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© 2020 Federation of American Societies for Experimental Biology.BACKGROUND SNCA multiplication is a genomic cause of familial PD, showing dosage-dependent toxicity. Until now, nonallelic homologous recombination was suggested as the mechanism of SNCA duplication, based on various types of repetitive elements found in the spanning region of the breakpoints. However, the sequence at the breakpoint was analyzed only for 1 case. OBJECTIVES We have analyzed the breakpoint sequences of 6 patients with PD who had duplicated SNCA using whole-g
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