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Article Dans Une Revue Bulletin de l'Académie Nationale de Médecine Année : 2015

Experimental modelling of -synuclein aggregation and spreading in synucleinopathies.

Résumé

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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Dates et versions

inserm-02448823 , version 1 (22-01-2020)

Identifiants

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

Citer

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

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