New CRISPR screen flags dozens of genes that suppress toxicity of the Parkinson’s protein. Tweaking multiple genes strengthened the protection.
Using modified MRI protocols, researchers were able to visualize these vessels in the dura mater of living people. The discovery challenges conventional wisdom.
Researchers claim this failed drug allows Aβ to accumulate inside cells, while small peptides cleaved from the C-terminal end of APP become trapped in membranes.
Human endothelial cells, smooth muscle cells, and astrocytes combine to form a vessel that ferries away Aβ, particularly Aβ42.
PET scans show a tangle patch in the entorhinal cortex when people report subjective cognitive concerns.
Young tau knockout mice maintain healthy brain tissue after ischemia, while older knockouts lose this stroke protection due to brain iron buildup.
Three developers of cryo-electron microscopy—the technique researchers recently used to unveil atomic structures of γ-secretase, Aβ, and tau fibrils—won this year’s Nobel Prize in chemistry.
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?