ParkinsonFranceV1, Hal, Curation, bibRecord, 000323

Downstream mechanisms triggered by mitochondrial dysfunction in the basal ganglia: From experimental models to neurodegenerative diseases

Identifieur interne : 000323 ( Hal/Curation ); précédent : 000322; suivant : 000324

Downstream mechanisms triggered by mitochondrial dysfunction in the basal ganglia: From experimental models to neurodegenerative diseases

Auteurs : Paolo Gubellini ; Barbara Picconi ; Massimiliano Di Filippo ; Paolo Calabresi

Source :

BBA - Molecular Basis of Disease [ 0925-4439 ] ; 2009-12-05.

RBID : Hal:hal-00543006

English descriptors

mix :
- 3-nitropropionic acid, Huntington's chorea, PINK1, Parkinson's disease, dopamine, huntingtin, long-term potentiation, parkin, rotenone, striatum.

Abstract

Mitochondrial dysfunctions have been implicated in the cellular processes underlying several neurodegenerative disorders affecting the basal ganglia. These include Huntington's chorea and Parkinson's disease, two highly debilitating motor disorders for which recent research has also involved gene mutation linked to mitochondrial deficits. Experimental models of basal ganglia diseases have been developed by using toxins able to disrupt mitochondrial function: these molecules act by selectively inhibiting mitochondrial respiratory complexes, uncoupling cellular respiration. This in turn leads to oxidative stress and energy deficit that trigger critical downstream mechanisms, ultimately resulting in neuronal vulnerability and loss. Here we review the molecular and cellular downstream effects triggered by mitochondrial dysfunction, and the different experimental models that are obtained by the administration of selective mitochondrial toxins or by the expression of mutant genes.

Url:

https://hal.archives-ouvertes.fr/hal-00543006

DOI: 10.1016/j.bbadis.2009.08.001

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Hal:hal-00543006

Le document en format XML

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<author><name sortKey="Picconi, Barbara" sort="Picconi, Barbara" uniqKey="Picconi B" first="Barbara" last="Picconi">Barbara Picconi</name>
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<author><name sortKey="Di Filippo, Massimiliano" sort="Di Filippo, Massimiliano" uniqKey="Di Filippo M" first="Massimiliano" last="Di Filippo">Massimiliano Di Filippo</name>
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<front><div type="abstract" xml:lang="en">Mitochondrial dysfunctions have been implicated in the cellular processes underlying several neurodegenerative disorders affecting the basal ganglia. These include Huntington's chorea and Parkinson's disease, two highly debilitating motor disorders for which recent research has also involved gene mutation linked to mitochondrial deficits. Experimental models of basal ganglia diseases have been developed by using toxins able to disrupt mitochondrial function: these molecules act by selectively inhibiting mitochondrial respiratory complexes, uncoupling cellular respiration. This in turn leads to oxidative stress and energy deficit that trigger critical downstream mechanisms, ultimately resulting in neuronal vulnerability and loss. Here we review the molecular and cellular downstream effects triggered by mitochondrial dysfunction, and the different experimental models that are obtained by the administration of selective mitochondrial toxins or by the expression of mutant genes.</div>
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Downstream mechanisms triggered by mitochondrial dysfunction in the basal ganglia: From experimental models to neurodegenerative diseases

Downstream mechanisms triggered by mitochondrial dysfunction in the basal ganglia: From experimental models to neurodegenerative diseases

Source :

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri