A postmortem study found that people who had more aggregation-prone, hyperphosphorylated, oligomeric forms of tau in their brains also had a more aggressive form of Alzheimer’s disease during life. Will we personalize tauopathy care like cancer care?
New research suggests the R47H variant protects neurons from neurodegeneration, raising questions about staging and direction of future TREM2-based therapy.
Islet amyloid protein and Aβ fibrils share similar folds.
When these tiny mural cells carried APOE4, they secreted more ApoE, causing Aβ to deposit in capillary walls. Blocking ApoE production prevented angiopathy.
Acting downstream of TREM2, PLCγ2 facilitates phagocytic microglial behavior such as lipid processing. PLCγ2 also acts downstream of toll-like receptors, where it can throw a switch to inflammation.
A GWAS of co-expression modules identifies a haplotype that disrupts lysosomes and myelination. ApoE4 and Aβ regulate the same module.
People who lived in impoverished neighborhoods in their last year of life had greater odds of having died with AD neuropathology.