The Val66Met Polymorphism of the BDNF Gene Influences Trigeminal Pain-Related Evoked Responses

Lorenzo, Cherubino Di; Lorenzo, Giorgio Di; Daverio, Andrea; Pasqualetti, Patrizio; Coppola, Gianluca; Giannoudas, Ioannis; Barone, Ylenia; Grieco, Gaetano S.; Niolu, Cinzia; Pascale, Esterina; Santorelli, Filippo M.; Nicoletti, Ferdinando; Pierelli, Francesco; Siracusano, Alberto; Seri, Stefano

doi:10.1016/j.jpain.2012.05.014

Cited by 24 publications

(26 citation statements)

References 36 publications

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“…BDNF herein exerts pro-nociceptive effects and contributes to descending pain facilitation and chronic pain hypersensitivity [49], [50]. On the other hand, BDNF can manifest protective anti-nociceptive effects under repeated painful conditions as a result of multiple mechanisms, including a direct neurotransmitter-like effect or processes of neural plasticity in the anti-nociceptive systems, induction of serotonin-related analgesia, and a modulatory effect at the supraspinal level [51]. BDNF can therefore be consociated with both an enhancement of nociceptive impact, and a dampened response to protect the brain from pain overstimulation [51].…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, BDNF can manifest protective anti-nociceptive effects under repeated painful conditions as a result of multiple mechanisms, including a direct neurotransmitter-like effect or processes of neural plasticity in the anti-nociceptive systems, induction of serotonin-related analgesia, and a modulatory effect at the supraspinal level [51]. BDNF can therefore be consociated with both an enhancement of nociceptive impact, and a dampened response to protect the brain from pain overstimulation [51]. Thus, the overall effect of BDNF on pain perception and experience depends on the net interaction output of these apparently contrasting activities at different neural structures in which BDNF is produced, secreted, and left to act [17], [50], [51].…”

Section: Discussionmentioning

confidence: 99%

“…BDNF can therefore be consociated with both an enhancement of nociceptive impact, and a dampened response to protect the brain from pain overstimulation [51]. Thus, the overall effect of BDNF on pain perception and experience depends on the net interaction output of these apparently contrasting activities at different neural structures in which BDNF is produced, secreted, and left to act [17], [50], [51]. The BDNF Val66Met polymorphism can lead to impaired BDNF signaling in the brainstem pain modulatory system and it may be associated with altered menstrual pain modulation in PDMs.…”

Section: Discussionmentioning

confidence: 99%

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Association of Brain-Derived Neurotrophic Factor Gene Val66Met Polymorphism with Primary Dysmenorrhea

Lee

Chen

et al. 2014

PLoS ONE

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Primary dysmenorrhea (PDM), the most prevalent menstrual cycle-related problem in women of reproductive age, is associated with negative moods. Whether the menstrual pain and negative moods have a genetic basis remains unknown. Brain-derived neurotrophic factor (BDNF) plays a key role in the production of central sensitization and contributes to chronic pain conditions. BDNF has also been implicated in stress-related mood disorders. We screened and genotyped the BDNF Val66Met polymorphism (rs6265) in 99 Taiwanese (Asian) PDMs (20–30 years old) and 101 age-matched healthy female controls. We found that there was a significantly higher frequency of the Met allele of the BDNF Val66Met polymorphism in the PDM group. Furthermore, BDNF Met/Met homozygosity had a significantly stronger association with PDM compared with Val carrier status. Subsequent behavioral/hormonal assessments of sub-groups (PDMs = 78, controls = 81; eligible for longitudinal multimodal neuroimaging battery studies) revealed that the BDNF Met/Met homozygous PDMs exhibited a higher menstrual pain score (sensory dimension) and a more anxious mood than the Val carrier PDMs during the menstrual phase. Although preliminary, our study suggests that the BDNF Val66Met polymorphism is associated with PDM in Taiwanese (Asian) people, and BDNF Met/Met homozygosity may be associated with an increased risk of PDM. Our data also suggest the BDNF Val66Met polymorphism as a possible regulator of menstrual pain and pain-related emotions in PDM. Absence of thermal hypersensitivity may connote an ethnic attribution. The presentation of our findings calls for further genetic and neuroscientific investigations of PDM.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Association of Brain-Derived Neurotrophic Factor Gene Val66Met Polymorphism with Primary Dysmenorrhea

Lee

Chen

et al. 2014

PLoS ONE

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“…On the other hand, it is well known that BDNF acts as a pain modulator at multiple levels, including pain processing and drug-seeking behavior. For instance, BDNF rs6265 has been previously reported to influence trigeminal pain-related evoked responses in healthy subjects (45) or to modulate analgesic drug consumption in patients with medication overuse headache (46). Also of note is that the minor T allele of rs6330 of nerve growth factor gene was significantly associated with MA in a Turkish case–control population (21).…”

Section: Discussionmentioning

confidence: 99%

Brain-Derived Neurotrophic Factor Val66Met Gene Polymorphism Impacts on Migraine Susceptibility: A Meta-analysis of Case–Control Studies

et al. 2017

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Inconclusive results have been reported in studies investigating the association between the brain-derived neurotrophic factor (BDNF) rs6265 polymorphism and migraine. In the present study, we conducted a systematic review and meta-analysis on the published data in order to quantitatively estimate the relationship between rs6265 and migraine susceptibility. A comprehensive search was performed through PubMed, Web of Knowledge, and Cochrane databases up to October 2016. The pooled odds ratio (OR) with the corresponding 95% confidence interval (CI) was calculated to estimate the strength of the association with rs6265 under an additive, dominant, or recessive model of inheritance. A total of five studies including 1,442 cases and 1,880 controls were identified for the meta-analysis. The pooled data showed an increased risk of migraine for the allelic (OR: 1.17, 95% CI: 1.03-1.34, p = 0.014) or the dominant model of rs6265 (OR: 1.22, 95% CI: 1.05-1.41, p = 0.011). Statistical significance of rs6265 was lost when one single study was excluded from the analysis (dominant OR: 1.17, 95% CI: 1.00-1.38, p = 0.054; allelic OR: 1.14, 95% CI: 0.99-1.31, p = 0.067), suggesting lack of robustness of pooled estimates. When stratified by migraine type, a similar trend of association was detected with both MA and MO, but a statistically significant association of rs6265 was reached only with the MA subtype in the dominant model (OR: 1.22, 95% CI: 1.00-1.47, p = 0.047). The present meta-analysis supports that BDNF rs6265 may act as a genetic susceptibility factor for migraine. Nevertheless, large-scale studies are required to confirm our findings and to assess potential modifiers of the relationship between rs6265 and migraine.

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“…Such changes in behavioural response offers insight into the adaptive short-and long-term plasticity mechanisms that correspond to changes in neuronal excitability. These include a decrease in evoked potential amplitudes that further depend on the underlying genetic load [22][23][24].…”

Section: Discussionmentioning

confidence: 99%

1. Cortical functional correlates of responsiveness to short-lasting preventive intervention with ketogenic diet in migraine: A multimodal evoked potentials study

Bracaglia¹,

Lorenzo²,

Lenola³

et al. 2016

Clinical Neurophysiology

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Background: Here, we aim to identify cortical electrofunctional correlates of responsiveness to short-lasting preventiveintervention with ketogenic diet (KD) in migraine. Methods: Eighteen interictal migraineurs underwent visual (VEPs) and median nerve somatosensory (SSEPs) evokedpotentials before and after 1 month of KD during ketogenesis. We measured VEPs N1-P1 and SSEPs N20-P25 amplitudes respectively in six and in two sequential blocks of 100 sweeps as well as habituation as theslope of the linear regression between block 1 to 6 for VEPs or between 1 to 2 for SSEPs. Results: After 1-month of KD, a significant reduction in the mean attack frequency and duration was observed (all P< 0.001). The KD did not change the 1st SSEP and VEP block of responses, but significantly inducednormalization of the interictally reduced VEPs and SSEPs (all p < 0.01) habituation during the subsequentblocks. Conclusions: KD could restore normal EPs habituation curves during stimulus repetition without significantly changing theearly amplitude responses. Thus, we hypothesize that KD acts on habituation regulating the balancebetween excitation and inhibition at the cortical level.

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The Val66Met Polymorphism of the BDNF Gene Influences Trigeminal Pain-Related Evoked Responses

Cited by 24 publications

References 36 publications

Association of Brain-Derived Neurotrophic Factor Gene Val66Met Polymorphism with Primary Dysmenorrhea

Association of Brain-Derived Neurotrophic Factor Gene Val66Met Polymorphism with Primary Dysmenorrhea

Brain-Derived Neurotrophic Factor Val66Met Gene Polymorphism Impacts on Migraine Susceptibility: A Meta-analysis of Case–Control Studies

1. Cortical functional correlates of responsiveness to short-lasting preventive intervention with ketogenic diet in migraine: A multimodal evoked potentials study

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