Parkinson’s disease

Giulia Ambrosi, Silvia Cerri, Fabio Blandini

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Parkinson’s disease (PD), the second most common neurodegenerative disease after Alzheimer’s disease, affects approximately 1 % of the population over 65 years of age. PD is primarily a sporadic disease and aging is the principal risk factor. Sporadic PD is a complex multifactorial disorder with variable contribution of genetic susceptibility and environmental factors. Several mechanisms are involved in the disease pathogenesis, such as mitochondrial dysfunctions, oxidative damage, autophagic alterations, proteasome impairment and protein aggregation [1]. There are also familial forms of PD, accounting for 5–10 % of all cases, associated with mutations in PARK genes. Interestingly, PARK genes encode for proteins involved in the maintenance of protein homeostasis, mitochondrial integrity and release of neurotransmitter-containing vesicles [2]. One of the major pathological hallmarks of PD is the accumulation of α-synuclein-containing aggregates (Lewy bodies) in neuronal perikarya and processes as a consequence of the proteolytic deficit, typical of the pathology.

Original languageEnglish
Title of host publicationMetabolism of Human Diseases: Organ Physiology and Pathophysiology
PublisherSpringer-Verlag Wien
Pages29-33
Number of pages5
ISBN (Print)9783709107157, 9783709107140
DOIs
Publication statusPublished - Jan 1 2014

ASJC Scopus subject areas

  • Medicine(all)

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