Nerve growth factor and chronic daily headache: a potential implication for therapy - PubMed (original) (raw)
Review
Nerve growth factor and chronic daily headache: a potential implication for therapy
Paola Sarchielli et al. Expert Rev Neurother. 2004 Jan.
Abstract
The pivotal role of nerve growth factor in inducing hyperalgesia and central sensitization has been emphasized in experimental pain models. Higher nerve growth factor levels have recently been found in the cerebrospinal fluid of patients with chronic daily headache. These levels were significantly correlated with the cerebrospinal fluid levels of substance P and calcitonin gene-related peptide, supporting the involvement of this neurotrophin in enhancing the production of the two sensory neuropeptides of the trigemino-vascular system in chronic daily headache. This may, in part, account for the long-lasting sensitization and activation of this system, which could contribute to headache chronicity. More recent research has shown a significant correlation between the higher cerebrospinal fluid levels of nerve growth factor and those of another neurotrophin, the brain-derived neurotrophic factor, as well as glutamate in chronic daily headache patients. These findings suggest the potential involvement of nerve growth factor-mediated upregulation of brain-derived neurotrophic factor in persistent head pain. Therefore, nerve growth factor appears to indirectly exert its effect through enhancing glutamatergic transmission involved in the processing of head pain via brain-derived neurotrophic factor. Based on these data, a potential application can be hypothesized for novel strategies targeting neurotrophins (nerve growth factor and brain-derived neurotrophic factor) and their receptors to chronic daily headache. To date, the majority of the molecules discovered in this regard have been scarcely or never proved in animal pain models and are far from clinical use in chronic pain, including chronic daily headache. If this approach is to be developed in the near future, research should be focused on identifying strategies with few central side effects and specific selective action on central sites involved in chronic head pain and more generally in chronic pain conditions. This will represent a very difficult challenge, taking into account the pleiotropic effect of nerve growth factor and the wide range of intracellular signalling pathways activated by this neurotrophin which are not limited to the nociceptive system.
Similar articles
- Increased levels of neurotrophins are not specific for chronic migraine: evidence from primary fibromyalgia syndrome.
Sarchielli P, Mancini ML, Floridi A, Coppola F, Rossi C, Nardi K, Acciarresi M, Pini LA, Calabresi P. Sarchielli P, et al. J Pain. 2007 Sep;8(9):737-45. doi: 10.1016/j.jpain.2007.05.002. Epub 2007 Jul 5. J Pain. 2007. PMID: 17611164 - The role of brain-derived neurotrophic factor in different animal models of neuropathic pain.
Vanelderen P, Rouwette T, Kozicz T, Roubos E, Van Zundert J, Heylen R, Vissers K. Vanelderen P, et al. Eur J Pain. 2010 May;14(5):473.e1-9. doi: 10.1016/j.ejpain.2009.09.006. Epub 2009 Dec 2. Eur J Pain. 2010. PMID: 19959385 Review. - The effect of site and type of nerve injury on the expression of brain-derived neurotrophic factor in the dorsal root ganglion and on neuropathic pain behavior.
Obata K, Yamanaka H, Kobayashi K, Dai Y, Mizushima T, Katsura H, Fukuoka T, Tokunaga A, Noguchi K. Obata K, et al. Neuroscience. 2006 Feb;137(3):961-70. doi: 10.1016/j.neuroscience.2005.10.015. Epub 2005 Dec 2. Neuroscience. 2006. PMID: 16326015 - Promoting neurotrophic effects by GPCR ligands.
Jeanneteau F, Chao MV. Jeanneteau F, et al. Novartis Found Symp. 2006;276:181-9; discussion 189-92, 233-7, 275-81. Novartis Found Symp. 2006. PMID: 16805430 Review. - Age-dependent time course of cerebral brain-derived neurotrophic factor, nerve growth factor, and neurotrophin-3 in APP23 transgenic mice.
Schulte-Herbrüggen O, Eckart S, Deicke U, Kühl A, Otten U, Danker-Hopfe H, Abramowski D, Staufenbiel M, Hellweg R. Schulte-Herbrüggen O, et al. J Neurosci Res. 2008 Sep;86(12):2774-83. doi: 10.1002/jnr.21704. J Neurosci Res. 2008. PMID: 18438945
Cited by
- Inhibition of endogenous NGF degradation induces mechanical allodynia and thermal hyperalgesia in rats.
Osikowicz M, Longo G, Allard S, Cuello AC, Ribeiro-da-Silva A. Osikowicz M, et al. Mol Pain. 2013 Jul 29;9:37. doi: 10.1186/1744-8069-9-37. Mol Pain. 2013. PMID: 23889761 Free PMC article. - Tanezumab for Patients with Osteoarthritis of the Knee: A Meta-Analysis.
Kan SL, Li Y, Ning GZ, Yuan ZF, Chen LX, Bi MC, Sun JC, Feng SQ. Kan SL, et al. PLoS One. 2016 Jun 13;11(6):e0157105. doi: 10.1371/journal.pone.0157105. eCollection 2016. PLoS One. 2016. PMID: 27294371 Free PMC article. Review. - Sensitization, glutamate, and the link between migraine and fibromyalgia.
Sarchielli P, Di Filippo M, Nardi K, Calabresi P. Sarchielli P, et al. Curr Pain Headache Rep. 2007 Oct;11(5):343-51. doi: 10.1007/s11916-007-0216-2. Curr Pain Headache Rep. 2007. PMID: 17894924 Review. - Investigation of the functional brain-derived neurotrophic factor gene variant Val66MET in migraine.
Marziniak M, Herzog AL, Mössner R, Sommer C. Marziniak M, et al. J Neural Transm (Vienna). 2008 Sep;115(9):1321-5. doi: 10.1007/s00702-008-0056-1. Epub 2008 May 14. J Neural Transm (Vienna). 2008. PMID: 18478177
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical