Monday, October 01, 2007

Mitochondrial downfall in Parkinson’s disease

The mutation of two genes associated with the development of Parkinson’s disease cooperate to regulate mitochondrial function when cells are stressed, reports a paper online in Nature Cell Biology this week. This link will help researchers understand the mechanisms underlying the neuronal degeneration seen in pathologies such as Parkinson‘s disease.

Julian Downward and colleagues investigated the mitochondrial protease Omi – the loss of which leads to a neurodegenerative disorder resembling Parkinson’s. They found that Omi is regulated by PINK1, which has been identified as an early-onset Parkinson’s disease susceptibility factor. The researchers show that, in response to various cellular stresses, PINK1 is essential for mitochondrial protection by Omi and keeps cells healthy. Strikingly, they also find that this cooperation is impaired in brain samples from Parkinson's disease patients carrying mutations in PINK1.

Finding this new interaction suggests that in the normal brain, PINK1 and Omi prevent the death of neuronal cells by protecting their mitochondria. The development of Parkinson’s disease would thus be linked to a higher susceptibility to neuronal death following stress.
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