Article

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

University Department of Clinical Neurosciences and Institute of Neurology, University College London, London, UK.
The Lancet Neurology (impact factor: 23.46). 02/2008; 7(1):97-109. DOI:10.1016/S1474-4422(07)70327-7 pp.97-109
Source: PubMed

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.

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Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.

Keywords

biochemical abnormalities
 
brains
 
cause PD
 
cell dysfunction
 
converging
 
familial
 
free radical damage
 
Insights
 
leucine-rich repeat kinase 2
 
mitochondrial dysfunction
 
mitochondrial proteins
 
oxidative stress
 
Parkinson's disease
 
pathogenesis
 
PD
 
PINK1
 
slow
 
specific gene mutations