Dürdane Aksoy

Cholecalciferol (vitamin D 3) improves cognitive dysfunction and reduces inflammation in a rat fatty liver model of metabolic syndrome

AIM The aim of this study was to examine the effects of cholecalciferol on systemic inflammation and memory in the setting of fatty liver disease in rats. MATERIALS AND METHODS To induce the development of fatty liver disease, the rats were fed a 35% fructose solution over 8 weeks. Group I (n=6) was designated as the control group and fed with standard rat chow. Group II (n=6) was provided with, standard rat chow, and 0.3 μg/kg/day of oral cholecalciferol over a duration of 2 weeks. In addition to standard rat chow, group III (n=6) and group IV (n=6) were given 4 mL of the 35% fructose solution per day via oral gavage for 8 weeks. However, group IV was also given 0.3 μg/kg/day of oral cholecalciferol over 2 weeks. After the treatment period, passive avoidance tasks were performed by all groups. The liver and brain were harvested for subsequent biochemical and histopathologic analyses. KEY FINDINGS The development of fatty liver extends the memory latency period of passively avoiding tasks after 1 trial. Moreover, there were increases in brain TNF-α and plasma MDA levels according to two-way analysis of variance. Cholecalciferol supplementation decreased the latency period of passively avoiding tasks in rats with hepatosteatosis, and also significantly reduced brain TNF-α and plasma MDA levels. SIGNIFICANCE Fatty liver may contribute to the development of systemic inflammation, which affects cognition and causes deficits in memory; however, the anti-inflammatory and antioxidant properties of vitamin D may improve the cognitive function of rats with hepatosteatosis.

Montelukast Inhibits Pentylenetetrazol-Induced Seizures in Rats

Background Montelukast is an antiinflammatory drug with an antioxidant property. In this study, we aimed to reveal whether montelukast has a preventive effect against seizures and post-seizure oxidative stress in pentylenetetrazol (PTZ)-induced seizures in rats. Material/Methods Of the 48 male Sprague-Dawley rats used in the study, 24 were assigned to EEG recordings (group A) and 24 were assigned to behavioral studies (group B). In group A, the electrodes were implanted on dura over the left frontal cortex for EEG recording. After 10 days, in group A, i.p. saline, 25, 50, or 100 mg/kg montelukast+35 mg/kg PTZ was administered to the rats. EEG was recorded and spike percentage was evaluated. In group B, i.p. saline, 25, 50, or 100 mg/kg montelukast+70 mg/kg PTZ was administered to the rats. Racine’s Convulsion Scale (RCS) and onset times of first myoclonic jerk (FMJ) was used to evaluate the seizures. Malondialdehyde (MDA) and superoxide dismutase (SOD) levels were determined in the brain tissue of animals. Results Animals treated with 50 or 100 mg/kg montelukast had significantly lower RCS and significantly increased FMJ onset time compared to the saline-treated animals. Moreover, groups given 25, 50, or 100 mg/kg montelukast had significantly lower MDA and higher SOD levels compared to the saline-treated group. The differences were more pronounced in the 100 mg/kg montelukast-pretreated group (p<0.001). Conclusions Montelukast showed anticonvulsant action and led to amelioration of oxidative stress markers in PTZ-induced seizures in rats.

Central corneal thickness and its relationship to Parkinson's disease severity

OBJECTIVE To investigate the effect of Parkinsons disease (PD) on blink rate (BR), tear breakup time test (TBUT), Schirmers test, and corneal thickness, and the relationship of these effects with disease severity. DESIGN Prospective controlled study. PARTICIPANTS Fifty-five eyes from 55 patients with PD and 40 eyes from 40 healthy subjects were analyzed in the study. METHODS The patients were divided into 2 groups according to their Hoehn-Yahr (H-Y) scores; patients classified as H-Y 1-2 were designated as the mild group, and those classified as H-Y 3-5 were designated as the moderate group. Subjects were screened for BR, TBUT, and Schirmers test, and the central corneal thickness (CCT) was measured. RESULTS The BR, Schirmers test, TBUT, and CCT values of the patient group were significantly lower than those of the control group. The BR and TBUT of the mild group were significantly lower than those of the control group, but the decreases in the Schirmers test values and CCT were not statistically significant. In addition, significant decreases in the BR, TBUT, Schirmers test scores, and CCT were observed in the patient group as the H-Y score increased. CONCLUSIONS A reduced BR and poor tear quality in the early stages of PD, as well as decreased tear production as the disease progresses, can result in reduced CCT. The possibility of a thin cornea should be taken into consideration while measuring the intraocular pressure in patients with severe PD.

Analysis of MMP2-1306C/T and TIMP2G-418C polymorphisms with relapsing remitting multiple sclerosis

Aims Multiple sclerosis (MS) is an autoimmune, inflammatory disease characterized by loss of myelin forming oligodendrocytes and changes in the blood–brain barrier. Matrix metalloproteinase (MMP) -2 and -9 are known to cause disruption of the blood–brain barrier, remodeling of the basal lamina, regeneration of axons, and remyelination in MS. The imbalance between MMPs and tissue inhibitor metalloproteinases (TIMPs) may lead to the emergence of pathological processes such as MS. The roles of MMP2-1306 C/T and TIMP2-418 G/C genetic variants in MS have not been studied before. We aimed to investigate whether MMP2-1306C/T and TIMP2-418 G/C gene variants are risk factors for patients with relapsing remitting multiple sclerosis (RRMS). Methods The study included 102 RRMS and 102 healthy controls. Genomic DNA was extracted from peripheral leukocytes from ethylenediaminetetraacetic acid anticoagulated blood. Genotyping of the MMP2-1306C/T and TIMP2G-418C polymorphisms was performed using real-time PCR. Results There were significant differences in terms of distribution of genotype (MMP2-1306- CT, TT) and T allele frequency between the patients with RRMS and the control group (p<0.0001; p<0.0001). The groups were not different in terms of TIMP2G-418C polymorphisms. Conclusions In the RRMS group, the genotype and allele frequencies of MMP2-1306C/T polymorphism showed significant differences from the controls. These results indicate that MMP2 might play a role in the pathogenesis of MS even during the inflammation stage.

Inhibitor effect of dexketoprofen in rat model of pentylenetetrazol-induced seizures

Objectives: The relationship between epilepsy and inflammation is known, and it has been reported that there is an increase in cyclooxygenase (COX) levels in epilepsy. We aim to reveal the anticonvulsant effects of dexketoprofen in pentylenetetrazol (PTZ)-induced seizures in rats. Materials and Methods: Forty-eight male Sprague-Dawley rats, 24 of them for EEG recording and 24 of them are for behavioral studies, were randomly divided in two groups: Group A for EEG recordings and Group B for behavioral assessment. A weight of 70 mg/kg PTZ was used for behavioral studies after dexketoprofen administration. Thirty-five milligrams per kilogram PTZ were used for EEG recording after dexketoprofen administration. The electrodes were implanted on dura over the left frontal cortex and the reference electrode was implanted over the cerebellum for EEG recording. The Racine convulsion scale (RCS), first myoclonic jerk (FMJ) onset time, and spike percentages were evaluated between the two groups. Results: There was a significant (P< 0·05) difference between the RCS, FMJ onset time (P< 0·001), and spike percentage (P< 0·05) between the groups (Group 2 compared with Groups 3 and 4). Conclusion: Dexketoprofen has an antiepileptic feature and this effect increases as the dosage increases, however it is currently unknown through which mechanism this drug shows its anticonvulsant effect. Dexketoprofen, in the group of NSAIDs, shows an anticonvulsant effect on PTZ-induced epilepsy model. This study suggests that dexketoprofen can preferably be used with NSAIDs for epileptic patients in clinical practice.

Clinical, demographic and prognostic features of sporadic amyotrophic lateral sclerosis in Northern Turkey

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease for which progression cannot be prevented. In this study, we evaluated 37 patients diagnosed with sporadic definitive-probable ALS who were monitored in our neurology clinic between 2002 and 2012 in terms of age, gender, profession, onset, and clinical course within the disease process. The hospital ethics committee approved the study. Nineteen female and 18 male patients diagnosed with sporadic definitive or probable ALS were evaluated for age, gender, level of education, residence, onset of disease, the time between the first symptom and diagnosis, and average lifetime after diagnosis. Twenty-eight of the patients had graduated from primary-secondary school, six were illiterate, and three of them were college graduates. Eighteen patients were living in city center, 19 were living in the country. Fourteen patients were farmers, 11 were housewives, and the remaining was working in various different occupations. The age of onset was 62.13. The men and women were diagnosed 10.27 months and 17.91 months after the first symptom, respectively (p = 0.001). The average survival time after diagnosis was 36.70 months for males and 49.80 months for females (p < 0.05). This difference was particularly evident among patients from rural areas. In addition, our female patients required interventions such as ventilation at a later period than did males. In conclusion, female gender seems to be one of the good prognostic factors for our ALS patients. This may be due to the protection by hormonal mechanisms in women or differences in their responses to exogenous toxins.

Neuroprotective Effects of Eexenatide in a Rotenone-Induced Rat Model of Parkinson’s Disease☆

Backround: Several studies suggest an association between Parkinsons disease (PD) and type 2 diabetes mellitus; these 2 diseases are both known to affect the common molecular pathways. As a synthetic agonist for the glucagon‐like peptide 1 receptor, exenatide has been evaluated as a neuroprotective agent in multiple animal models. Rotenone models of PD have great potential for the investigation of PD pathology and motor and nonmotor symptoms, as well as the role of gene‐environment interactions in PD causation and pathogenesis. Therefore, in this study, the neurochemical, behavioral and histologic effects of exenatide on a rotenone‐induced rat model of PD were examined. Materials and Methods: Eighteen adult male rats were randomly divided into the following 3 groups (n = 6): 1 group received stereotaxical infusion of dimethyl sulfoxide (vehicle, group 1) and the others received stereotaxical infusion of rotenone (groups 2 and 3). Apomorphine‐induced rotation test was applied to the rats after 10 days. Thereafter, group 2 was administered isotonic saline, whereas group 3 was administered exenatide for 28 days. Results: Malondialdehyde and tumor necrosis factor alpha levels increased in the rats with PD induced by rotenone, whereas malondialdehyde and tumor necrosis factor alpha levels markedly decreased in the rats treated with exenatide. The apomorphine‐induced rotation test scores of exenatide‐treated rats were determined to be lower compared with the untreated group. Additionally, treatment with exenatide significantly reduced the loss of dopaminergic neurons in striatum. Conclusions: These results have shown that exenatide has neuroprotective, anti‐inflammatory and antioxidant effects in a rotenone‐induced rat model of PD.

Hypokalemia and hypomagnesaemia related to levetiracetam use

Levetiracetam (LEV), used for both partial and generalized seizures, is a frequently preferred antiepileptic because of its few side effects. We present a 23-year-old man who developed hypokalemia after switching from valproate to LEV. The patient was sent to our clinic due to hypokalemia 1 month after initiation of LEV, and his neurological examination was normal. Further examinations revealed hypokalemia (3.1 mmol/L) and hypomagnesaemia (0.56 mmol/L). His hemogram, blood urea nitrogen, creatinine, total cortisol, thyroid function tests, creatinine clearance, and renal Doppler ultrasound were normal. LEV was tapered off and treatment with 200mg/day lamotrigine begun. Potassium and magnesium levels returned to normal ranges in subsequent tests. While hypokalemia and hypomagnesaemia have not been reported before to our knowledge, interstitial nephritis and renal failure after the use of LEV have been. Hypokalemia, found in the early period in this case, may be an indicator of a recently developed renal tubular disorder. This experience indicates that unpredictable side effects of increasingly used new antiepileptic drugs should be taken into consideration.

Sexual dysfunction in women with migraine and tension-type headaches

Primary headaches (PHAs) prominently affect the performance and life quality of people. Sexual dysfunction (SD) is an important health problem caused by several factors. This study aimed to compare the sexual function of women who have PHAs. Forty-one female patients who were diagnosed with migraine, 39 female patients who were diagnosed with tension-type headache (TTHA) and 41 healthy subjects were included in study. Sexual function of the cases were evaluated by using the ‘Female Sexual Function Index (FSFI)’. Beck Depression Scale was applied to subjects and those who were diagnosed with depression were excluded from the study. SD was detected in both the migraine and TTHA groups. FSFI subgroup scores were statistically significantly lower in the migraine and TTHA groups compared with the control group. No significant differences were detected between the migraine and TTHA groups in terms of FSFI and its components. In addition, no significant differences were detected between the blood prolactin levels or SD and headache. It was concluded that primary headaches (which are chronic diseases) itself may cause SD in female patients with migraine and TTHA independently of factors that may cause development of SD such as comorbid condition, depression, drug use and age.

Atypical Features in a Large Turkish Family Affected with Friedreich Ataxia

Here, we describe the clinical features of several members of the same family diagnosed with Friedreich ataxia (FRDA) and cerebral lesions, demyelinating neuropathy, and late-age onset without a significant cardiac involvement and presenting with similar symptoms, although genetic testing was negative for the GAA repeat expansion in one patient of the family. The GAA repeat expansion in the frataxin gene was shown in all of the family members except in a young female patient. MRI revealed arachnoid cysts in two patients; MRI was consistent with both cavum septum pellucidum-cavum vergae and nodular signal intensity increase in one patient. EMG showed demyelinating sensorimotor polyneuropathy in another patient. The GAA expansion-negative 11-year-old female patient had mental-motor retardation, epilepsy, and ataxia. None of the patients had significant cardiac symptoms. Description of FRDA families with different ethnic backgrounds may assist in identifying possible phenotypic and genetic features of the disease. Furthermore, the genetic heterogeneity observed in this family draws attention to the difficulty of genetic counseling in an inbred population and to the need for genotyping all affected members before delivering comprehensive genetic counseling.