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  • 1
    Publication Date: 2019
    Description: 〈p〉Publication date: 1 November 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Free Radical Biology and Medicine, Volume 143〈/p〉 〈p〉Author(s): Xiaojia Ren, Angela Hinchie, Aaron Swomley, David K. Powell, D. Allan Butterfield〈/p〉 〈div xml:lang="en"〉 〈h5〉Abstract〈/h5〉 〈div〉〈p〉Parkinson disease (PD) is the second most common neurodegenerative disease associated with aging. Dopaminergic neuronal degeneration and α-synuclein aggregation are commonly found in PD brain. Oxidative damage and inflammation often are considered as etiological factors of PD, although the detailed mechanisms still remain unknown. Gender and aging are two important risk factors to PD, and gene mutations and certain environmental factors have been implicated in this disease. The current study employed 〈em〉PTEN-induced putative kinase -1〈/em〉 (〈em〉PINK1〈/em〉) knockout (KO) rats, since mutations in 〈em〉PINK-1〈/em〉 lead to familial PD. We evaluated the oxidative damage in the brain of 〈em〉PINK1〈/em〉 KO rats, and we used MRI and MRS to measure the ventricle sizes and neurochemical metabolite profiles in these rats as a function of age and gender. Distinct gender- and age-related alterations were found. The results are discussed with respect to the suitabililty of this unique rat as a faithful model of known characteristics of PD.〈/p〉〈/div〉 〈/div〉 〈h5〉Graphical abstract〈/h5〉 〈div〉〈p〉PINK1 is a mitochondrial surveillance kinase that contributes to the processes involved in ridding the cell of damaged mitochondria. Mutations in the 〈em〉pink 1〈/em〉 gene lead to inherited Parkinson disease (PD). This study examined the effects of age and gender on the 〈em〉PINK1〈/em〉 knockout rat to determine its fidelity to certain biochemical and clinical characteristics of PD.〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0891584919309153-fx1.jpg" width="446" alt="Image 1" title="Image 1"〉〈/figure〉〈/p〉〈/div〉
    Print ISSN: 0891-5849
    Electronic ISSN: 1873-4596
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Published by Elsevier
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