A Trem2 R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques.

Kristine M TranShimako KawauchiEnikö A KramárNarges RezaieHeidi Yahan LiangJasmine S SakrAngela Gomez-ArboledasMiguel A ArreolaCelia da CunhaJimmy PhanShuling WangSherilyn CollinsAmber WalkerKai-Xuan ShiJonathan NeumannGhassan FilimbanZechuan ShiGiedre MilinkeviciuteDominic I JavonilloKatelynn TranMagdalena GantuzStefania FornerVivek SwarupAndrea J TennerFrank M LaFerlaMarcelo A WoodAli MortazaviGrant R MacGregorKim N Green

Published in: Molecular neurodegeneration (2023)

mouse is a valuable model that can be used to investigate age-dependent effects of the AD-risk R47H mutation on TREM2 and microglial function including its effects on plaque development, microglial-plaque interaction, production of a unique interferon signature and associated tissue damage.

Keyphrases

mouse model
inflammatory response
coronary artery disease
lipopolysaccharide induced
oxidative stress
neuropathic pain
dendritic cells