Better Living Through Polyamines?
In animals, polyamines such as spermidine enhance autophagy, rejuvenate mitochondria, and slow cognitive decline. Buzzword: hypusination. Human data not far behind.
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In animals, polyamines such as spermidine enhance autophagy, rejuvenate mitochondria, and slow cognitive decline. Buzzword: hypusination. Human data not far behind.
A set of 19 plasma proteins identified clinical Alzheimer’s cases with 97 percent accuracy, and it distinguished mild versus severe dementia. The panel was tested in two small cohorts.
Using isotope labeling and mass spectrometry imaging, researchers detail how plaques first assemble with an Aβ1-42 core, expand, then subsume Aβ1-38. Plaques start in cortex, then spread to hippocampus.
In an aging cohort, weak LC signal intensity on MRI correlated with plaques, tangles, and memory problems.
An unbiased “interactome” generated from human neurons could shed light on what goes wrong in tauopathies, and help identify new therapeutic targets.
In some people who had weathered COVID at home, olfactory regions in the brain shrank and executive function slowed. Will these changes resolve or persist?
In a game changer for the field, three papers report similar structures for TMEM106b fibrils. One claims they comprise the lion’s share of TDP-43 aggregates.
In a clever bit of sleuthing, Karen Ashe and colleagues appear to have solved the case of the mysterious...
Filaments of Aβ42 struck different poses in people with sporadic versus familial AD. The familial AD structure was also found in people with other neurodegenerative diseases, and even in APP knock-in mice.
These axonal swellings block action potentials, weakening neural networks in mice. PLD3, an Alzheimer’s disease risk gene, may be involved.
Plasma p-tau217 and p-tau181 better track amyloid PET, tangles, and subtle cognitive decline.
A protective variant promotes anti-inflammatory microglia, while a risk variant depletes them.
In cognitively unimpaired older adults, some gut bacteria correlated with plaques and tangles, but not neurodegeneration.
In the Finnish city of Kuopio, surgeons and scientists have built a unique protocol. It improves life for people with hydrocephalus—and it banks cortical tissue rife with preclinical pathology and gene variants for Alzheimer's research.
Proteins involved in the extracellular matrix, metabolism, immunity, proteostasis, and synaptic function change in the CSF and plasma up to 30 years before dementia sets in.
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