Matthew Xin

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.

Mar 11, 2024 | biorxiv.org | Katrin I. Andreasson |Edward Wilson |Congcong Wang |Matthew Xin

AbstractHuman genetics implicate defective myeloid responses in the development of late onset, age-associated Alzheimer disease (AD). Aging is characterized by a decline in myeloid metabolism that triggers maladaptive, neurotoxic immune responses. TREM1 is an amplifier of pro-inflammatory myeloid responses, and here we find that Trem1 deficiency prevents age-dependent changes in myeloid metabolism, inflammation, and hippocampal memory function.

Oct 18, 2023 | pericles.pericles-prod.literatumonline.com | Shawn Murphy |Yue Liu |Cora L. Petersen-Cherubini |Matthew Xin

Multiple sclerosis (MS) is an immune-mediated inflammatory disease of the central nervous system (CNS). A defining characteristic of MS is the ability of autoreactive T lymphocytes to cross the blood brain barrier (BBB) and mediate inflammation within the CNS. Previous work from our lab found the gene Enpp2 to be highly upregulated in murine encephalitogenic T cells.

Oct 18, 2023 | onlinelibrary.wiley.com | Cora L. Petersen-Cherubini |Shawn Murphy |Matthew Xin |Yue Liu

Multiple sclerosis (MS) is an immune-mediated inflammatory disease of the central nervous system (CNS). A defining characteristic of MS is the ability of autoreactive T lymphocytes to cross the blood brain barrier (BBB) and mediate inflammation within the CNS. Previous work from our lab found the gene Enpp2 to be highly upregulated in murine encephalitogenic T cells.