Neural Regeneration Research ›› 2020, Vol. 15 ›› Issue (7): 1191-1198.

Previous Articles     Next Articles

The N-formyl peptide receptors: contemporary roles  in neuronal function and dysfunction

Peter J.G. Cussell, Margarita Gomez Escalada, Nathaniel G.N. Milton, Andrew W.J. Paterson*
  

  1. Centre for Biomedical Science Research, School of Clinical and Applied Sciences, Leeds Beckett University, Leeds, UK
  • Online:2020-07-15 Published:2020-09-11
  • Contact: Andrew W.J. Paterson, PhD, A.Paterson@leedsbeckett.ac.uk. E-mail:A.Paterson@leedsbeckett.ac.uk.

PDF

231

Abstract:

N-formyl peptide receptors (FPRs) were first identified upon phagocytic leukocytes, but more than four de
cades of research has unearthed a plethora of non-myeloid roles for this receptor family. FPRs are expressed
within neuronal tissues and markedly in the central nervous system, where FPR interactions with endoge
nous ligands have been implicated in the pathophysiology of several neurodegenerative diseases including
Alzheimer’s disease and Parkinson’s disease, as well as neurological cancers such as neuroblastoma. Whilst
the homeostatic function of FPRs in the nervous system is currently undefined, a variety of novel physio
logical roles for this receptor family in the neuronal context have been posited in both human and animal
settings. Rapid developments in recent years have implicated FPRs in the process of neurogenesis and neu
ronal differentiation which, upon greater characterisation, could represent a novel pharmacological target
for neuronal regeneration therapies that may be used in the treatment of brain/spinal cord injury, stroke
and neurodegeneration. This review aims to summarize the recent progress made to determine the physi
ological role of FPRs in a neuronal setting, and to put forward a case for FPRs as a novel pharmacological
target for conditions of the nervous system, and for their potential to open the door to novel neuronal re
generation therapies.

Key words: Alzheimer’s disease, formyl peptide receptor, neural regeneration, neuroblastoma, neurodegeneration, neuroinflammation, neuronal differentiation, stroke