Could a Faulty Ubiquitin Trigger Amyloid and Tau Deposits?
In human three-dimensional brain cell cultures, UBB+1 caused plaques and tangles. Silencing UBB+1 prevented spontaneous amyloid pathology caused by AD mutations.
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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.
In mice, the long noncoding RNA MEG3 mediated the death of human neurons, which accumulated tau tangles.
In people over 60, sitting for 12 hours per day increased dementia risk. An exercise-induced hormone, irisin, protects via astrocytes, at least in vitro.
A curated panel of 48 proteins foretold cognitive decline. It also illuminated biological pathways involved in Alzheimer's disease.
A retrospective study found an increased risk of brain bleeds in people who received blood from someone else with such bleeds, hinting at a soluble agent. Aβ?
The NIA invites scientists to submit data to create diverse, open datasets and design diagnostic algorithms for more accurate, early prediction of Alzheimer’s.
In a mouse amyloidosis model, a protective variant tightened the reins on plaques and spared synapses; a risk variant did the opposite.
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