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First published online May 14, 2007
doi: 10.1242/10.1242/jcs.03443

Journal of Cell Science 120, 1707-1716 (2007)
Published by The Company of Biologists 2007
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Commentary

A cell biological perspective on mitochondrial dysfunction in Parkinson disease and other neurodegenerative diseases

Wim Mandemakers, Vanessa A. Morais and Bart De Strooper*

Center for Human Genetics, K.U.Leuven and Department of Molecular and Developmental Genetics, VIB, Herestraat 49, 3000 Leuven, Belgium

* Author for correspondence (e-mail: Bart.destrooper{at}med.kuleuven.be)

Accepted 13 March 2007

Dysfunction of mitochondria is frequently proposed to be involved in neurodegenerative disease. Deficiencies in energy supply, free radical generation, Ca2+ buffering or control of apoptosis, could all theoretically contribute to progressive decline of the central nervous system. Parkinson disease illustrates how mutations in very different genes finally impinge directly or indirectly on mitochondrial function, causing subtle but finally fatal dysfunction of dopaminergic neurons. Neurons in general appear more sensitive than other cells to mutations in genes encoding mitochondrial proteins. Particularly interesting are mutations in genes such as Opa1, Mfn1 and Dnm1l, whose products are involved in the dynamic morphological alterations and subcellular trafficking of mitochondria. These indicate that mitochondrial dynamics are especially important for the long-term maintenance of the nervous system. The emerging evidence clearly demonstrates the crucial role of specific mitochondrial functions in maintaining neuronal circuit integrity.

Key words: Neurodegenerative, Mitochondria, Oxidative stress, Parkinson disease, OXPHOS, Apoptosis, Mitochondrial dynamics




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