After a Decade, Amyloid PET Scans Receive Broad Insurance Coverage
CMS has lifted restrictions that allowed beneficiaries one scan per lifetime as part of a clinical study. Approval of immunotherapies was a key factor.
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CMS has lifted restrictions that allowed beneficiaries one scan per lifetime as part of a clinical study. Approval of immunotherapies was a key factor.
A comparative snRNA-Seq study of three regions from AD, PSP, and FTD brains identifies subtypes of neurons and glia hit hard in each disorder.
The oligomers beckon microglia and astrocytes to prune dendrites. This correlates with cognitive decline.
A consortium of pharma companies mined data from 50,000 people in the U.K. Biobank to turn up thousands of new gene-protein connections.
Reported in 21 papers, a collaborative effort describes brain-wide gene expression, epigenetics, morphology, and activity at single-cell resolution.
Resilient and vulnerable interneurons mark different stages of Alzheimer's. Gene regulation crumbles in late stages. Microglial states change with epigenomic shifts.
In human three-dimensional brain cell cultures, UBB+1 caused plaques and tangles. Silencing UBB+1 prevented spontaneous amyloid pathology caused by AD mutations.
Acetylation of lysine residues unique to 4R tau hinders protofibril folding. The findings might explain selective 3R tau deposition in Pick’s disease.
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.
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