The first whole-genome manipulation of protein expression in neurons by CRISPR reveals a deadly chain of events. Bad processing by lysosomes leads to build-up of lipids and iron. Oxidative stress revs up. Neurons die by ferroptosis.
African Americans are likelier than non-Hispanic Caucasians to carry low-expression TREM2 variants, and less likely to carry a high-expression variant. As a result, they have less soluble TREM2 in their cerebrospinal fluid.
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.
As life expectancy increases in countries such as Nigeria, Brazil, China, and others, so does the number of people with dementia. How to provide modern care for them?
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.
New data presented at the AD/PD conference offer the first evidence that a brain-shuttle strategy can work in people; the lecanemab and aducanumab antibody programs offer small updates.
A new PET tracer. Plasma glial fibrillary acidic protein. Two new, promising surrogates for astrogliosis are filling in the Alzheimer’s biomarker toolbox. Both reflect Aβ amyloid better than they do tau tangles.
At this year’s ICFTD meeting, researchers reviewed the lay of the land of current and planned trials for FTD, with glimpses of how the newly formed FTD Prevention Initiative seeks to coordinate treatment and prevention trials in the future.
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