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.
Subtle memory deficits resolved after volunteers stopped taking the Novartis BACE inhibitor.
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.
At AAT-ADPD, researchers report how they built on prior reports that a person’s blood level of p-tau181 tells if they have Alzheimer’s.
Poor coordination among grid cells in the entorhinal cortex and place cells in the hippocampus compromises navigation. Grid cells fail first.
New drug application is first for Alzheimer’s disease in the U.S. since 2003, and first based on amyloid hypothesis.
New synaptic profiling and imaging techniques are enabling scientists to zero in on synaptic proteins, including phospho-tau, that make the difference between clinical Alzheimer’s and resilience.
Plaque-busting antibodies reset the time course of amyloid accumulation, but so far provide only hints of a clinical benefit in mild AD. Good news: once gone, plaque stays gone for a while.
New genetic variants emerged by harmonizing whole-exome-sequencing data across continents, and by using imputation to plumb the depths of existing GWAS. One variant encodes a microglial phospholipid transporter.