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| and China have published research suggesting that a class of currently used anti-cancer drugs as well as several previously untested synthetic compounds show effectiveness in reversing memory loss in two animal models of Alzheimer's' disease. who led the research conducted in fruit flies and mice, says he and his colleagues were surprised with their results, which, he stressed, used two independent experimental approaches the results of which clearly converged. Specifically, the research converged on what Zhong's team suggests is a preferred target for treating memory loss associated with the amyloid-beta (A?) plaques seen in advanced Alzheimer's patients. That target is the epidermal growth factor receptor, often called by its acronym, EGFR. Overexpression of the EGFR is a characteristic feature of certain cancers, notably a subset of lung cancers. Two targeted treatments, erlotinib (Tarceva) and gefitinib (Iressa), can dramatically, albeit transiently, reverse EGFR-positive cancers, by blocking the EGFR receptor and thus preventing its activation. The newly published research by Zhong's team suggests that the signaling within cells that is induced by EGFR activation also plays a role in the pathology - still poorly understood - involved in A?-associated memory loss seen in Alzheimer's patients. Zhong and colleagues previously had studied A?-associated memory loss in fruit flies with brain cells expressing the A?-42 peptide (a specific version of the protein, composed of 42 amino acids, seen in Alzheimer's plaques). These fruit flies are regarded as models of the illness in part because the A?-42 they manifest is encoded by a human gene, inserted in their genome.
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In behavioral experiments, such flies have been shown to suffer memory deficiencies analogous to those seen in human Alzheimer's. Enhanced activation of EGFR exacerbates memory loss in flies In the current round of experiments, Zhong's team demonstrated that enhanced activation of EGFRs in brain cells exacerbated memory loss in the A?-42 fruit fly model of Alzheimer's disease. This led them to dose 3-day-old flies of the same type with the two anti-cancer EGFR inhibitors over a week's time, which was shown in behavioral tests on day 11 to prevent memory loss. The results were then confirmed in mouse models of Alzheimer's, also based on the human A?-42 gene. This was remarkable, but even more so, says Zhong, because of a parallel but independent experimental process that also suggested EGFR as a drug target for Alzheimer's. This parallel process consisted of screening, by Zhong's collaborators in China, of some 2,000 synthetic compounds for activity against A?-induced memory loss in model fruit flies. Of these, 45 compounds showed positive results in fruit flies after two months of dosing. Nine of these were selected for testing in mouse models, of which four showed positive results after two months.
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