In mouse models, the Alzheimer’s risk gene TREM2 affects microglial behavior but does not lead to more amyloid deposition.
Scientists report that astrocytes help neurons destroy their unwanted mitochondria.
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.
Plenty of genetic risk factors for sporadic ALS are still waiting to be found, according to a new meta-analysis of GWAS data.
Scientists have turned a yeast heat shock protein into a powerful disaggregase that attacks TDP-43, FUS, and α-synuclein mutants.
A man lacking ApoE appears to have no cognitive deficits, and his brain and CSF biomarker profiles appear normal. Some claim the findings support ApoE as a rational drug target for AD.
Mutated huntingtin may stow away in synaptic vesicles to sneak from one neuron to another.
X-ray crystallography reveals secrets of the glutamate receptor.
While mice sleep, neurons sprout synapses to solidify fresh skills, according to a new study. The brain also keeps amyloid-β levels low while we snooze.
Blocking calcium-dependent protease normalizes lifespan in mouse tauopathy model.
Researchers are looking to the eye for a cheap, easy way to detect Alzheimer’s pathology in the brain.
Perfectly healthy mitochondria can sicken neurons simply by being in the wrong place.
An amplification-based test picks up minute amounts of prion protein in the blood of asymptomatic carriers, but researchers wonder whether regulators will want to screen the population.
The first large-scale surveys of DNA methylation in Alzheimer’s brains turned up numerous altered regions that may point to new genes involved in pathology.
The largest meta-analysis done to date confirms dramatic variability in age at onset of autosomal-dominant Alzheimer's disease overall, but finds mutation type and parental age at onset to be strong predictive modulators.