Not So Fast—The Brain Has Three Meningeal Membranes After All
Using live imaging, electron microscopy, and gene expression studies, two groups show that a purported fourth membrane is instead the inner layer of the arachnoid mater.
Using live imaging, electron microscopy, and gene expression studies, two groups show that a purported fourth membrane is instead the inner layer of the arachnoid mater.
In mice, microglia that sprout vascular cell adhesion molecule 1 flock to amyloid aggregates. ApoE is required.
The second-generation PET ligand snuggles into the C-shaped protofilaments of tau fibrils extracted from an AD brain sample.
The transmembrane protein tempers an enzyme that destroys lipids comprising myelin. Sans TMEM106b, lipid levels drop, and the myelin may be compromised.
FTLD-causing mutations in tau turned down expression of lncRNAs including SNHG8. This goaded TIA1 to form stress granules, bringing tau along for the ride.
DOPA decarboxylase in blood or CSF, and damaged mitochondrial DNA in blood cells, separated cases from controls.
Raising TMEM164 prevents astrocytes from releasing the toxic lipids, protecting neurons in models of Alzheimer’s and Parkinson’s.
In mice, the long noncoding RNA MEG3 mediated the death of human neurons, which accumulated tau tangles.
A report earlier this year that the brain has a fourth meningeal membrane stirred excitement and controversy. Now papers from two groups contradict the claim. The researchers used a variety of techniques to show that the purported fourth membrane is instead the inner layer of the arachnoid mater. The new data and tools developed may help explore other meningeal mysteries as well.
Microglia survey brain tissue, searching for protein aggregates and other cellular debris to dispose of, but what leads the cells to their prey? In the case of amyloid, it might be ApoE. In mice, interleukin-33, a cytokine linked to Alzheimer’s disease, spurs microglia to sprout vascular cell adhesion molecule 1. VCAM1 senses ApoE within plaques, kick-starting phagocytosis. Neutralizing VCAM1 or ApoE prevented plaque clearance.
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