30^th International Conference on Neurology and Cognitive Neuroscience February 24-25, 2020 London, UK

Janean E Holden, PhD, RN, FAAN is the Barbara A. Therrien Collegiate Professor of Nursing. She received her PhD from the University of Michigan and did Post-doctoral research in Pharmacology at the University of Illinois at Chicago. Her research focus is on the role of the hypothalamus in descending pain modulation with emphasis on the role of norepinephrine in the spinal cord.

Statement of the Problem and Objectives: Approximately 70% of patients receiving oxaliplatin for colorectal cancer develop painful oxaliplatin-induced peripheral neuropathy (OIPN-P). OIPN-P can persist up to 11 years after treatment is stopped, affecting quality of life and contributing to falls, depression and sleep loss. OIPN-P also necessitates decreased dosage during treatment, thereby decreasing treatment effectiveness and increasing mortality risk. The serotonin and norepinephrine reuptake inhibitor, duloxetine is approved for treating OIPN-P, but is effective only in about 50% of patients. Recent work is suggestive that pretreating with tricyclic drugs can prevent onset of OIPN-P, but these drugs have serious side effects. We investigated whether pretreatment with duloxetine would prevent onset of OIPN-P in male and female rats in a model of oxaliplatin-induced hyperalgesia. Methodology: Rats were pretreated with duloxetine (15 mg; PO) for 7 days prior to and through oxaliplatin treatment and for 20 days post oxaliplatin treatment. Rats were then tested for 6 days after all treatment stopped. The measure used was a 15 g von Frey filament applied to the left foot, which measures hyperalgesia, a sign of neuropathic pain. Findings: We found that rats pretreated with duloxetine presented with significantly less hyperalgesia through the testing period compared to control and notably for the six days after all treatment stopped (p ≤ 0.003; p ≤ 0.13; males and females resp.). Conclusion and Significance: These pilot study findings are suggestive of the need for further study to determine whether pretreatment with duloxetine can prevent onset of OIPN-P.

Olga Petrovna Sidorova Graduated from Russian National Research Medical University named after N.I. Pirogov in Moscow, residency and graduate school in Neurology. She defended her doctoral dissertation in the specialty of Neurology. She works as a Professor in the Department of Neurology of the Faculty of Advanced Medical Doctors of the Moscow Regional Clinical Research Institute. The chief of Neurological Department is Professor Sergey Kotov. Her research interests - Mitochondrial disorders in neurological diseases, hereditary neurological diseases, myasthenia gravis, photopheresis (extracorporeal photochemotherapy) in autoimmune neurological diseases and porphyria in neurology (acute, chronic and latent course). Together with Hanns Lochmuller, a new mutation has been identified in the gene responsible for one of the forms of congenital myasthenic syndrome. Studies mitochondrial disorders using A.G.E. Pearse in patients with various neurological pathologies.

Introduction: Hypoxia is the main cause of neuron damage in stroke. Therefore, it is important to study the metabolism of mitochondria in the acute period of the disease. The study of the activity of mitochondrial enzymes will clarify the purpose of drug therapy and develop new approaches to treatment. The goal is to use a method that allows an objective assessment of mitochondrial disorders in the acute period of a stroke. Material and Methods: The quantitative assessment of the cytochemical activity of mitochlorine enzymes in peripheral blood lymphocytes was studied in 7 adult patients with ischemic stroke. For a quantitative cytochemical study of the activity of mitochondrial enzymes in peripheral blood lymphocytes, the method proposed by A.G.E. Pearse. Investigated the activity of succinate dehydrogenase (SDH) (complex 2 of the respiratory chain of mitochondria), α-glycerophosphate dehydrogenase (α-GPDH) (an indicator of fat metabolism involving carnitine), glutamate dehydrogenase (GDH) (an indicator of amino acid metabolism, LDH (a carbohydrate metabolism indicator). Blood sampling was performed in the first 24 hours from the start of the stroke. Two patients re-conducted the study after 7 days. Results: All patients had an increase in the activity of SDH in the first 24 hours after the onset of a stroke. Α-GPDH activity was reduced in 6 of 7 patients (85.7%). GDG activity in patients was 9.4 ± 1.1 g / lymphocyte (in the control group - 8.8 ± 0.3). The average LDH activity in patients was 14.8 ± 1.5 g / lymphocyte (15.4 ± 0.3 g / lymphocyte in the control group). In two patients with ischemic stroke, the activity of mitochondrial enzymes was re-determined 1 week after the first blood sampling. A week after the onset of the disease on the background of administration of the preparation of succinic acid (5% solution of mexidol 5.0), in the 1st patient with overweight, there was a decrease in the activity of SDH below the reference values, in the second patient (low power) more grown. Which indicates the need to take into account the body weight of patients in the appointment of the drug succinic acid or increase the dose of Mexidol for all patients. α-GPDH activity was lower than the reference values on the first day of the disease in both patients. A week later, in the first patient, the index increased (but remained below the reference values), while in the second patient it decreased to 7.85 g / lymphocyte (in the control group - 9.0-12.0 g / lymphocyte). The level of GDG and LDH activity did not deviate from normal values in both patients. Conclusion: The method used makes it possible to objectively evaluate the indicators of various types of metabolism in mitochondria and justify the appointment of energy-induced therapy, correct the dose of the drug.

Jovana Drljača is a Research Assistant at the Institute for Histology and Embryology, Faculty of Medicine, University of Novi Sad, Serbia. She holds a Master’s degree in Pharmacy since 2016 and now is a PhD candidate, highly engaged with science through participating in the project supported by the Ministry of Education, Science and Technological Development of Serbia. She is trained in working with laboratory animals and also has completed several training courses regarding the cell culture and molecular testing. Jovana has a great practical experience in cell biology, different staining methods of cells and mitochondrial respiration.

Background: L-Carnosine (b-alanyl-L-histidine) is a dipeptide, widely present in excitable tissues, such as muscle and neural tissue and has been shown to have a direct and indirect antioxidant effect, but its role in the brain remains unclear. Data suggests the possible neuroprotective potential of carnosine in vitro and in vivo models. Purpose: The objective of this study was to determine glio and neuroprotective potential of l- carnosine in vivo animal model of autoimmune encephalitis in mice. Methods: C67BL/6 mice underwent AIE and were treated with carnosine (420mg/kg) or saline per os once daily during 20 days until sacrifice. Histological characteristics of brain tissue were assessed. To determine demyelinating areas we have used immunohistochemical staining to Myelin Basic Protein (MBP). Infiltration with a mononuclear inflammatory infiltrate is detected by immunohistochemical staining on CD68. Results: Qualitative analysis of the tissue characteristics in carnosine group showed weaker inflammatory infiltrate, as well as a smaller number of demyelinating areas positive for MBP. L- carnosine produced a potentially significant neuro and glioprotective potential compared to the control group that received saline. Conclusions: The results highlight the potential of L-carnosine as a neuroprotective agent in autoimmune encephalitis model in mice.

Shiva Nematgorgani has completed his Master from Iran University of Medical Science. He is pursuing his PhD in Shahid Beheshti University of Medical Science, School of Nutrition. He has published 3 papers in reputed Iranian and international journals and has great experience in clinical nutrition research.

Aims: This study aimed to investigate the association between socio-demographic factors and child feeding practices with diet in 3- 6 years old children. Methods: A cross-sectional study of 208 mothers with their children aged 3-6 years was carried out in 30 primary schools of Rasht, Iran in 2018. Measures included socio-demographic factors, aspects of parental control practices and the child's diet. Mothers reported their own and their child's demographics. Aspects of child feeding practices were assessed using Comprehensive Feeding Practices Questionnaire (CFPQ) after investigating validity and reliability of questionnaire. Food Frequency Questionnaire (FFQ) was then used to assess the child's dietary intake. Height and weight of mothers and children participated in the study were also measured. The role of parental and child social and demographic factors and child feeding practices in predicting children's diet was assessed using multiple block entry linear regression. P value was adjusted by Beforerroni correction to account for multiple comparisons (pc<.0002). Results: The results showed a significant relationship in between some socio-demographic factors and feeding control practices with some aspects of the child's dietary intake. Conclusion: To conclude, the results showed a significant relationship between some socio-demographic factors and feeding control practices with some aspects of the child's dietary intake. Higher education of parents is significantly associated with increase of healthy foods intake and decrease of unhealthy snacks. The boys eat more unhealthy snacks and mothers's job inversely influence on some aspect of child's diet.