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.
Repeat peptides made by the mutant C9ORF72 gene in ALS and FTD enter the nucleolus and obstruct RNA biogenesis.