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Human protein may trigger Parkinson’s disease

Research led by the Research Institute Vall d’Hebron (VHIR), has shown that pathological forms of the α-synuclein protein present in deceased patients with Parkinson’s disease are able to initiate and spread in mice and primates the neurodegenerative process that typifies this disease. The discovery, published in the March issue of Annals of Neurology, opens the door to the development of new treatments that may stop the progression of Parkinson’s disease, by blocking the expression, the pathological conversion and the transmission of this protein.

In the present study, the researchers extracted α-synuclein aggregates from brains of dead patients with Parkinson’s disease, and injected them into the brains of rodents and primates.

Four months after the injection into mice, and nine months after the injection into monkeys, these animals began to present degeneration of dopaminergic neurons and intracellular cumulus of α-synuclein pathology in these cells, as occurs in Parkinson’s disease. Months later, the animals also showed cumulus of this protein in other brain remote areas, with a pattern of similar extension to that observed in the brains of patients after years of disease evolution.

Journal Reference:
Ariadna Recasens, Benjamin Dehay, Jordi Bové, Iria Carballo-Carbajal, Sandra Dovero, Ana Pérez-Villalba, Pierre-Olivier Fernagut, Javier Blesa, Annabelle Parent, Celine Perier, Isabel Fariñas, José A. Obeso, Erwan Bezard, Miquel Vila. Lewy body extracts from Parkinson disease brains trigger α-synuclein pathology and neurodegeneration in mice and monkeys. Annals of Neurology, 2014; 75 (3): 351 DOI: 10.1002/ana.24066

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