Hereditary Early-Onset Parkinson's Disease Caused by Mutations in <i>PINK1</i>

Enza Maria Valente(Medway School of Pharmacy), Patrick M. Abou‐Sleiman(Medway School of Pharmacy), Viviana Caputo(Medway School of Pharmacy), Miratul M. K. Muqit(Medway School of Pharmacy), Kirsten Harvey(Medway School of Pharmacy), Suzana Gispert(Goethe University Frankfurt), Zeeshan Ali(Goethe University Frankfurt), Domenico Del Turco(Goethe University Frankfurt), Anna Rita Bentivoglio(Medway School of Pharmacy), Daniel G. Healy(Medway School of Pharmacy), Alberto Albanese(Medway School of Pharmacy), Robert Nussbaum(Medway School of Pharmacy), Rafael González-Maldonado(Medway School of Pharmacy), Thomas Deller(Goethe University Frankfurt), Sergio Salvi(Medway School of Pharmacy), Pietro Cortelli(University of Modena and Reggio Emilia), William P. Gilks(Medway School of Pharmacy), David S. Latchman(Medway School of Pharmacy), Robert J. Harvey(Medway School of Pharmacy), Bruno Dallapiccola(Medway School of Pharmacy), Georg Auburger(Medway School of Pharmacy), Nicholas Wood(Medway School of Pharmacy)
Science
April 19, 2004
Cited by 3,462Open Access
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Abstract

Parkinson's disease (PD) is a neurodegenerative disorder characterized by degeneration of dopaminergic neurons in the substantia nigra. We previously mapped a locus for a rare familial form of PD to chromosome 1p36 (PARK6). Here we show that mutations in PINK1 (PTEN-induced kinase 1) are associated with PARK6. We have identified two homozygous mutations affecting the PINK1 kinase domain in three consanguineous PARK6 families: a truncating nonsense mutation and a missense mutation at a highly conserved amino acid. Cell culture studies suggest that PINK1 is mitochondrially located and may exert a protective effect on the cell that is abrogated by the mutations, resulting in increased susceptibility to cellular stress. These data provide a direct molecular link between mitochondria and the pathogenesis of PD.


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