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.
A recent genetics symposium drew positive reviews for its approach of following up prerecorded, on-demand talks with a live Q&A session.
Carriers of a rare hypomorphic gene variant develop a frontotemporal dementia that features Alzheimer’s-like neurofibrillary tangles.
The day-long advisory committee meeting will be broadcast live online. Prerecorded presentations are to be available November 4; the public can submit comments.
While one anti-Aβ antibody thwarts initial seeding of fibrils, and others keep fibrils from lengthening, aducanumab prevents oligomers forming on their surface. In vitro, that is.
Comprising mostly Aβ40, these large plaques are shot through with strange tubular structures and BBB markers. They are common in early onset AD.
Three studies agree that TMEM106b/progranulin double knockouts develop more extreme lysosomal dysfunction, inflammation, and motor deficits than PGRN KOs.
Phospholipase C-γ2 acts downstream of TREM2 to rev up beneficial inflammation, phagocytosis, and cell survival.