alpha-secretase does not necessarily pick up the slack when β-secretase cleavage of amyloid precursor protein wanes, a study in primates finds. It suggests APP can be processed in other ways.
The insoluble proteome from Alzheimer’s brains points to RNA processing proteins as a novel component of aggregates.
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.
Tau and amyloid PET tracers demonstrate potential to sharpen the diagnosis of Alzheimer’s disease and frontotemporal dementias.
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.
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.
As NIH researchers are preparing to return to their laboratories, Alzheimer's researchers warn about the greater consequences of cutting already limited resources.
People with previous head injuries may be more prone to amyloid deposition and have a higher risk for Alzheimer's.
Researchers have sliced and digitally reassembled a famous brain in neuroscience to view its detailed three-dimensional architecture.
Live imaging of the mouse brain offers a rare view of α-synuclein dynamics at presynaptic terminals, and raises questions about which form of the protein triggers synaptic dysfunction.
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.
Sleeping in an MRI scanner, babies with ApoE4 genotype reveal myelination and structural differences in brain areas affected in people with Alzheimer’s disease.
Plenty of genetic risk factors for sporadic ALS are still waiting to be found, according to a new meta-analysis of GWAS data.