In a retrospective study, people with vitiligo had 12 times the risk of developing Alzheimer’s disease than did healthy controls. Why is that?
This pathway may transmogrify microglia during neurodegeneration, without the help of TREM2.
Sensor algorithms can accurately capture patterns of resting tremor and dyskinesia. This could help clinicians manage symptoms and medication.
People who report not participating in social or cognitive activities are more likely to develop dementia within the next few years, but not after that. The findings cast nonparticipation as a consequence, not a cause, of neurodegeneration.
Transcriptomic and epigenomic data pin PD risk genes in GWAS loci; six affect splicing, five expression, four are new.
Researchers envision p-tau-based blood tests for Alzheimer’s disease within a few years, but maybe not a stand-alone test.
Two mouse models presented at AD/PD may hand scientists more translationally relevant tools to explore LOAD pathophysiology and treatment. The tricks: targeted replacement and knocking in multiple GWAS variants.
New research implicates IL-6 signaling and even Aβ42 itself as BACE targets, complicating efforts to resurrect BACE inhibitors at a low dose.
The field is shifting from targeting tau’s tips to its mid-region, especially where tau binds microtubules. Several new candidates are in the clinic; whether the strategy will work remains to be seen.
Scientists report at AAT-AD/PD that they tightened a causal connection between gut microbes, microglial function, and protein deposits. In mice, that is.
In a Phase 2 trial, the vaccine reportedly normalized the rise in plasma NfL, and appeared to lower CSF tau and retard brain atrophy.
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.
New Assay, New Cohorts—Plasma p-Tau181 Looks Even Better 217—The Best Phospho-Tau Marker for Alzheimer’s? In DIAN-TU, Gantenerumab Brings Down Tau. By a Lot. Open Extension Planned Confused About the DIAN-TU Trial Data? Experts Discuss Active Tau Vaccine: ...
Researchers at the online AAT-AD/PD meeting touted therapies that target neuroinflammation, synapses, epigenetic regulation, or the cortisol stress response.
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.