4
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Mitochondrial dysfunction in Parkinson's disease.

      1 , 2
      Journal of neurochemistry
      Wiley-Blackwell
      MAM, DJ1, HTRA2, PINK1, VPS35, α-synuclein

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Parkinson's disease (PD) is the second most common neurodegenerative disease. About 2% of the population above the age of 60 is affected by the disease. The pathological hallmarks of the disease include the loss of dopaminergic neurons in the substantia nigra and the presence of Lewy bodies that are made of α-synuclein. Several theories have been suggested for the pathogenesis of PD, of which mitochondrial dysfunction plays a pivotal role in both sporadic and familial forms of the disease. Dysfunction of the mitochondria that is caused by bioenergetic defects, mutations in mitochondrial DNA, nuclear DNA gene mutations linked to mitochondria, and changes in dynamics of the mitochondria such fusion or fission, changes in size and morphology, alterations in trafficking or transport, altered movement of mitochondria, impairment of transcription, and the presence of mutated proteins associated with mitochondria are implicated in PD. In this review, we provide a detailed overview of the mechanisms that can cause mitochondrial dysfunction in PD. We bring to the forefront, new signaling pathways such as the retromer-trafficking pathway and its implication in the disease and also provide a brief overview of therapeutic strategies to improve mitochondrial defects in PD. Bioenergetic defects, mutations in mitochondrial DNA, nuclear DNA gene mutations, alterations in mitochondrial dynamics, alterations in trafficking/transport and mitochondrial movement, abnormal size and morphology, impairment of transcription and the presence of mutated proteins associated with mitochondria are implicated in PD. In this review, we focus on the mechanisms underlying mitochondrial dysfunction in PD and bring to the forefront new signaling pathways that may be involved in PD. We also provide an overview of therapeutic strategies to improve mitochondrial defects in PD. This article is part of a special issue on Parkinson disease.

          Related collections

          Author and article information

          Journal
          J. Neurochem.
          Journal of neurochemistry
          Wiley-Blackwell
          1471-4159
          0022-3042
          Oct 2016
          : 139 Suppl 1
          Affiliations
          [1 ] Appel Alzheimer's Disease Research Institute, Brain and Mind Research Institute, Weill Cornell Medicine, New York City, New York, USA. anb2055@med.cornell.edu.
          [2 ] Brain and Mind Research Institute, Weill Cornell Medicine, New York City, New York, USA. fbeal@med.cornell.edu.
          Article
          10.1111/jnc.13731
          27546335
          bec64969-a595-4579-9dd1-7dacb82ad4a7
          History

          MAM,DJ1,HTRA2,PINK1,VPS35,α-synuclein
          MAM, DJ1, HTRA2, PINK1, VPS35, α-synuclein

          Comments

          Comment on this article