Alzheimer’s Research Restarts, Cautiously
As the SARS-Cov-2 infection peak passes in some areas, scientists are resuming lab work and clinical studies, albeit with new safety protocols in place. Regions differ greatly in how fast they can reopen.
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As the SARS-Cov-2 infection peak passes in some areas, scientists are resuming lab work and clinical studies, albeit with new safety protocols in place. Regions differ greatly in how fast they can reopen.
Many Alzheimer’s trials had minimal dosing interruptions, but recruitment stopped for a time. Others trials fared worse, with some scrapped altogether. One administered study drug in an ambulance.
By suppressing a single gene, scientists triggered the transformation of astrocytes into neurons in the mouse substantia nigra, where the converts released dopamine and connected with the striatum.
A mouse study claims that the small GTPase restrains pro-inflammatory responses in microglia. Aβ oligomers inhibit RhoA, promoting Aβ deposition and neurodegeneration.
Researchers used PET scans from 4,000 people to link RBFOX1 risk variants to amyloidosis. People with lower RBFOX1 expression in their brains had more amyloid and worse cognition.
Cognitive enrichment in early life correlated with less Alzheimer’s pathology, and slower cognitive decline, in late life.
Sex-specific polygenic hazard scores predict pathology and cognitive decline.
As mice age, a busy receptor-mediated protein transport across the barrier wanes; inhibiting an alkaline phosphatase restores it. Meanwhile, the aging barrier becomes generally leaky to large molecules.
Released from hippocampal neurons in response to experience, the cytokine prompted microglia to eat extracellular matrix around synapses. This facilitated growth of new spines, and sharpened memory.
New drug application is first for Alzheimer’s disease in the U.S. since 2003, and first based on amyloid hypothesis.
The findings hint at a liver-brain axis that transmits inflammation from periphery to brain, and could suggest therapeutic targets for preserving brain function.
The tracer distinguished people with progressive supranuclear palsy from controls with a sensitivity of 85 percent, suggesting potential as a diagnostic for 4R tauopathies.
Behold single proteins on the move: Super-resolution microscopy of living cells suggests the infamous protease does not form complexes with other secretases in the plasma membrane—in mouse fibroblasts, that is.
Tissue from 13-week-old fetuses carrying the huntingtin repeat expansion shows defects in neuronal polarity and proliferation, which lead to fewer neurons populating some brain regions.
A 2018 report that had spotted extra copies of APP lurking in neuronal genomes has come under scrutiny, with claims that the result is due to contamination. Does a response from the original authors bolster their claim?