Decressac 1..15

, 163ra156 (2012); 4 Sci Transl Med et al. Mickael Decressac in Nigral Dopamine Neurons Induced Down-Regulation of Nurr1 Disrupts GDNF Signaling − -Synuclein α Editor's Summary -synuclein toxicity and highlight Nurr1 as a promising new target for neuroprotective therapy. α against -synuclein toxicity. These results suggest that Nurr1 is a key player in the cellular defense α neurons subjected to induced expression of Nurr1, Ret receptor expression was restored as well as the response to GDNF in the dopamine complete failure of dopamine neurons to respond to exogenously applied GDNF. However, when the investigators downstream target, the GDNF receptor Ret. Deletion of Nurr1 resulted in reduced Ret expression, accompanied by a evidence that blockade of GDNF signaling is caused by reduced expression of the transcription factor Nurr1 and its -synuclein effectively block the trophic response of dopamine neurons to GDNF. They provide α concentrations of now show that excess cellular et al. mediated PD, Decressac − -synuclein α -synuclein toxicity. Using a rat model of α disease, GDNF has failed to afford protection in PD rodent models in which dopamine neurons are killed by this neuroprotection in patients with Parkinson disease (PD). Although effective in classic neurotoxin animal models of derived neurotrophic factor (GDNF) and its close relative neurturin are currently in clinical trials for − Glial cell line NURRishing Dopamine Neurons with GDNF