Human neuronal networks for modelizing Parkinson’s disease

Research published in 2015Press release from June 10, 2015: http://www2.cnrs.fr/presse/communique/4077.htm showed that altered and aggregated forms of the alpha-synuclein protein increased in the brains of rodents, and caused various Parkinsonian symptoms.

In this new study, researchersResearchers from l’Institut des Cellules Souches pour le traitement et l'étude des maladies monogéniques (Inserm/Université d’Evry Val d’Essonne/AFM), the Laboratoire de maladies neurodégénératives (CNRS/CEA/Université Paris-Sud), as well as the laboratories Adaptation Biologique et Vieillissement (CNRS/Sorbonne Université) and Neurosciences Paris-Seine (CNRS/Inserm/Sorbonne Université), both of which are part of l’Institut de Biologie de Paris-Seine. used human pluripotent stem cells, differentiated them into neurons, and designed a simplified and robust neuronal network typical of the human brain. They then exposed these neurons to altered forms of alpha-synuclein, and observed the appearance of pathological signs characteristic of Parkinson’s disease and multiple system atrophy (MSA), another neurodegenerative disease. Alpha-synuclein actually aggregates differently for each of these diseases, thereby forming a “signature” of each one.

The scientists also showed that “sick” neurons transfer altered alpha-synuclein to healthy neurons, particularly through synaptic connections. By passing from neuron to neuron and multiplying in similar fashion to the infectious protein prion, the altered forms of alpha-synuclein affect the integrity and function of the neuronal network.