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Experimental modelling of -synuclein aggregation and spreading in synucleinopathies.

Abstract : During the past two decades, a myriad of studies have suggested a central pathogenic role for a-synuclein in Parkinson's disease. Recent studies have unravelled self-aggregation and prion-like spreading properties for a-synuclein. Of particular importance was the seminal observation of Lewy body-like structures in grafted fetal dopaminergic neurons of patients with Parkinson's disease. This conceptual breakthrough generated the " host-to-the-graft " hypothesis orprion-like hypothesis. Nowadays, mechanisms underlying these new properties appear as putative disease-modifying targets. As the lack of valid animal models for Parkinson's disease is considered as a roadblock toward therapeutic intervention, the use of the newly developed models based on the prion-like properties of a-synuclein should allow future target validation.
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Contributor : Benjamin Dehay Connect in order to contact the contributor
Submitted on : Wednesday, January 22, 2020 - 3:09:34 PM
Last modification on : Thursday, November 12, 2020 - 9:30:16 AM


  • HAL Id : inserm-02448823, version 1
  • PUBMED : 29901880



Mathieu Bourdenx, Benjamin Dehay, Erwan Bezard'. Experimental modelling of -synuclein aggregation and spreading in synucleinopathies.. Bulletin de l'Académie Nationale de Médecine, Elsevier Masson, 2015, 199 (6), pp.797-808. ⟨inserm-02448823⟩



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