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Published online before print December 16, 2005, doi:10.1212/01.wnl.0000192311.78890.3e)
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Accepted ,

Treatment and prevention of the amyloidoses. Can the lessons learned be applied to sporadic inclusion-body myositis?

Joel N. Buxbaum MD*

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


* To whom correspondence should be addressed. E-mail: jbux{at}scripps.edu.

Abstract--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.




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Reply from the Author
Joel Buxbaum
Neurology Online, 13 Feb 2006 [Full text]
Treatment and prevention of amyloidoses: Can the lessons learned be applied to sporadic IBM?
Kostas Konstantopoulos, et al.
Neurology Online, 13 Feb 2006 [Full text]

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