In mouse brain slices at least, tau shuffles in and out of protein inclusions. The tangles grew more inert as the tissue aged.
When cultured with human neurons expressing a familial Alzheimer’s gene, both microglia and astrocytes were necessary to spike complement C3 and send inflammation into overdrive.
By comparing protein changes with GWAS data, scientists identified new links to AD. This method can unearth genes that otherwise fall short of genome-wide significance.
In mouse models of Aβ toxicity and amyloidosis, inhibiting the integrated stress response restored protein production, spared synapses, and brought back memory.
Plaques abound, cytokines spike, microglia swell with lipids and send out spermine SOS signals in Denali model. Mice will be shared, allowing unrestricted use.
In mice, an anti-ApoE antibody removed plaques from the brain’s parenchyma and blood vessels better than aducanumab. Importantly, it caused no microhemorrhages.
Whole-genome sequencing combined with expression data identifies five LBD loci: three known and two new. Four increased LBD risk while one appears protective.
Based on pooled data from five well-characterized cohorts, women appear to initially outperform men, but then slide faster, on global cognition and executive function. Oddly, this was not true for memory.
Neurons take up extracellular vesicles containing tau oligomers more readily than they do free tau. Some gift: This speeds the march of tauopathy through mouse brain.
In both mice and (wo)men, the sex difference comes down to an Aβ-glutamate receptor-prion protein troika.
High amyloid burden and neuroinflammation, neuronal excitability, and tangles and oligodendrocyte loss distinguish the disease types.
The blood-based marker may be far more scalable and cost-effective for tracking the disease than PET imaging and CSF biomarkers.
Aging macrophages and microglia poorly burn glucose and enter an inflammatory state. Revving their metabolism preserved synapses and memory in mice. What does prostaglandin have to do with it?
Some people with severe COVID-19 have neurovascular injury and elevated markers of neural damage in their blood and CSF. What’s going on in their brains?
In response to an FDA request, the drug’s sponsor submitted new data analyses. The agency moved the action date to June 7.