HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Figures Only Full Text Full Text (PDF) All Versions of this Article: 01.wnl.0000192311.78890.3ev1 66/1_suppl_1/S110    most recent Correspondence: Submit a response Correspondence: View responses 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 HighWire Citing Articles via Google Scholar Google Scholar Articles by Buxbaum, J. N. Search for Related Content PubMed PubMed Citation Articles by Buxbaum, J. N.

Treatment and prevention of the amyloidoses

Can the lessons learned be applied to sporadic inclusion-body myositis?

From the Department of Molecular and Experimental Medicine, The Keck Autoimmune Disease Center, Division of Rheumatology Research, The Scripps Research Institute, La Jolla, CA.

Address correspondence and reprint requests to Dr. Joel N. Buxbaum, The Scripps Research Institute, Department of Molecular and Experimental Medicine, The Keck Autoimmune Disease Center, Division of Rheumatology Research, 10550 N. Torrey Pines Road, MEM-230, La Jolla, CA 92037; e-mail: jbux{at}scripps.edu

The amyloid fibril represents a final common pathologic pathway for a variety of human proteins, all of which have a propensity to misfold. Each seems to require a predisposing event to realize its fibrillogenic potential. It may be mutation, inappropriate or incomplete cleavage, overproduction, or the availability of a template for misfolding. Therapies have been based on decreasing the stimulus (inflammation in the case of AA) reducing the number of producing cells (AL) and a variety of approaches to removing the extracellular aggregates. Sporadic inclusion-body myositis (sIBM), while physically resembling the extracellular amyloidoses, is an intracellular disease, hence imposes the additional requirement of developing a therapy that can access and function inside the affected or potentially affected, cell. Current approaches to the treatment of other forms of amyloidosis are discussed in the context of their applicability, or lack thereof, to sIBM.

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

Supported by National Institutes of Health Grant 1R01 AG19259.

Disclosure: The authors report no conflicts of interest.

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

This article has been cited by other articles:

				S. A Greenberg How citation distortions create unfounded authority: analysis of a citation network BMJ, July 23, 2009; 339(jul20_3): b2680 - b2680. [Abstract] [Full Text] [PDF]

				K. Konstantopoulos, G. Vaiopoulos, A. Mailis, and J. N. Buxbaum Treatment and prevention of the amyloidoses: Can the lessons learned be applied to sporadic inclusion-body myositis? Neurology, June 27, 2006; 66(12): 1959 - 1959. [Full Text] [PDF]

				C. E. Finch A perspective on sporadic inclusion-body myositis: The role of aging and inflammatory processes Neurology, January 24, 2006; 66(1_suppl_1): S1 - S6. [Abstract] [Full Text] [PDF]

Correspondence: