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- Title
Mortality, oxidative stress and tau accumulation during ageing in parkin null mice.
- Authors
Rodríguez-Navarro, Jose A.; Casarejos, M. Jos; Menéndez, Jaime; Solano, Rosa M.; Rodal, Izaskun; Gómez, Ana; Yébenes, Justo García de; Mena, Maria A.
- Abstract
Young parkin null (pk−/−) mice have subtle abnormalities of behaviour, dopamine (DA) neurotransmission and free radical production, but no massive loss of DA neurons. We investigated whether these findings are maintained while ageing. Pk−/− mice have reduced life span and age-related reduced exploratory behaviour, abnormal walking and posture, and behaviours similar to those of early Parkinson’s disease (PD), reduced number of nigrostriatal DA neurons and proapoptotic shifts in the survival/death proteins in midbrain and striatum. Contrary to young pk−/− animals 24-month-old pk−/− 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−/− mice accumulate high levels of tau and fail to up-regulate CHIP and HSP70. Our results suggest that aged pk−/− 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’s disease.
- Subjects
AGING; BRAIN; NEURONS; OXIDATIVE stress; PROTEINS; PARKINSON'S disease; NEURAL transmission
- Publication
Journal of Neurochemistry, 2007, Vol 103, Issue 1, p98
- ISSN
0022-3042
- Publication type
Article
- DOI
10.1111/j.1471-4159.2007.04762.x