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Glutamate and Mitochondria: Two Prominent Players in the Oxidative Stress-Induced Neurodegeneration.
Cassano, Tommaso; Pace, Lorenzo; Bedse, Gaurav; Lavecchia, Angelo Michele; De Marco, Federico; Gaetani, Silvana; Serviddio, Gaetano.
Afiliación
  • Cassano T; Department of Clinical and Experimental Medicine, University of Foggia, Viale Luigi Pinto 1, Foggia 71100, Italy. tommaso.cassano@unifg.it.
Curr Alzheimer Res ; 13(2): 185-97, 2016.
Article en En | MEDLINE | ID: mdl-26679860
ABSTRACT
The aetiology of major neurodegenerative diseases such as Alzheimer's disease (AD) and Parkinson's disease (PD) is still unknown, but increasing evidences suggest that glutamate and mitochondria are two prominent players in the oxidative stress (OS) process that underlie these illnesses. Although AD and PD have distinct pathological and clinical features, OS is a common mechanism contributing to neuronal damage. Glutamate is an important neurotransmitter in neurons and glial cells and is strongly dependent on calcium homeostasis and on mitochondrial function. In the present work we focused on glutamate- induced calcium signaling and its relation to the mitochondrial dysfunction with cell death processes. In addition, we have discussed how alterations in this pathway may lead or aggravate the neurodegenerative diseases. Finally, this review aims to stimulate further studies on this issue and thereby engage a new perspective regarding the design of possible therapeutic agents or the identification of biomarkers.
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Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Estrés Oxidativo / Ácido Glutámico / Enfermedades Neurodegenerativas / Mitocondrias Límite: Animals / Humans Idioma: En Revista: Curr Alzheimer Res Asunto de la revista: NEUROLOGIA Año: 2016 Tipo del documento: Article País de afiliación: Italia
Buscar en Google
Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Estrés Oxidativo / Ácido Glutámico / Enfermedades Neurodegenerativas / Mitocondrias Límite: Animals / Humans Idioma: En Revista: Curr Alzheimer Res Asunto de la revista: NEUROLOGIA Año: 2016 Tipo del documento: Article País de afiliación: Italia