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Rethinking Alzheimer's Disease Therapy: Are Mitochondria the Key?

Issue title: Mitochondria and Neurodegenerative Diseases

Guest editors: Xiongwei Zhu, M. Flint Beal, Xinglong Wang, George Perry and Mark A. Smith

Article type: Review Article

Authors: Ankarcrona, Mariaa; * | Mangialasche, Francescab; c | Winblad, Bengta

Affiliations: [a] KI-Alzheimer's Disease Research Center, Karolinska Institutet, Department of Neurobiology, Care Sciences and Society (NVS), Huddinge, Sweden | [b] Aging Research Center, Karolinska Institutet, Stockholm, Sweden | [c] Institute of Gerontology and Geriatrics, Department of Clinical and Experimental Medicine, University of Perugia, Italy

Correspondence: [*] Correspondence to: Maria Ankarcrona, KI-Alzheimer's Disease Research Center, Karolinska Institutet, Department of Neurobiology, Care Sciences and Society (NVS), Novum 5th floor, SE-141 86 Huddinge, Sweden. Tel.: +46 8 58583617; Fax: +46 8 58583610; E-mail: maria.ankarcrona@ki.se.

Keywords: Alzheimer's disease, drug target, mitochondria, therapy

DOI: 10.3233/JAD-2010-100327

Journal: Journal of Alzheimer's Disease, vol. 20, no. s2, pp. S579-S590, 2010

Accepted 5 April 2010
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Published: 3 June 2010
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Abstract

The number of people suffering from Alzheimer's disease (AD) is constantly increasing worldwide since humans live longer and age is the strongest risk factor for AD. Currently available medications for AD do not interfere with the progressive loss of synapses and neurons in the AD brain. Therefore, the development of disease modifying therapies is a major future goal. Mitochondria provide cellular energy and are crucial for proper neuronal activity and survival. Mitochondrial dysfunction is evident in early stages of AD and is involved in AD pathogenesis. The development of drugs that protect mitochondria from damage is therefore a promising strategy for AD therapy. In this review, we will discuss current available medications for AD, drugs under clinical testing, and mitochondria as a novel drug target.

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