Mitochondrial biology in Alzheimer's disease pathogenesis

Authors: Galindo, María F.¹; Ikuta, Ichiro²; Zhu, Xiongwei³; Casadesus, Gemma⁴; Jordán, Joaquín⁵

Source: Journal of Neurochemistry, Volume 114, Number 4, August 2010 , pp. 933-945(13)

Publisher: Wiley-Blackwell

Abstract:

J. Neurochem. (2010) 114, 933-945. Abstract

Despite the increasing knowledge of Alzheimer's disease (AD) management with novel pharmacologic agents, most of them are only transiently fixing symptomatic pathology. Currently there is rapid growth in the field of neuroprotective pharmacology and increasing focus on the involvement of mitochondria in this devastating disease. This review is directed at understanding the role of mitochondria-mediated pathways in AD and integrating basic biology of the mitochondria with knowledge of possible pharmacologic targets for AD treatment in an attempt to elucidate novel mitochondria-driven therapeutic interventions useful to both clinical and basic research.

Keywords: apoptosis; Bax; beta-amyloid; mitochondrial membrane permeabilization; mitochondrial membrane potential; mitochondrial permeability transition pore; reactive oxygen species

Document Type: Research article

DOI: http://dx.doi.org/10.1111/j.1471-4159.2010.06814.x

Affiliations: 1: Unidad de Neuropsicofarmacología Translacional, Complejo Hospitalario Universitario de Albacete, Albacete, Spain 2: College of Medicine, SUNY Upstate Medical University, Syracuse, New York, USA 3: Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA 4: Department of Neurosciences, Case Western Reserve University, Cleveland, Ohio, USA 5: Grupo de Neurofarmacología, Centro Regional de Investigaciones Biomédicas and Departamento de Ciencias Médicas, Facultad de Medicina, Universidad Castilla-La Mancha, Albacete, Spain

Publication date: 2010-08-01

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