213 RESULTS
Sort By:
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
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 i
Merged Consortia Forge Path to Trials in Frontotemporal Dementia FTD Fluid Markers for Degeneration: Check. For Pathology: Not Yet. Imaging Exposes Hugely Heterogeneous Brain Changes Among FTDs Moving Target: Can Standardized Tests Track Symptoms of FTD?
Donanemab Confirms: Clearing Plaques Slows Decline—By a Bit Astroglial Markers Poised for Stardom? Shuttle Unloads More Gantenerumab Into the Brain N-Terminal Tau Antibodies Fade, Mid-Domain Ones Push to the Fore Where to Now, Phospho-Tau? Clinicians from
Scientists report at AAT-AD/PD that they tightened a causal connection between gut microbes, microglial function, and protein deposits. In mice, that is.
Massive meta-analysis finds the longevity gene’s VS haplotype staves off mild cognitive impairment and AD. It reduces amyloid burden.
For people with Parkinson’s, carrying Alzheimer’s genetic risk variants upped their odds of harboring Aβ and tau pathology and getting dementia. In people with DLB, Aβ plaques worsened tau and Lewy pathology, and cognition.
Trialists are shooting new arrows at the disease, including compounds that tweak autophagy, neuroinflammation, and glycolipid recycling.
In a mouse model of amyloidosis, human wild-type TREM2 kept Aβ deposition at bay early on, but this defense became overwhelmed as plaques grew. The R47H AD risk variant never offered protection early on, and made things worse later.
The first topline Phase 2 results from an antibody targeting Parkinson’s pathology, Roche’s prasinezumab, were a mixed bag. Next steps are unclear.
In nonhuman primates, three classes of LRRK2 kinase inhibitor cause microscopic changes in lung morphology, but they are reversible and do not impair breathing. Parkinson’s programs remain on track.
Award recognizes discoveries of genetic variants that perturb liquid-liquid phase separation and increase risk for ALS-FTD and other neurodegenerative diseases.
Loss-of-function variants in the demethylase TET2 raise a person’s risk for early and late-onset Alzheimer’s, as well as FTD and ALS, suggesting a common mechanism.
For several neurodegenerative diseases, scientists identified which cell types exert a person’s inherited risk. In Alzheimer’s, it’s microglia; in Parkinson’s, it’s dopaminergic and enteric neurons—and oligodendrocytes.
Avid’s postmortem validation data indicate Alzheimer’s can be diagnosed by visual examination of flortaucipir PET scans.
