In postmortem brain, proteins involved in all manner of vesicular functions waxed or waned with increasing phases of disease, starting years prior to symptoms.
People who develop Type 2 diabetes before age 60 have more than double the dementia risk, and earlier dementia onset, than those without diabetes.
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 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.
The fewer their meningeal lymphatic vessels, the slower treated mice clear plaques. Lymphatic dysfunction also drives microglial activation, hinting at a role in pathology.
Machine learning analysis of 912 PET scans says neurofibrillary tangles spread through the AD brain in one of four distinct patterns.
The APP/PS1 double knock-ins begin to deposit amyloid in the brain by 3 months of age.
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.
Grappling with a rare disease whose variability is daunting, international cohort studies are charting the natural history of FTD. They have discovered biomarkers and honed physiological tests that underlie its behavioral symptoms.
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.
In animals, polyamines such as spermidine enhance autophagy, rejuvenate mitochondria, and slow cognitive decline. Buzzword: hypusination. Human data not far behind.
Epidemiology study reveals 1.5-times higher risk of dementia after herpes virus infection. Short-term antiviral treatment appears to lower risk.
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?
Regulators in the U.S. and Europe have certified a mass-spectrometry-based blood test for amyloid-β. Plasma phospho-tau markers are poised to come next.
In mice, an IgG4 version of semorinemab better protected neurons, but for AX004, an IgG1 version better cleared tau. How to make the choice?