Eran Blacher

Mar 27, 2024 | nature.com | Edward Wilson |Yann Le Guen |Eran Blacher |Matthew Xin |Melanie R. McReynolds |Chinyere A. Iweka

AbstractHuman genetics implicate defective myeloid responses in the development of late-onset Alzheimer disease. A decline in peripheral and brain myeloid metabolism, triggering maladaptive immune responses, is a feature of aging. The role of TREM1, a pro-inflammatory factor, in neurodegenerative diseases is unclear. Here we show that Trem1 deficiency prevents age-dependent changes in myeloid metabolism, inflammation and hippocampal memory function in mice.