Neural Regeneration Research ›› 2015, Vol. 10 ›› Issue (9): 1403-1405.doi: 10.4103/1673-5374.165505

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Substance P and its tachykinin NK1 receptor: a novel neuroprotective target for Parkinson’s disease

Emma Thornton, Robert Vink   

  1. School of Medical Sciences, University of Adelaide, Adelaide, Australia; Division of Health Sciences, University of South Australia, Adelaide, Australia
  • Received:2015-08-10 Online:2015-09-28 Published:2015-09-28
  • Contact: Robert Vink, Ph.D., Robert.Vink@unisa.edu.au.
  • Supported by:

    This work has been presented at the International Congress of Parkinson’s Disease and Movement Disorders (2009 and 2010), and in part has been supported by the Neurosurgical Research Foundation, South Australia, Australia. The authors would like to thank Tavik Morgenstern for assistance with the Figure 1 graphics.

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Abstract:

Substance P-induced neurogenic inflammation may play an important role in the pathogenesis of Parkinson’s disease (PD), including L-DOPA induced dyskinesia (LID), by increasing BBB permeability and subsequent peripheral immune cell infiltration, as well as activation of resident immune cells. These injury cascades not only directly contribute to the ongoing neurodegeneration of dopaminergic neurons in PD but can also exacerbate other secondary injury mechanisms such as oxidative stress and mitochondrial dysfunction. Treatment with an NK1-R antagonist attenuated the progression of PD and significantly reduced the onset of LID, presumably by inhibiting multifactorial injury mechanisms involving SP and NK1-R. Blocking the effects of SP with a NK1-R antagonist therefore presents a potentially promising new avenue for neuroprotection in PD.