Cholesteryl Esters Hobble Proteasomes, Increase p-Tau
Reducing these esters with statins and cholesterol-hydroxylase-activating drugs lowers phospho-tau and Aβ in neurons. One such drug is approved to treat HIV AIDS.
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Reducing these esters with statins and cholesterol-hydroxylase-activating drugs lowers phospho-tau and Aβ in neurons. One such drug is approved to treat HIV AIDS.
In cognitively normal people, a set of blood proteins may predict whether or not amyloid plaques have deposited in a person’s brain.
Among cognitively normal people with amyloid plaques, women have more tau tangles in the entorhinal cortex than do men. Does this indicate susceptibility, or resilience?
When it seeps into the brain, fibrinogen activates innate immune responses that zap dendrites. And amyloid deposition has little to do with it.
In several animal models, stimulating mitophagy lowered amyloid deposits and tau phosphorylation while improving learning and memory.
New work implicates changes in chromatin structure and failed DNA repair in neurodegeneration.
In mouse models of Alzheimer’s, neutrophils stick to capillaries in the cerebral cortex, reducing blood flow. Keeping those cells moving or depleting them altogether improved memory.
In a tiny pilot trial, people with amyotrophic lateral sclerosis who took a “cellular health and optimization” supplement were reported to have improved on several clinical outcome measures.
A longitudinal study finds that middle-aged people with the highest levels of inflammation markers in their blood succumb to the greatest cognitive decline over the next 20 years.
The approach provides an in vitro system that more closely resembles the brain milieu than do cell cultures, and can be used to model other proteinopathies as well.
Knocking down or blocking the CCR5 receptor with an HIV drug improved motor symptoms and learning and memory in a mouse model of stroke. Recently, researchers in China knocked out this gene in babies using CRISPR.
Human cells show more phenotypic variation than mouse microglia, but the two match up well overall.
A score based on the combined burden of a person’s Alzheimer’s risk variants correlated with plaques, tangles, cognitive decline, and even non-AD pathology. Are polygenic hazard scores ready for direct-to-consumer marketing?
Aberrant gene-expression patterns found to be common to human neurodegenerative disease and animal models. MicroRNA and epigenetic modification may be to blame.
A flavonoid reportedly spices up oxidative phosphorylation in microglial mitochondria, revving up phagocytosis of amyloid plaques in mouse models. The small study needs independent replication.
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