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.
Scientists at AD/PD 2019 see a Goldilocks of microglial activation: Both too little and too much is bad in an injured brain. How could a therapy make it just right?
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.
In Barcelona, data ran the gamut from a few hopeful little hints on new treatments to mixed signals on familiar players, and failed drugs thrown on the scrap heap.
Proteomics and protein-protein interaction research may yield clues to etiology, tracking, and treatment of granulin-related and other forms of FTD/ALS.
Working with human microglia is fraught with technical challenges, but that didn’t stop researchers at Keystone from sharing a flurry of data on how these cells act in neurodegenerative disease.
This past year, therapeutic antibodies massively reduced brain amyloid, blood tests came into their own, and systems-based approaches transformed the study of gene expression, glial cells, and selective vulnerability.
New potential immunotherapies and insight into single-cell responses were highlights of a small meeting in Denmark.