At the HAI 2020 conference, the tracers PI-2620 and APN-1607 appeared to bind frontotemporal dementia tau. MK-6240 looked highly sensitive. And JNJ-067 and SNFT-1 are two new kids in town.
The findings hint at a liver-brain axis that transmits inflammation from periphery to brain, and could suggest therapeutic targets for preserving brain function.
The tracer distinguished people with progressive supranuclear palsy from controls with a sensitivity of 85 percent, suggesting potential as a diagnostic for 4R tauopathies.
In striatal spiny projection neurons with mutant huntingtin, mitochondria spill immunogenic RNAs into the cytosol. These touch off innate antiviral signaling inside the neurons, which may spell their demise.
A slight drop in hospital admissions after amyloid PET, especially in people with positive scans, fell well short of the prespecified endpoint. Still, IDEAS is broadening into a research platform, and IDEAS 2 will add racial diversity.
In updating their broad evaluation of the risk literature, the commission blamed three more modifiable factors for causing 6 percent of all dementia, concluding that 40 percent of cases can be prevented.
New research pushes back the age at which dementia risk from cardiovascular and metabolic factors begins. Should protective lifestyle interventions start in youth?
Plasma p-Tau217 Set to Transform Alzheimer’s Diagnostics Could Common Vaccines Protect Against Alzheimer’s Disease? Doubling Down on Sequencing Serves up More Alzheimer’s Genes IDEAS Finds Small Drop in Hospitalizations, Missing Goal Lancet Commission’s ...
The AAT-AD/PD conference hosted a virtual conversation about what the trial’s disappointing cognitive and tantalizing biomarker data might mean. Hidden between thank you’s and pledges to stay committed were substantive points of debate and context.
Early data suggest that CT1812 and AL001 shift biomarker levels in Alzheimer’s disease and frontotemporal dementia, respectively. BI 425809 fails to improve cognition.
The FDA will decide whether to approve the antibody as a treatment for Alzheimer’s disease on or before March 7, 2021.
Three weeks of on-demand seminars to culminate in live Q&A.
Restoring proper gene editing assuaged mitochondrial defects in patient-derived neurons and organoids. Splicing errors may underlie other PD cases as well.
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.