A Single Microglial Protein Controls Suite of Alzheimer’s Risk Genes
Genetic studies have turned up numerous genes linked to Alzheimer’s disease (AD), but in most cases, researchers have no idea how the genes raise or lower risk. A new genetic analysis now suggests that most of these genes act in the brain’s immune cells, microglia, not in neurons. A large group of researchers led by Alison Goate at the Icahn School of Medicine at Mount Sinai, New York, identified a protective genetic variant that delays when Alzheimer’s disease starts. The authors discovered that this variant lowered expression of the master microglial regulator PU.1. PU.1 regulates the expression of other microglial genes, controlling the cells’ survival and behavior. Notably, the authors found a huge number of AD risk genes among its downstream targets. Of 112 such genes they examined, 60 of them were expressed in microglia and controlled by PU.1. The results suggest that microglia, rather than neurons, may wield the most influence over AD pathogenesis.
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14th International Conference on Neurology, Neuroscience and Neuromuscular Disorders
June 17-18, 2019; Tokyo
CARS 2019 Computer Assisted Radiology and Surgery
June 18-21, 2019; Rennes, France
18th Meeting of WSSFN
June 24-27, 2019; New York
International Summer School Transnasal Endoscopic Surgery: From Sinuses to Skull Base
June 24-28, 2019; Brescia, Italy
The Society of University Neurosurgeons Annual Meeting
June 26-30, 2019; Dubrovnik, Croatia