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Going Viral: Alzheimer’s Research at Herpes Conference Herpesvirus: Trigger for Many Brain Pathologies? In light of recent work implicating human herpesviruses in AD, virologists invited Alzheimer’s researchers to join them at the 11th International ...
TREM2, Microglia Dampen Dangerous Liaisons Between Aβ and Tau Down to Sex? Boy and Girl Microglia Respond Differently Dopaminergic Neurons Conjured from Astrocytes Restore Motion In PD Model, α-Synuclein Spreads from Intestine to Brain Do Microglia Finish ...
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.
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.
At Quebec conference, researchers considered multiple aspects of herpesvirus biology that may come in to play in AD.
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.
Researchers gain traction in the study of these rare tau disorders, which are sometimes confused with Alzheimer’s disease.
Antisense Oligonucleotides: Can They Take on ALS, SMA, Prions? Drug Reported to Help Alzheimer’s Patients Sleep Better American Academy of Neurology 2019 Annual Meeting ...
By aging cultured neurons and manipulating them to stimulate endocytosis or interfere with vesicle release, researchers can bring about characteristics of Alzheimer’s—without adding APP or Aβ.
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?
