Downregulation of a chemokine receptor traps T cells in the meninges. Glymph drainage slows, amyloid burden rises.
A “mammalian-wide interspersed repeat-natural antisense transcript” blocks translation of tau mRNA. Other MIR-NATS may act on α-synuclein and APP.
Certain neurons crank up ApoE expression with age in mice. Ditto with AD progression in people. These same neurons ramp up immune response genes. The shift could foreshadow their demise.
Longitudinal studies in DS have pegged biomarkers and cognitive measures as potential clinical trial readouts. Hundreds of adults are anticipated to join trial-ready cohorts this year.
ACI-24 prompted an immune response without serious side effects, according to AC Immune. Researchers are gearing up for other treatment trials in DS.
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?
In animals, polyamines such as spermidine enhance autophagy, rejuvenate mitochondria, and slow cognitive decline. Buzzword: hypusination. Human data not far behind.
In mice, an IgG4 version of semorinemab better protected neurons, but for AX004, an IgG1 version better cleared tau. How to make the choice?
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.
The APP/PS1 double knock-ins begin to deposit amyloid in the brain by 3 months of age.
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.
Machine learning analysis of 912 PET scans says neurofibrillary tangles spread through the AD brain in one of four distinct patterns.
The fewer their meningeal lymphatic vessels, the slower treated mice clear plaques. Lymphatic dysfunction also drives microglial activation, hinting at a role in pathology.
People who develop Type 2 diabetes before age 60 have more than double the dementia risk, and earlier dementia onset, than those without diabetes.
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.