Peroxisome proliferator-activated receptor oxidative stress

The activation of the retinoid X receptor, which dimerizes with peroxisome proliferator-activated receptors (PPARs), leads to an enhanced clearance of A(f from the brain of a transgenic mouse model of AD, with increased expression of ApoE and its main transporters. Both a PPARy agonist (ciplitazone) and a PPARa agonist (WT 14.643) are able to protect neurons by modulating mitochondrial fusion and fission, leading to a better response of neurons to oxidative stress, suggesting that a PPAR-based therapy could act simultaneously in different cellular components [437]. 

Coleman, J.D., K.S. Prabhu, J.T. Thompson, P.S. Reddy, J.M. Peters, B.R. Peterson, C.C. Reddy, and J.P. Vanden Heuvel. 2007. The oxidative stress mediator 4-hydroxynonenal is an intracellular agonist of the nuclear receptor peroxisome proliferator-activated receptor-B/8 (PPARB/6 >. Free Radical Biolotv Medicine 42 1155-64. 

Almeida, M., E. Ambrogini, L. Han et al. Increased lipid oxidation causes oxidative stress, increased peroxisome proliferator-activated receptor-gamma expression, and diminished pro-osteogenic Wnt signaling in the skeleton. 284(40), 2009 27438-48. 

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