In several model systems, α-synuclein boosts oleic acid production and the fatty acid worsens α-synuclein pathology.
In presynapses, binding sequesters synaptic vesicles.
The first rule of triage is do no harm, but try telling that to microglia...
Rare mutations in a microglial receptor contribute as much to Alzheimer’s risk as does the more common ApoE4 genotype...
When told what to kill, the complement system deftly deals the final blows...
Scientists report that astrocytes help neurons destroy their unwanted mitochondria.
Animal models suggest excessive NFκB-TNFα signaling brings on compulsive behavior in a frontotemporal dementia mouse model and early death in flies.
Microfluidic tri-culture of neurons, astrocytes, and microglia models how glia impose deadly neuroinflammation on top of amyloid and tau pathology.
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.
Boosting sTREM2 in the brain rallied microglia to clear Aβ plaques, restored synaptic plasticity, and even rescued memory deficits in mice.
By prying open chromatin, neurofibrillary tau may expose dormant transposable elements for transcription.
The discovery hints that microglia, rather than neurons, may control much of a person’s genetic susceptibility to Alzheimer’s disease.
In response to the peptide, these little cells squeeze capillaries, constricting them. This may contribute to neuronal dysfunction.
Longitudinal data identifies four stages of amyloid plaque buildup, with the earliest deposits appearing in the precuneus and posterior cingulate.