Introduction: Alzheimer's disease (AD) is the most common cause of dementia and is defined as a progressive neurodegenerative disease. Main clinical features of AD are progressive impairment in learning and memory loss. Several studies have indicated that mitochondria play a critical role in the pathogenesis of AD. In this study, we investigated the effect of melatonin on mitochondria-dependent TRPA1 ion channels in neuroblastoma cells by creating an in vitro model of Alzheimer's disease. Methods: Okadaic acid was applied to SH-SY5Y (human neuroblastoma cell line) cells to create an AD model. After cellular differentiation, the following 7 main groups were created: Group 1 (Control), Group 2 (Mel+AD), Group 3 (Mel+AD+AP18), Group 4 (AD), Group 5 (AD+AP18), Group 6 (AD+Mel), and Group 7 (AD+Mel+AP18), and Alzheimer's disease was determined in vitro by examining the effect of melatonin on calcium-dependent TRPA1 channels in neuroblastoma cells. Results: The Ca2+ concentration was greater in the melatonin+AD, AD and AD+melatonin groups than in the control (p<0.001). However, there was no statistically significant difference between Mel+AD+AP18, AD+Mel+AP18 and the control. We determined that Ca2+ levels were lower in the melatonin+AD and AD+melatonin groups than in the AD group (p<0.001 and p<0.05). Additionally, cytosolic Ca2+ concentrations were found to be lower in the melatonin+AD group than in the AD+melatonin group (p<0.05). In evaluating the apoptosis and oxidative stress levels, we found that the apoptosis and intracellular ROS values were higher in the melatonin+AD, AD and AD+melatonin groups than in the control (p<0.001). In this respect, the mitochondrial depolarization and caspase-3 and caspase-9 levels were higher in the melatonin+AD, AD and AD+melatonin groups than in the control group (p<0.001). Additionally, the mitochondrial depolarization, caspase-3 and caspase-9 values were higher in the AD group than in the melatonin+AD and AD+melatonin groups (p<0.001), while mitochondrial depolarization and caspase-3 levels were lower in the melatonin+AD group than in the AD+melatonin group (p<0.001). However, in the same groups, there was no statistically significant difference in caspase-9 results. Additionally, the caspase-9 values were lower in the melatonin+AD group, AD group and AD+melatonin groups than in the melatonin+AD+AP18, AD+AP18 and AD+melatonin+AP18 groups, respectively (p<0.001 and p<0.05). Conclusion: Our results suggest that melatonin may be an effective option in the treatment and prophylaxis of Alzheimer's disease by reducing cytosolic Ca2+ concentration, apoptosis and intracellular ROS through TRPA1 channels.

We aimed to investigate changes in electrophysiological findings in Turkish patients with restless legs syndrome (RLS), including F-wave latency (FWL), peripheral silent period (PSP), and Hoffmann reflex. The study took place in a university hospital in Turkey and involved 30 newly diagnosed RLS patients and 30 healthy controls who were matched for age and gender. Participant’s demographics (age, gender, weight, and height), laboratory findings, and electrophysiological test outcomes were gathered and analyzed. There was no significant difference in the FWL of the median and ulnar nerves, whereas the H-wave maximum amplitude and H/M ratio were significantly higher in the RLS patients than in the controls at rest. All of the PSP parameters were similar between patients and controls for the abductor pollicis brevis and gastrocnemius muscles. However, for the tibialis anterior muscle, all the PSP duration parameters were shorter in the RLS patients, whereas the PSP latency parameters were similar. The data suggest that there may be a reduction in spinal segmental inhibition at the L4–L5–S1 level, but the mechanisms of inhibition at the L4–L5 and S1 levels may be different; furthermore, there may be no pathology in the peripheral nerves. Further prospective studies with larger cohorts are now needed to evaluate the pathophysiology of RLS with different neurophysiological assessment tools.

Introduction: The effect of Ginkgo biloba (GB) on mitochondria dependent TRPV1 ion channels in neuroblastoma cells was investigated by creating an Alzheimer's disease (AD) model.Methods: Okadaic acid was applied on SH-SY5Y cells to create an AD model. After cellular differentiation, the study was organized with the seven main groups, examining the effect of GB on calcium depended TRPV1 channels in neuroblastoma cells AD, has been established in vitro.Results: The higher Ca2+ concentration was detected in the GB+AD, AD and AD+GB groups when compared with the control (p<0.001). The Ca2+ level was lower in GB+AD and AD+GB groups than in the AD group (p<0.001). Also, cytosolic Ca2+ concentration was lower in the GB+AD than in the AD+GB group (p<0.05), the apoptosis and intracellular reactive oxygen species (ROS) values were higher in the GB+AD, AD and AD+GB groups than in the control (p<0.001). The apoptosis and intracellular ROS values were higher in AD group than in the GB+AD and AD+GB group (p<0.001) and the apoptosis level was higher in AD+GB group than GB+AD group (p<0.001) and the mitochondrial depolarization, caspase 3 and caspase 9 levels were higher in the GB+AD, AD and AD+GB groups when compared to the control group (p<0.001). Also, the values were lower in the GB+AD group, AD group and AD+GB groups when compared with the GB+AD+capsazepine group, AD+capsazepine group and AD+GB+capsazepine respectively (p<0.001).Conclusion: These results show us that GB has a protective effect besides its therapeutic effect in Alzheimer's disease via TRPV1 channel.

Aim: We aimed to compare 25-hydroxy vitamin D (25-OH vitamin D) and Ca2+ levels of patients admitted to our clinic with the complaint of dizziness and diagnosed with idiopathic benign paroxysmal positional vertigo (BPPV) with those of healthy control group without dizziness and investigate the role of Ca2+ and 25-OH vitamin D in the development of BPPV.Material and methods: This study is a retrospective case-control study. The study sample consisted of 409 patients admitted to Alanya Training and Research Hospital Neurology outpatient clinic and diagnosed with idiopathic BPPV between 01.01.2018 and 01.08.2021, and of 338 control patients without any physician consultation due to vertigo, dizziness or imbalance in the last 1 year before admission to our clinic and whose serum vitamin D levels were measured, the Chi-square and T-test were utilized for statistical analysis.Results: Mean blood 25-OH vitamin D levels were 15.74 ng/mL and 17.91 ng/mL in BPPV and control groups, respectively. Serum 25-OH vitamin D levels were significantly lower in BPPV group than control group (p=0.01, p<0.05). Mean serum Ca2+ levels did not exhibit any difference in BPPV and control groups.Conclusion: Decreased serum levels of 25-OH vitamin D have been associated with the occurrence of BPPV independently of other key markers.

Aim: We investigated the connection between D vitamin and factors such as the type of antiepileptic agent, patient age and gender.Methods: This retrospective case-control study enrolled a total of 301 participants, including 141 epilepsy patients with (n= 120) without drug (n=21) regimens followed up in Alanya Alaaddin Keykubat University neurology outpatient clinic and 160 healthy individuals who applied to the neurology outpatient clinic for different reasons from January 2018 to January 2021. Demographics, detailed history, use of medications, duration of antiepileptic use, plasma 25-hydroxy Vitamin D and calcium levels were determined.Results: The mean level of Vitamin D was 15.46 in the epilepsy group and 16.95 in the control group. Level of D Vitamine did not differ significantly by groups (p>0.05). There were no significant relationship regarding age and vitamin D levels in both groups while decreased Vitamin D levels were detected epileptic women. Vitamin D level was below 20 in 69.6% of healthy control group, 78.9% of carbamazepine users, 62.5% of lacosamide users, all lamotrigine users, 66.7% of levatiracetam users, and 72.4% of sodium valproate users. No significant connection were detected between levels of Vitamin D and the drug used (p>0.05) while a significant association was confirmed only between calcium levels and carbamazepine (p<0.05).Conclusion: Vitamin D and calcium levels can be found to be low in antiepileptic users; however, except for the calcium levels in the carbamazepine group, this decrease does not constitute a significant difference.