In a mouse model of ALS, removing mutant SOD1 from peripheral myeloid cells relieved neuroinflammation and extended lifespan.
Regulators in the U.S. and Europe have certified a mass-spectrometry-based blood test for amyloid-β. Plasma phospho-tau markers are poised to come next.
Phospholipase C-γ2 acts downstream of TREM2 to rev up beneficial inflammation, phagocytosis, and cell survival.
Three studies agree that TMEM106b/progranulin double knockouts develop more extreme lysosomal dysfunction, inflammation, and motor deficits than PGRN KOs.
TRP cation channels combine with extrasynaptic NMDA glutamate receptors to set off mitochondrial meltdown and cell death. Blocking the interaction stops excitotoxicity.
ApoE4 does so much more strongly than the other known genes collected in a polygenic risk score.
Could this forestall the amyloid cascade and the onset of Alzheimer’s disease?
The designer chimera stabilizes synapses in various mouse models of neurodegenerative disease.
Comprising mostly Aβ40, these large plaques are shot through with strange tubular structures and BBB markers. They are common in early onset AD.
Expert panel concludes there’s little risk based on current evidence.
AMX0035, a mix of sodium phenylbutyrate and taurursodiol, slowed functional decline over six months by about as much as the approved ALS drug edaravone.
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.
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.
The transcription factor NFATc2 mediates this response.
By looking for SNPs that affect how transcription factors bind DNA, researchers nominated causal genes for 30 Alzheimer’s and Parkinson’s GWAS hits.