Sci. Aging Knowl. Environ., 1 December 2004
Vol. 2004, Issue 48, p. pe42
[DOI: 10.1126/sageke.2004.48.pe42]


Mitochondrial Injury: A Hot Spot for Parkinsonism and Parkinson's Disease?

Benoit I. Giasson

The author is in the Department of Pharmacology at the University of Pennsylvania School of Medicine, Philadelphia, PA, 19104, USA. E-mail: giassonb{at}

Key Words: Parkinson's disease • Mitochondria • {alpha}-synuclein • parkin • E3 ligase • DJ-1 • PINK1

Abstract: The recent identification of genes (parkin, DJ-1, and PINK1) involved in recessive autosomal parkinsonism, and the indications that these proteins may have protective effects on the mitochondria, has led to the reemergence of the notion that mitochondrial dysfunction might play a central role in the etiology of sporadic Parkinson's disease (PD). This idea has previously been supported by biochemical analyses showing reduced mitochondrial activity in PD patients and in animal models of PD generated by the selective inhibition of mitochondria activity. However, the involvement of DJ-1 or PINK1 loss of function in classical idiopathic PD, characterized by pathological inclusions composed of aggregated {alpha}-synuclein protein, has still not been evaluated. More detailed studies of the possible interactions between parkin, DJ-1, PINK1, and {alpha}-synuclein and their effects on mitochondria are needed to more adequately define the biological pathways that may convergently or independently lead to parkinsonism.

Citation: B. I. Giasson, Mitochondrial Injury: A Hot Spot for Parkinsonism and Parkinson's Disease? Sci. Aging Knowl. Environ. 2004 (48), pe42 (2004).

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Mutations in PTEN-induced putative kinase 1 associated with recessive parkinsonism have differential effects on protein stability.
A. Beilina, M. Van Der Brug, R. Ahmad, S. Kesavapany, D. W. Miller, G. A. Petsko, and M. R. Cookson (2005)
PNAS 102, 5703-5708
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