ApoE4 does so much more strongly than the other known genes collected in a polygenic risk score.
By looking for SNPs that affect how transcription factors bind DNA, researchers nominated causal genes for 30 Alzheimer’s and Parkinson’s GWAS hits.
The first steps of endocytosis faltered in astrocytes expressing ApoE4, but pumping in PICALM reversed the problem. A new study places two Alzheimer’s risk factors into the same cellular mechanism.
Three amino acid substitutions in the Aβ sequence accelerate BACE cleavage of APP and ramp up Aβ production in rats and mice. The mice can serve as better controls for mutant APP knock-ins already in use.
Researchers have devised a way to measure how long ago a reporter transcript was made. It allows them to detect distinct transcriptional events within a cell.
Armed with snazzy new hardware, scientists solve protein structures to a resolution of 1.22Å. Cryo-EM now rivals X-ray crystallography.
Most pathways that emerged were common between African Americans and non-Hispanic whites, though some individual variants differed. Kidney development jumped out as a possibly unique aspect of AD in African Americans.
A new single-nucleus RNA-Seq study of 3,900 endothelial cells finds a boost in angiogenesis and antigen presentation genes, drawing attention to the vascular component of AD.
A survey of 16 purported conformation-specific antibodies found that most bound nearly equally well to oligomers and fibrils, and weakly to monomers.
Two papers report that skin samples from people with Parkinson’s disease contain α-synuclein seeds that can be robustly amplified, paving the way for a reliable test for the disease.
Reducing levels of monounsaturated fatty acids lowered α-synuclein toxicity and prevented movement symptoms in mice. Scientists say the data boost the α-synuclein tetramer hypothesis.
Technical limitations may have misrepresented the transcriptional state of these cells, obscuring detection of their activation signature in frozen postmortem tissue from Alzheimer’s brain.
TRP cation channels combine with extrasynaptic NMDA glutamate receptors to set off mitochondrial meltdown and cell death. Blocking the interaction stops excitotoxicity.
Expert panel concludes there’s little risk based on current evidence.
The R1279Q variant of angiotensin-converting enzyme associates with AD and causes neurodegeneration in mice. In a model of amyloidosis, it accelerates decline.