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This Article Figures Only Full Text Full Text (PDF) All Versions of this Article: 01.wnl.0000192309.26571.a7v1 66/1_suppl_1/S118    most recent Correspondence: Submit a response Alert me when this article is cited Alert me when Correspondence are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by May, B. C.H. Articles by Cohen, F. E. Search for Related Content PubMed PubMed Citation Articles by May, B. C.H. Articles by Cohen, F. E.

Developing therapeutics for the diseases of protein misfolding

From the Institute for Neurodegenerative Diseases (B.C.H.M.) and Department of Cellular and Molecular Pharmacology (C.G., F.E.C.), University of California, San Francisco, CA.

Address correspondence and reprint requests to Dr. Barnaby C.H. May, Institute for Neurodegenerative Diseases, University of California San Francisco, Genentech Hall, 600 16th Street, Box 2240, San Francisco, CA 94143-2240; e-mail: alchemi{at}itsa.ucsf.edu.

Our current structural and biologic understanding of the misfolding diseases has restricted the development of therapies that target these diseases at a molecular level. The prion diseases are illustrative of this group of misfolding disorders and provide a model system for therapeutic intervention. Strategies to inhibit the replication and accumulation of the prion protein are being developed and have entered animal and clinical studies. Due to the underlying molecular basis of this disease class, many of the therapeutic approaches used to target prion misfolding have parallels in other misfolding diseases.

This article was previously published in electronic format as an Expedited E-Pub at www.neurology.org.

Supported by National Institutes of Health Grants AG21601, AG10770, AG02132, and NS41997, and the Taube Family Foundation Program in Huntington's Disease Research.

Disclosure: The authors report no conflicts of interest.

Received June 22, 2005. Accepted in final form October 14, 2005.