Journal of Neural Transmission

, Volume 121, Issue 4, pp 371–378 | Cite as

C-type natriuretic peptide in Parkinson’s disease: reduced secretion and response to deprenyl

  • E. A. Espiner
  • J. C. Dalrymple-Alford
  • T. C. R. Prickett
  • Y. Alamri
  • T. J. Anderson
Neurology and Preclinical Neurological Studies - Original Article

Abstract

C-type natriuretic peptide (CNP) is a neurotrophic factor widely expressed in the central nervous system including the basal ganglia, limbic system and hypothalamus. Nothing is known of CNP’s role in the human brain but in rodents CNP promotes axon growth and branching, and interacts with dopaminergic function in models of addiction. Because preliminary evidence showed reduced levels in Parkinson’s disease (PD), we examined concentrations of CNP peptides in cerebrospinal fluid (CSF) in 146 PD patients from the DATATOP study to determine changes over time in relation to medication status and cognitive function. CNP and an aminoterminal product of proCNP (NTproCNP) were measured in extracts from stored CSF by radioimmunoassay. CSF samples were obtained twice—at enrolment and at the study’s endpoint (requirement for levodopa treatment) after treatment with placebo or deprenyl. At enrolment, median baseline concentration of CSF NTproCNP (776 pmol/L, n = 146) was significantly lower than that in a reference group without neurological disorder (1,010 pmol/L, p < 0.001). Concentrations declined significantly during placebo (p = 0.02) and lower values at enrolment were associated with more rapid functional decline (p < 0.01). In contrast, deprenyl—a treatment which delayed the need for levodopa—nullified the time-dependent decline in CSF NTproCNP. In conclusion subnormal CSF NTproCNP which declines with time and associates with increasing functional disability implicates CNP in PD. Concordant clinical and peptide responses to deprenyl suggest that some of the benefits of monoamine oxidase inhibitors in PD are mediated by preserving tissue CNP activity.

Keywords

Parkinson’s disease CSF NTproCNP Monoamine oxidase inhibitors 

Supplementary material

702_2013_1123_MOESM1_ESM.doc (171 kb)
Supplementary material 1 (DOC 171 kb)

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Copyright information

© Springer-Verlag Wien 2013

Authors and Affiliations

  • E. A. Espiner
    • 1
  • J. C. Dalrymple-Alford
    • 3
  • T. C. R. Prickett
    • 1
  • Y. Alamri
    • 2
  • T. J. Anderson
    • 2
  1. 1.Department of MedicineUniversity of OtagoChristchurchNew Zealand
  2. 2.New Zealand Brain Research InstituteUniversity of OtagoChristchurchNew Zealand
  3. 3.Department of PsychologyUniversity of CanterburyChristchurchNew Zealand

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