Format

Send to

Choose Destination
Lancet Neurol. 2008 Jan;7(1):97-109.

Mitochondria in the aetiology and pathogenesis of Parkinson's disease.

Author information

1
University Department of Clinical Neurosciences and Institute of Neurology, University College London, London, UK. a.schapira@medsch.ucl.ac.uk

Abstract

Several biochemical abnormalities have been described in the brains of patients with Parkinson's disease (PD), including oxidative stress and mitochondrial dysfunction. The identification of specific gene mutations that cause PD has reinforced the relevance of oxidative stress and mitochondrial dysfunction in the familial and the sporadic forms of the disease. The proteins that are associated with familial PD--PTEN-induced putative kinase 1 (PINK1), DJ-1, alpha-synuclein, leucine-rich repeat kinase 2, and, possibly, parkin--are either mitochondrial proteins or are associated with mitochondria, and all interface with the pathways of oxidative stress and free radical damage. Insights into the aetiology and pathogenesis of PD provide hope that drugs or cocktails of drugs that might successfully intervene in the pathogenesis and slow the progression of the disease can be derived from the study of the converging rather than diverging pathways to cell dysfunction and death.

PMID:
18093566
DOI:
10.1016/S1474-4422(07)70327-7
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center