Premium
P2‐129: A Small Molecule Anti‐Neuroinflammatory Experimental Therapeutic Inhibited IL‐1Beta Levels After Traumatic Brain Injury with no Effect on Microglia Physiological Responses
Author(s) -
Van Eldik Linda J.,
Zhou Zhengqiu,
Watterson D. Martin,
Bachstetter Adam D.
Publication year - 2016
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2016.06.1499
Subject(s) - proinflammatory cytokine , neuroinflammation , microglia , traumatic brain injury , medicine , cytokine , inflammation , neuroprotection , neuroscience , brain damage , immunology , pharmacology , biology , psychiatry
received mitochondrial lysate injection had increased messenger RNA (mRNA) levels of TNFa, while mice injected with mtDNA displayed a trend towards increased TNFa mRNA. TREM2 mRNA levels were significantly reduced in both groups. CCL11 mRNA levels trended higher in both groups. Mice injected with mitochondrial lysates or mtDNA had increased phosphorylated NFkB. However, only mice injected with mtDNA had increased levels of phosphorylated AKT and colony stimulating factor 1 receptor (CSF1R) protein expression. A trend towards increased GFAP mRNA and protein expression was observed. Further immunohistochemical analysis confirmed an increase in GFAP expression in mice injected with mtDNA, but not mice injected with mitochondrial lysates. A trend towards increased GFAP positive cells was observed in mice injected with mtDNA. APP mRNA and protein levels were significantly increased in mice injected with mitochondrial lysates but not in mice injected with mtDNA. Conclusions: These data indicate molecules derived frommitochondria can induce neuroinflammation in vivo, and alter APP biology.