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Review
. 2010 Mar;13(2):235-46.

Novel therapeutics for Alzheimer's disease: an update

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Review

Novel therapeutics for Alzheimer's disease: an update

David J Bonda et al. Curr Opin Drug Discov Devel. 2010 Mar.

Abstract

As the most prevalent form of dementia worldwide, Alzheimer's disease (AD) continues to be a burden for patients and their families. In addition, with the global population of aged individuals increasing exponentially, AD represents a significant economic burden to society. The development of an effective approach for the treatment of AD is thus of major importance, as current treatment strategies are limited to agents that attenuate disease symptomatology without addressing the causes of disease. A considerable need exists for the development of an effective therapy to prevent, or at least delay, the progression of AD. Current hypotheses for the pathogenesis of AD are discussed in this review, with a particular emphasis on the implications of these hypotheses with respect to treatment strategies and preventive measures.

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References

    1. Mancuso M, Orsucci D, Siciliano G, Murri L. Mitochondria, mitochondrial DNA and Alzheimer's disease. What comes first? Curr Alzheimer Res. 2008;5(5):457–468. - PubMed
    1. Zhu X, Lee HG, Perry G, Smith MA. Alzheimer disease, the two-hit hypothesis: An update. Biochim Biophys Acta. 2007;1772(4):494–502. - PubMed
    1. Selkoe DJ. Toward a comprehensive theory for Alzheimer's disease. Hypothesis: Alzheimer's disease is caused by the cerebral accumulation and cytotoxicity of amyloid β-protein. Ann N Y Acad Sci. 2000;924:17–25. - PubMed
    1. Smith MA, Nunomura A, Zhu X, Takeda A, Perry G. Metabolic, metallic, and mitotic sources of oxidative stress in Alzheimer disease. Antioxid Redox Signal. 2000;2(3):413–420. - PubMed
    1. Atamna H, Frey WH., 2nd Mechanisms of mitochondrial dysfunction and energy deficiency in Alzheimer's disease. Mitochondrion. 2007;7(5):297–310. - PubMed

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