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Brain aging and late-onset Alzheimer's disease: many open questions

Published online by Cambridge University Press:  12 July 2012

Christian Behl*
Affiliation:
Institute for Pathobiochemistry, University Medical Center of the Johannes Gutenberg University Mainz, Germany
*
Correspondence should be addressed to: Christian Behl, Director, Institute for Pathobiochemistry, University Medical Center of the Johannes Gutenberg University Mainz, D-55099 Mainz, Germany. Phone: +49 6131 3925890; Fax: +49 6131 39 25792. Email: cbehl@uni-mainz.de.

Abstract

Despite decades of research in the field of Alzheimer's disease (AD), a real understanding of its molecular pathophysiology and treatments relevant to the day-to-day lives of patients remain out of reach. Research has, with good reason, focused on certain key pathways and potential mechanisms, but sometimes this has been at the expense of work on other theories, which may be slowing down progress in this field. Interesting theories at present include oxidative stress and caloric restriction. Work on the Aβ cascade should continue but with a shift in focus to its intracellular effects and an awareness that additional pathogenetic factors and processes must be involved – most importantly, brain aging. Hyperphosphorylation of tau, for instance, provides another interesting pathway, with one old drug showing promise in this regard. Moreover, work in epigenetics and on protein homeostasis has produced interesting findings and both lines of investigation may reveal suitable targets for future intervention. Taken together, analysis of the biochemistry of aged neurons and the interplay with pathways of neurodegeneration may lead to a better understanding of AD and how to treat and prevent this condition.

Type
Research Article
Copyright
Copyright © International Psychogeriatric Association 2012

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