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AimsThe aggregation of Huntingtin (HTT) protein and of its moiety encoded by its Exon1 (HTTExon1) into fibrillar structures inside neurons is the molecular hallmark of Huntington's disease. Prion‐like transmission of these aggregates between cells has been demonstrated. The cell‐to‐cell transmission mechanisms of these protein aggregates and the susceptibility of different kinds of neuronal cells...
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