| First Author | Rodríguez-Navarro JA | Year | 2007 |
| Journal | J Neurochem | Volume | 103 |
| Issue | 1 | Pages | 98-114 |
| PubMed ID | 17623040 | Mgi Jnum | J:125148 |
| Mgi Id | MGI:3757725 | Doi | 10.1111/j.1471-4159.2007.04762.x |
| Citation | Rodriguez-Navarro JA, et al. (2007) Mortality, oxidative stress and tau accumulation during ageing in parkin null mice. J Neurochem 103(1):98-114 |
| abstractText | 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. |
