Mitochondria are organelles with multiple functions essential for neural activities, and the dysfunction of which is implicated in the pathogenesis of AD, especially for sporadic and late-onset cases. The main research interest of my lab is to illustrate the underlying mechanisms of mitochondrial dysfunction in Alzheimer's disease and aging, with a goal of identifying novel targets for Alzheimer's disease prevention and therapy.
Yoo SE, Chen L, Na R, Liu Y, Rios C, Van Remmen H, Richardson A, Ran Q. Gpx4 ablation in adult mice results in a lethal phenotype accompanied by neuronal loss in brain. Free Radic Biol Med. 2012 May 1;52(9):1820-7.
Chen L, Yoo SE, Na R, Liu Y, Ran Q. Cognitive impairment and increased Aβ levels induced by paraquat exposure are attenuated by enhanced removal of mitochondrial H(2)O(2). Neurobiol Aging. 2012 Feb;33(2):432.e15-26.
Liang H, Yoo SE, Na R, Walter CA, Richardson A, Ran Q. Short form glutathione peroxidase 4 is the essential isoform required for survival and somatic mitochondrial functions. J Biol Chem. 2009 Nov 6;284(45):30836-44.
Chen L, Na R, Gu M, Salmon AB, Liu Y, Liang H, Qi W, Van Remmen H, Richardson A, Ran Q. Reduction of mitochondrial H2O2 by overexpressing peroxiredoxin 3 improves glucose tolerance in mice. Aging Cell. 2008 Dec;7(6):866-78.
Chen L, Na R, Gu M, Richardson A, Ran Q. Lipid peroxidation up-regulates BACE1 expression in vivo: a possible early event of amyloidogenesis in Alzheimer's disease. J Neurochem. 2008 Oct;107(1):197-207.