Pleiotrophin over-expression rescues nigral dopaminergic neurons from 6-hydroxydopamine injury in an animal model of Parkinson's disease.

TARAVINI IR; CHERTOFF M; MURER MG; PITOSSI FJ; GERSHANIK OS

Congreso; 13th Congress of the European Federation of Neurological Societies; 2009

European Federation of Neurological Societies

Parkinson´s disease is characterized by the loss of striatal dopamine as the result of the degeneration of dopaminergic neurons of the substantia nigra pars compacta. The current pharmacological and surgical therapies only offer symptomatic relief as they are not able to modify the neurodegeneration process. At present, neuroprotection treatments are being studied with the hope of delaying or stopping neurodegeneration by restoring dopaminergic function or protecting the affected dopaminergic neurons from the degenerative process. Use of neurotrophic factors is one of the possibilities. In a previous study, we characterized the pattern of distribution of Pleiotophin (PTN) in the striatum and substantia nigra of adult normal rats. Our results showed that cholinergic and GABAergic interneurons of the striatum express PTN. In the substantia nigra, dopaminergic neurons express PTN and their receptors. In this work, we studied the effects of in vivo over-expression of PTN on the integrity of the partially damaged (6-OHDA) dopaminergic system. We found that PTN promotes a partial recovery of this system after analyzing the neurons of the substantia nigra and axonal terminals in the striatum. These results support the idea that PTN and their receptors could be therapeutic targets for the design of strategies for neuroprotection and neurorestoration in Parkinson´s disease.