Dying neurons trigger a transcriptional change in microglia that requires APOE and TREM2. Does this altered phenotype fight or fuel disease?
A surprising fold emerges from a low-complexity domain. Videos show core holding steady, N and C termini dancing around.
Multiple lines of new evidence are tying disparate cellular neurodegenerative pathologies together. One result: The FTD risk factor progranulin is now firmly placed in lysosomes.
Tau in the plasma rises after traumatic brain injury, with cognitive decline, and progression to mild cognitive impairment.
ApoE, especially E4, interacts directly and indirectly with tau. This worsens outcomes along the pathogenic process, from soluble tau to glial activation and brain atrophy. All without Aβ.
A birth cohort study in New York City finds a sharp drop in dementia incidence in people born after 1929. Neither better cardiovascular health nor more education explain the data.
Autophagy spares motor neurons from synaptic ruin early in disease, but stokes the fires of neuroinflammation later on.
Engineering mice to express a tagged polyA-binding protein in specific cell types allows researchers to pull out neuronal, astroglial, or microglial mRNAs from the intact brain and examine each cell type′s mix of mRNA 3' ends.
RIPK1 catapults microglia into an inflammatory frenzy, disrupting their lysosomal pathway and undermining Aβ clearance. A new drug target?
Two new mouse studies show that a ketogenic diet that avoids obesity improves the health of mind and body, increasing median lifespan. Related studies hint at possible benefits for Alzheimer’s disease.
CryoEM reveals high-resolution view of full length of Aβ42 in a novel conformation.
Liquid droplets of tau subsume and concentrate tubulin, which then rapidly forms microtubules.
Dopaminergic neurons made from human iPS cells take root in monkey brains and reverse PD-like motor problems. Matching donor and host immune signatures mitigates graft rejection.
Agonists of β2-adrenergic receptor dampened transcription of α-synuclein, and protected neurons in mice and patient cells. Norwegians taking the drugs had half the risk of PD.
Large study using GAAIN data reveals subtle sex differences in chances for AD.