BANish Aβ? BAN2401 Antibody Makes Its Move in Phase 3 Program BAN2401 Forges AHEAD into Phase 3, Preclinical AD TRC-PAD Funnel Finally Touches Down Learning Troubles Spied by Smartphone Track with Biomarkers In Phase 2 Trial, Neflamapimod Aids Cognition ...
Three weeks of on-demand seminars to culminate in live Q&A.
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.
Restoring proper gene editing assuaged mitochondrial defects in patient-derived neurons and organoids. Splicing errors may underlie other PD cases as well.
The antiviral protein enhances γ-secretase processing of APP. More of it is present in Alzheimer’s disease.
Learning tests may prove more informative in clinical trials of early AD. A new one claims it can spot a difference in six days.
Comprising mostly Aβ40, these large plaques are shot through with strange tubular structures and BBB markers. They are common in early onset AD.
In a career spanning four decades, Davies spearheaded the cholinergic hypothesis, unlocked secrets of tau, and readily shared antibodies in the field.
Three studies agree that TMEM106b/progranulin double knockouts develop more extreme lysosomal dysfunction, inflammation, and motor deficits than PGRN KOs.
The day-long advisory committee meeting will be broadcast live online. Prerecorded presentations are to be available November 4; the public can submit comments.
A recent genetics symposium drew positive reviews for its approach of following up prerecorded, on-demand talks with a live Q&A session.
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.
The designer chimera stabilizes synapses in various mouse models of neurodegenerative disease.
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.
Carriers of a rare hypomorphic gene variant develop a frontotemporal dementia that features Alzheimer’s-like neurofibrillary tangles.