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.
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.
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.
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.
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.
New work implicates changes in chromatin structure and failed DNA repair in neurodegeneration.
In several animal models, stimulating mitophagy lowered amyloid deposits and tau phosphorylation while improving learning and memory.
When it seeps into the brain, fibrinogen activates innate immune responses that zap dendrites. And amyloid deposition has little to do with it.
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?
In cognitively normal people, a set of blood proteins may predict whether or not amyloid plaques have deposited in a person’s brain.
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.
Building on results in AD mouse models, researchers now report that immune checkpoint inhibitors reduce pathology and improve cognition in tauopathy mice, too. Other scientists are skeptical.
Neural progenitor cells derived from people with sporadic AD are missing the transcriptional repressor REST in the nucleus. This lets neurogenesis run wild, exhausting a person’s stem cell pool.
Binding occurs around lipid deposits in the choroid plexus, near Aβ deposits, and also in atherosclerotic plaques in blood vessels.
Amyloid plaques in postmortem human cortex correlated with the proportion of microglia that were activated, not with microglial numbers. Tau pathology and cognitive decline come later.
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