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.
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 D
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.
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?
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.
Early data suggest that CT1812 and AL001 shift biomarker levels in Alzheimer’s disease and frontotemporal dementia, respectively. BI 425809 fails to improve cognition.
Restoring proper gene editing assuaged mitochondrial defects in patient-derived neurons and organoids. Splicing errors may underlie other PD cases as well.
Researchers at the online AAT-AD/PD meeting touted therapies that target neuroinflammation, synapses, epigenetic regulation, or the cortisol stress response.