The RNA-binding protein FUS promotes synthesis of an isoform of SynGAP, a protein that bolsters dendritic spines. Restoring SynGAP expression partially rescued deficits in FUS–deficient mice.
A study suggests hypertension arising in the 30s or 40s puts only women at risk for later dementia. Other scientists caution that this study missed the same effect in men because they died sooner.
In old and in diabetic mice, ApoE4 sequesters the insulin receptor in early endosomes of neurons, interrupting its signaling. This may help explain ApoE effects seen in intranasal insulin trials.
Large, long-term prospective study finds deficits years before PD diagnosis.
A longitudinal study suggests that distinct populations of immune cells in the blood expand as the disease progresses, while others shrink.
Researchers are finding ways to prevent this protein machine from assembling and spewing toxic cytokines.
In a Phase 3 trial, Axovant’s acetylcholine-boosting drug failed to improve cognition or activities of daily living.
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.