I know that amyloidosis refers to conditions wherein soluble proteins become insoluble and are deposited in the extracellular space of various tissues. Accordingly, many different types of amyloïdosis derived from different proteins exist. I would like to know whether A-beta peptides derived from peripheral APP are able to form oligomers and plaques as they do in the brain.
Jeffery Kelly at Scripps has studied this disease at a molecular level in great detail. I recall a lecture of his on the effects of aggregation of transthyretin on other organs such as the kidney and heart. He has a list of his publications on his web page. Just google in his name.
There Abeta-containing plaques in the eyes. See this paper, for example:
http://www.ncbi.nlm.nih.gov/pubmed/19834067
Also, Abeta oligomers can be detected in CSF and serum. See this, for example:
http://www.ncbi.nlm.nih.gov/pubmed/23811027
Check V. Askanas and W. K. Engel, “Newest pathogenetic considerations in inclusion-body myositis: possible role of amyloid-beta, cholesterol, relation to aging and to Alzheimer's disease,” Current Rheumatology Reports, vol. 4, no. 5, pp. 427–433, 2002.
there are some great reviews by the Gladstone Group (Robert Mahley is one of the authors) - also to review:
a pancreas paper by J. Miklossy (neurobiol of aging 2010), The DJ. Selkoe (Science 1989) and AE Roher examined temporalis muscle (American J. Pathology 2000)
but beware of IHC staining data of amyloid in the periphery- it can have artifactual staining due to the differences in tissue types.
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