Microtubule Regulator Connects TDP-43 to Axonal Dysfunction
Two independent studies find that loss of nuclear TDP-43 leads to mis-splicing of stathmin 2, an essential protein for axon growth and repair.
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Two independent studies find that loss of nuclear TDP-43 leads to mis-splicing of stathmin 2, an essential protein for axon growth and repair.
Aberrant gene-expression patterns found to be common to human neurodegenerative disease and animal models. MicroRNA and epigenetic modification may be to blame.
The largest study so far to compare brain scans and CSF among African-Americans and Caucasians finds differences, but participant numbers remain small.
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.
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.
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 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.
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?
How the element relates to neurodegeneration remains unclear.
IBM researchers in Australia identify a combination of four proteins in plasma that predicts amyloid positivity in cerebrospinal fluid, and correlates with progression to AD.
Exposing AD mice to multisensory gamma therapy induced 40-Hz waves in their brains, plus effects on amyloid, tau, microglia, blood vessels, and cognitive function.
Analysis of 19 H1 MAPT subhaplotypes ties five to progressive supranuclear palsy.
Regulatory T cells rush into the brain after a stroke, quelling astrocytosis and aiding neural recovery.
In a fly model of neurodegeneration, CDK5 slams autophagy, which leads to a runaway immune response that shoves aging neurons over the edge.
The ligand binds the microglia-specific CSF1 receptor in animal and postmortem studies; human trials are forthcoming.