Migraine is one of the most common neurological diseases worldwide. Migraine pathophysiology is very complex. Genetic factors play a major role in migraine. Neurotrophic factors, such as brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF), play an important role in central nervous system functioning, development, and modulation of pain. This study investigates whether polymorphisms in the BDNF and NGF genes are associated with migraine disease in a Turkish case–control population. Overall, 576 subjects were investigated (288 patients with migraine and 288 healthy controls) for the following polymorphisms: rs6265(G/A), rs8192466(C/T), rs925946(G/T), rs2049046(A/T), and rs12273363(T/C) in the BDNF gene, and rs6330(C/T), rs11466112(C/T), rs11102930(C/A), and rs4839435(G/A) in the NGF gene using 5′-exonuclease allelic discrimination assays. We found no differences in frequency of the analyzed eight polymorphisms between migraine and control groups. However, the frequency of minor A alleles of rs6265 in BDNF gene was borderline significant in the patients compared with the healthy controls (P=0.049; odds ratios [ORs] [95% confidence intervals {CIs}] =0.723 [0.523–0.999]). Moreover, when the migraine patients were divided into two subgroups, migraine with aura (MA) and migraine without aura (MO), the minor TT genotype of rs6330 in NGF was significantly higher in MA patients than in MO patients (P=0.036) or healthy controls (P=0.026), and this disappeared after correction for multiple testing. Also, the rs6330*T minor allele was more common in the MA group than in the MO group or controls (P=0.011, ORs [95% CIs] =1.626 [1.117–2.365] or P=0.007, ORs [95% CIs] =1.610 [1.140–2.274], respectively). In conclusion, this is the first clinical study to evaluate the association between BDNF and NGF polymorphisms in migraine patients compared with health controls. Our findings suggest that the NGF rs6330*T minor allele might be nominated as a risk factor for developing aura in migraine disease. Our results should be considered as preliminary, and they need to be confirmed by future studies.
Summary: Cyclic vomiting syndrome (CVS) is a disorder characterized by recurrent, stereotypic episodes of nausea, vomiting, and other symptoms, separated by intervals of comparative wellness. These episodes carry on for hours or days. The patient is healthy between the episodes and has no clinical finding. For the treatment of the CVS, antiemetic, antimigraine and sedative medications were used. However, in some cases CVS treatment is very difficult. We report about a young patient, who did not respond to many agents, but was succesfully treated with chlorpomazine
ÖzetAmaç: Hipoksi-iskemi ve reperfüzyon sonrasında gelişen apopitozisin şiddeti, beyin hasarının bir göstergesidir. Serebral iskemide hücre ölümüne uzanan olayları başlatan birçok faktör bulunmaktadır. En önemli faktörlerin başında hücre içi kalsiyum konsantrasyonundaki aşırı artış gelmektedir. N-metil-D-aspartat (NMDA) reseptörlerindeki iyon kanalları Ca ++ 'nın hücreye girişini artırarak hücre ölümüne neden olmaktadırlar. Memantin, NMDA reseptörünün nonkompetitif eksitatör aminoasid blokörüdür. İskemi öncesi veya sonrası memantin uygulamasının nöronal hasarı azalttığını ileri süren çalışmalar yayınlanmıştır. Bu çalışmada; memantinin iskemi sonrası, özellikle penumbra alanındaki apopitoz ile sonuçlanan nöronal hasarı azaltıcı ve beyin dokularında antioksidan ve oksidan düzeylerine olan etkilerinin araştırılması amaçlandı. Sum maryObjective: The severity of apoptosis developing after hypoxia-ischemia and reperfusion is an indicator of cerebral injury. In cerebral ischemia, there are many factors initiating the events progressing to cell death. The most common leading cause is excessive increase in intracellular calcium concentration. Ion channels in NMDA receptors cause cell death by increasing Ca ++ entries into the cell. Memantine is a non-competitive excitatory amino acid blocker of the NMDA receptor. Studies suggesting administration of memantine before and after ischemia decreasing the neural injury have been published. In this study we aimed to examine the memantine could have a decreasing effect on neuronal injury resulting with apoptosis especially in the penumbra region after ischemia and its effects on antioxidants and oxidants in brain tissues. Ma te ri al and Met hod: Experimental study was performed in three groups; each of them including 7 rats. The control group (without any intervention) was used for evaluation of the normal brain tissue. Transient focal cerebral ischemia was performed by clipping the right common carotid arteries of the rats in ischemia and ischemia-drug groups. Ten mg/kg intraperitoneal memantine was administered in ischemia-drug group 30 minutes after ischemia and for 5 days thereafter. All of the rats were sacrificed after the experiment. Antioxidant and oxidant levels of the cerebral tissues were measured. Apoptotic cells were determined immunohistochemically using TUNEL method. Re sults: When the memantine administered group was compared with the ischemia group, we observed that memantine decreased apoptotic cells in the brain tissue and there was an improvement in the oxidant levels (p<0.05). Dis cus si on: In conclusion, memantine may be effective in prevention of apopitosis and neuronal injury in cerebral ischemic tissue via decreasing cerebral oxidant formations. (Turkish Journal of Neurology 2013; 19:85-9)
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.