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Clin Chim Acta. 2015 Sep 20;449:68-76. doi: 10.1016/j.cca.2015.04.042. Epub 2015 Jun 3.

Candidate genes for Parkinson disease: Lessons from pathogenesis.

Author information

1
IRCCS Casa Sollievo della Sofferenza, CSS-Mendel Institute, San Giovanni Rotondo, Italy.
2
IRCCS Casa Sollievo della Sofferenza, CSS-Mendel Institute, San Giovanni Rotondo, Italy; Dept. of Biological and Environmental Sciences, University of Messina, Messina, Italy.
3
IRCCS Casa Sollievo della Sofferenza, CSS-Mendel Institute, San Giovanni Rotondo, Italy; Section of Neurosciences, Dept. of Medicine and Surgery, University of Salerno, Salerno, Italy. Electronic address: e.valente@css-mendel.it.

Abstract

Parkinson disease (PD) is a multifactorial neurodegenerative disease characterized by the progressive loss of specific neuronal populations and accumulation of Lewy bodies in the brain, leading to motor and non-motor symptoms. In a small subset of patients, PD is dominantly or recessively inherited, while a number of susceptibility genetic loci have been identified through genome wide association studies. The discovery of genes mutated in PD and functional studies on their protein products have provided new insights into the molecular events leading to neurodegeneration, suggesting that few interconnected molecular pathways may be deranged in all forms of PD, triggering neuronal loss. Here, we summarize the most relevant findings implicating the main PD-related proteins in biological processes such as mitochondrial dysfunction, misfolded protein damage, alteration of cellular clearance systems, abnormal calcium handling and altered inflammatory response, which represent key targets for neuroprotection.

KEYWORDS:

Autophagy; Genetics; Inflammation; Misfolded protein damage; Mitochondria; Parkinson disease

PMID:
26048192
DOI:
10.1016/j.cca.2015.04.042
[Indexed for MEDLINE]

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