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Etiology and pathogenesis of Parkinson’s disease: role of mitochondrial pathology

Authors Ottolini D, Calì T, Brini M

Received 28 January 2013

Accepted for publication 15 March 2013

Published 16 May 2013 Volume 2013:3 Pages 55—70


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 4

Denis Ottolini, Tito Calì, Marisa Brini

Department of Comparative Biomedicine and Food Science, University of Padova, Padova, Italy

Abstract: Neurons critically rely on mitochondrial activity: they are characterized by high energy demand and they are totally dependent on the process of oxidative phosphorylation to produce adenosine triphosphate. Thus, any impairment in mitochondrial function results in neuronal damage and degeneration. Some particular neuronal populations are more susceptible to mitochondrial damage, as it has been recently proposed for the ventral midbrain dopaminergic neurons, the degeneration of which represents a clinical sign of Parkinson’s disease. Different cellular pathways are involved in the pathogenesis of this neurodegenerative disease, but intriguingly both sporadic and familial forms share common features that essentially recapitulate mitochondrial dysfunction. Mitochondrial biogenesis, bioenergetics, mitochondria dynamics, and quality-control process are the main affected pathways. General consensus agrees on the possibility that deficiency in these processes may represent the cause rather than the consequence of neurodegeneration. In this review, we will discuss these aspects and the substantial achievements that have been reached in recent years in identifying specific defects in precise biological processes, eg, mitochondrial quality control. The development of cell and animal genetic models has been an important tool to dissect numerous molecular details; for this reason, we will mainly refer to experiments performed on them.

Keywords: mitochondria, Parkinson’s disease, α-synuclein, PINK1/parkin, DJ-1, LRRK2

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