Make Proteins, Save Memory: The Cellular Stress Response and Synapses
In mouse models of Aβ toxicity and amyloidosis, inhibiting the integrated stress response restored protein production, spared synapses, and brought back memory.
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In mouse models of Aβ toxicity and amyloidosis, inhibiting the integrated stress response restored protein production, spared synapses, and brought back memory.
In mouse brain slices at least, tau shuffles in and out of protein inclusions. The tangles grew more inert as the tissue aged.
When cultured with human neurons expressing a familial Alzheimer’s gene, both microglia and astrocytes were necessary to spike complement C3 and send inflammation into overdrive.
Plaques abound, cytokines spike, microglia swell with lipids and send out spermine SOS signals in Denali model. Mice will be shared, allowing unrestricted use.
Three young monkeys missing exon 9 of presenilin 1 seem to have an elevated Aβ42/40 ratio. It remains to be seen if they will develop plaques and tangles as they age.
Centenarians who scored high on the MMSE stayed cognitively and physically active over the next two years, even if they carried genetic risk factors for Alzheimer’s. What protects these lucky few?
The slowdown of proteasomes stymied TDP-43’s entry into the nucleus and promoted its aggregation in the cytoplasm.
Massive meta-analysis finds the longevity gene’s VS haplotype staves off mild cognitive impairment and AD. It reduces amyloid burden.
Grown on doughnut-shaped supports, the cultures survive for years. They offer a versatile system for studying Alzheimer’s disease, the authors claim.
This update of the Allen Brain Institute atlas reveals detailed anatomical structures and provides a common framework for comparing brain datasets.
Separately, cerebrovascular disease drove an uptick in neurofilament light in the brain, indicating neurodegeneration.
The plasma biomarker neurofilament light was able to distinguish individual mutation carriers from noncarriers three years prior to onset.
The modeling approach reinforces the idea that tau pathology propagates through the brain’s physical architecture, including neuronal networks.
Researchers identify a way to isolate human astrocytes generated from induced pluripotent stem cells. And astrocytes stand out in FTD-prone brain areas.
A GWAS of co-expression modules identifies a haplotype that disrupts lysosomes and myelination. ApoE4 and Aβ regulate the same module.