Danse-thérapie et Parkinson

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Neuroprotective strategies for basal ganglia degeneration: Parkinson’s and Huntington’s diseases

Identifieur interne : 000413 ( Main/Exploration ); précédent : 000412; suivant : 000414

Neuroprotective strategies for basal ganglia degeneration: Parkinson’s and Huntington’s diseases

Auteurs : Tajrena Alexi [Nouvelle-Zélande] ; Cesario V. Borlongan [États-Unis] ; Richard L. M. Faull [Nouvelle-Zélande] ; Chris E. Williams [Nouvelle-Zélande] ; Ross G. Clark [Nouvelle-Zélande] ; Peter D. Gluckman [Nouvelle-Zélande] ; Paul E. Hughes [Nouvelle-Zélande]

Source :

RBID : ISTEX:A5141262231446D599DF5115C9C1597A402317CB

Abstract

There are three main mechanisms of neuronal cell death which may act separately or cooperatively to cause neurodegeneration. This lethal triplet of metabolic compromise, excitotoxicity, and oxidative stress causes neuronal cell death that is both necrotic and apoptotic in nature. Aspects of each of these three mechanisms are believed to play a role in the neurodegeneration that occurs in both Parkinson’s and Huntington’s diseases. Strategies to rescue or protect injured neurons usually involve promoting neuronal growth and function or interfering with neurotoxic processes. Considerable research has been done on testing a large array of neuroprotective agents using animal models which mimic these disorders. Some of these approaches have progressed to the clinical arena. Here, we review neuroprotective strategies which have been found to successfully ameliorate the neurodegeneration associated with Parkinson’s and Huntington’s diseases. First, we will give an overview of the mechanisms of cell death and the background of Parkinson’s and Huntington’s diseases. Then we will elaborate on a range of neuroprotective strategies, including neurotrophic factors, anti-excitotoxins, antioxidants, bioenergetic supplements, anti-apoptotics, immunosuppressants, and cell transplantation techniques. Most of these approaches hold promise as potential therapies in the treatment of these disorders.

Url:
DOI: 10.1016/S0301-0082(99)00032-5


Affiliations:


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