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Both diseases are characterized by amyloid deposition in target tissues: aggregation of amylin in T2DM is associated with loss of insulin\u2010secreting \u03b2\u2010cells, while amyloid \u03b2 (A\u03b2) aggregation in AD brain is associated with neuronal loss. Here, we used quantitative iTRAQ proteomics as a discovery tool to show that both A\u03b2 and human amylin (HA) deregulate identical proteins, a quarter of which are mitochondrial, supporting the notion that mitochondrial dysfunction is a common target in these two amyloidoses. A functional validation revealed that mitochondrial complex IV activity was significantly reduced after treatment with either HA or A\u03b2, as was mitochondrial respiration. In comparison, complex I activity was reduced only after treatment with HA. A\u03b2 and HA, but not the non\u2010amyloidogenic rat amylin, induced significant increases in the generation of ROS. Co\u2010incubation of HA and A\u03b2 did not produce an augmented effect in ROS production, again suggesting common toxicity mechanisms. In conclusion, our data suggest that A\u03b2 and HA both exert toxicity, at least in part, <jats:italic>via<\/jats:italic> mitochondrial dysfunction, thus restoring their function may be beneficial for both AD and T2DM.<\/jats:p>","DOI":"10.1002\/pmic.200900651","type":"journal-article","created":{"date-parts":[[2010,2,22]],"date-time":"2010-02-22T11:09:39Z","timestamp":1266836979000},"page":"1621-1633","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":125,"title":["A\u03b2 and human amylin share a common toxicity pathway <i>via<\/i> mitochondrial dysfunction"],"prefix":"10.1002","volume":"10","author":[{"given":"Yun\u2010An","family":"Lim","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Virginie","family":"Rhein","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ginette","family":"Baysang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fides","family":"Meier","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anne","family":"Poljak","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark","family":"J. 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