A compound that only blocks presenilin 1-containing secretases beat back leukemia in mice—without side effects caused by broad-spectrum inhibitors.
In Taiwan, interferon treatment for chronic hepatitis C infection appears to have reduced the incidence of Parkinson’s disease.
Expression of VCAM1 on the endothelial cells that line the blood-brain barrier allowed aging factors in the plasma to exact their toll on the brain.
By slipping human microglia inside the mouse brain, researchers hope to better monitor their response to pathologies, such as Aβ.
Researchers publish 14 new AD variants. This includes one near WWOX, a gene that encodes a protein linked to tau and lipid metabolism.
Human cells show more phenotypic variation than mouse microglia, but the two match up well overall.
Longitudinal and genetic studies reveal that intelligence underlies cognitive reserve.
Many genes that increase risk for late-onset AD are expressed in microglia, and researchers are going cell by cell to unravel the pathways involved in the immune response to amyloid and tau.
At SfN and in new papers, scientists describe how synapses crater under the combined onslaught of Aβ and tau. They also link gene-expression signatures to the selective vulnerability of excitatory neurons to tau pathology.
At AAIC, competitors vied for advantage, and discussion moved swiftly to the issue of assay standardization.
One rare variant protects ApoE4 carriers, others put noncarriers at risk.
At AD/PD Conference, New Alzheimer’s Genes Reinforce Known Pathways Expression, Expression, Expression—Time to Get on Board with eQTLs APP Upp: Mutation Nixes Six Amino Acids from Aβ, Spurs Aggregation Parsing How Alzheimer’s Genetic Risk Works Through ...
A tool of modern genetics, expression studies link GWAS hits to specific cell types, providing clues to pathogenesis. Microglia come up again and again.
Speakers at AD/PD 2019 reported that AD risk factors mess up lipid metabolism in glial cells. In cellular models, speeding the clearance of fats lessened pathology.
Greater lifetime estrogen exposure protects cognition, while hormone replacement therapy taken at menopause has no cognitive effects at all.