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.
Aging lymphatic vessels in the meninges hinder waste clearance from the brain and exacerbate Aβ build-up.
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?
At CTAD, tau-PET data from people in different stages of various neurodegenerative diseases highlighted both commonalities and peculiarities.
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.
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, an IgG4 version of semorinemab better protected neurons, but for AX004, an IgG1 version better cleared tau. How to make the choice?
Early dysfunction in Alzheimer’s may start in the lateral entorhinal cortex and spread from there to connected cortical brain regions.
Using an array of receptors to sense neurons in peril, microglia make matters worse by taking bites out of the struggling cells.
Using single-nuclei or cell sorting, three separate research groups sequenced RNA from human postmortem brains. They unveiled AD-associated gene-expression signatures, but disease-related transcriptomes from human microglia were quite different from those in mice.
A person's blood phospho-tau level, combined with his or her APOE genotype and scores on executive function and memory tests, outperforms the clinician in predicting dementia within the next four years.
In the plaque-ridden mouse brain, microglia that had taken up Aβ activated a unique gene-expression profile. It faded after microglia were moved to plaque-free environs.
Scientists know that both genetic and environmental risk factors contribute to sporadic Parkinson’s disease, and that one suspected environmental culprit is manganese...