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.
A panel of experts concludes the evidence for this scary prospect is weak, but recommends neurosurgeons use separate neurosurgical instruments for young and old patients. The experts called for further studies.
Learning tests may prove more informative in clinical trials of early AD. A new one claims it can spot a difference in six days.
Restoring proper gene editing assuaged mitochondrial defects in patient-derived neurons and organoids. Splicing errors may underlie other PD cases as well.
AMX0035, a mix of sodium phenylbutyrate and taurursodiol, slowed functional decline over six months by about as much as the approved ALS drug edaravone.
A C9ORF72 polydipeptide repeat induces aggregation by direct interaction with TDP-43, while progranulin mutations that trigger microglial toxicity cause TDP-43 to accumulate via complement.