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Pk\u2212\/\u2212 mice have reduced life span and age\u2010related reduced exploratory behaviour, abnormal walking and posture, and behaviours similar to those of early Parkinson\u2019s disease (PD), reduced number of nigrostriatal DA neurons and proapoptotic shifts in the survival\/death proteins in midbrain and striatum. Contrary to young pk\u2212\/\u2212 animals 24\u2010month\u2010old pk\u2212\/\u2212 mice do not have compensatory elevation of GSH in striatum, glutathione reductase (GR) and glutathione peroxidase (GPx) activities are increased and catalase unchanged. Aged pk\u2212\/\u2212 mice accumulate high levels of tau and fail to up\u2010regulate CHIP and HSP70. Our results suggest that aged pk\u2212\/\u2212 mice lack of the compensatory mechanisms that maintain a relatively normal DA function in early adulthood. This study could help to explain the effects of ageing in patients with genetic risks for Parkinson\u2019s disease.<\/jats:p>","DOI":"10.1111\/j.1471-4159.2007.04762.x","type":"journal-article","created":{"date-parts":[[2007,7,10]],"date-time":"2007-07-10T12:31:18Z","timestamp":1184070678000},"page":"98-114","source":"Crossref","is-referenced-by-count":76,"title":["Mortality, oxidative stress and tau accumulation during ageing in parkin null mice"],"prefix":"10.1111","volume":"103","author":[{"given":"Jose A.","family":"Rodr\u00edguez\u2010Navarro","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. 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