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.
Alzforum encourages users to visit the Virtual Exhibit Hall, where companies showcase their newest initiatives, products, and services. We welcome Dash Genomics, Inc. and Abcam, which join our other exhibitors — Biogen, BioLegend, BrainXell, NanoString Technologies, and the Jackson Laboratory.
According to the results of a small pilot study, people with ALS who took a supplement touted for its anti-aging properties not only stopped declining, but got better, on several clinical outcomes. The trial came with many caveats, including a small size and high drop-out rate. Hence, researchers called for larger, independent trials.
Blood leaks in the brain increase the risk for Alzheimer’s disease and dementia, and a new study suggests that immune responses to blood-clotting proteins are to blame. In a mouse model of amyloid deposition, fibrinogen that entered the brain activated microglia, leading to synaptic pruning. The process does not require Aβ, because fibrin foci devoid of amyloid induced neurite dystrophy. Preventing fibrinogen from binding microglia improved learning and memory in the mice, suggesting a possible new avenue for dementia treatment.
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