The iPSC Neurodegenerative Disease Initiative is creating 100+ isogenic cell lines. Each carries a different risk variant for Alzheimer's or a related dementia. Scientists around the world can obtain the cells through Jackson Labs.
The first detailed look at expression profiles in blood vessels of the human brain identifies new cell subtypes. These cells express 30 of the top 45 AD risk genes.
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.
Incorporation of a cryptic exon scuttles translation of UNC13A, but only in neurons lacking nuclear TDP-43. UNC13A ALS/FTD risk variants exacerbate the aberrant splicing.
In mice, polyamines boost autophagy and promote clearance of soluble Aβ species. In cells, they counteract tau aggregation. In the Alzheimer’s brain, their metabolism is ramped up. Could spermidine supplements prevent or treat AD?
After news on “new data” they won’t see, three committee members argue against approval.
Researchers split $200,000 for their theories on the role of six microbes—one virus, four bacteria, and one parasite—in Alzheimer’s.
People with FTD wrestle with behavioral, cognitive, language, and motor impairments. Scientists are designing standardized tests that capture such symptoms.
International cohort studies reveal that the brain starts to shrink, and neural connections to crumble, many years before FTD symptoms arise. Where and when those changes occur depends on the offending mutation.
Disturbed social and emotional cognition are among the most troubling features of FTD. They, too, can be quantified with new tools.
The global platform trial for Alzheimer’s due to mutations in APP or presenilin will try to treat or prevent symptoms by deploying a therapeutic antibody that homes in on a piece of tau known to aggregate into neurofibrillary tangles.