2^nd International Conference on Brain Disorders and Therapeutics October 26-28, 2016 Chicago, USA

Biography:

Yuri P Danilov is a system neuroscientist with over 35 years’ experience in research on brain functions and the special senses, including vision, taste, hearing and balance. He is the lead discoverer of the balance retention effect and continues to identify potential clinical and non-clinical application of neuromodulation and sensory substitution technology. He received the PhD degree in Neuroscience, in 1984, from the Pavlov Institute of Physiology, USSR Academy of Science. He was co-inventor of the Brain Port vision and balance systems. He is a co-inventor of the CN-NINM technology and his interest areas are neuroplasticity, neurorehabilitation and enhancement of human performance.

Abstract:

Th e neurorehabilitation of sensory and motor functions aft er brain damage and loss of brain functions is underdeveloped,
including the recovery of eye-movement control. Th ere are very few methods that show the possibility of eye movements
enhancement aff ected by brain injuries or disease. Th e goal of our research was to investigate how cranial-nerve non-invasive
neuromodulation (CN-NINM) can recover the oculomotor function impairments and help to improve eye movement control
for people with stroke, Parkinson’ s disease (PD), multiple sclerosis (MS) and traumatic brain injury (TBI) symptoms. Th e CNNINM
therapy includes a combination of targeted exercises for recovery of balance and gait motor control with electrotactile
tongue stimulation, using the Portable Neuromodulation Stimulator (PoNStm device). Assessment of oculomotor function was
performed before and aft er the CN-NINM intervention using special 4-channel binocular eye tracking goggles (VisualEyes,
Micromedical Inc) and custom analysis soft ware. To evaluate the state of subjects’ eye movements, we used three static
nystagmus tests (vertical and horizontal gaze, and spontaneous nystagmus) and two dynamic tests (random saccade and
smooth pursuit). All of the tests were performed without tongue stimulation.
Balance, gait, and eye movement control gradually improved in all tests. We observed improvement of eye fi xation, accuracy
and stability in nystagmus and gaze tests, increased eye movement accuracy and precision, improved gain and velocity of target
tracking, and changes in both smoothness and synchronization of binocular movement control in oculomotor tests. Th e
improvements of eye movement control demonstrated by this set of case studies suggest that CN-NINM therapy may benefi t
people aff ected by stroke, PD, MS, and TBI, and would off er a novel treatment option for oculomotor disorders.

Biography:

Jordan L Holtzman, Graduated from University of Chicago, the Pritzker School Of Medicine in 1959. He Complete internship from University Ill Rsc/Ed in 1960. He Completed Residency training from University of Minnesota in 1973, Department of Medicine, University of Minnesota Minneapolis, MN, USA at present he is in Department of Pharmacology, University of Minnesota Minneapolis, MN, USA. Department of Environmental Health Sciences, University of Minnesota Minneapolis, USA.

Abstract:

Alzheimer’s disease is described as a progressive dementia associated with the extracellular deposits in the brain of a garbage protein, β-amyloid (Aβ) and the intracellular deposits of tangles. The vast majority of the patients develop the disease in old age while a small portion has an early onset, familial form. Since the 1970’s it has been generally assumed that the dementia seen in the two forms is due to the neurotoxicity of the Aβ. With the purification and sequencing of Aβ in the 1990’s investigators were able to identify the mutations associated with the familial forms. A number of laboratories transfected mice with these mutated genes. Since these animals exhibited many of the pathological and clinical manifestations of the late onset disease, they have been used to screen for new therapeutic agents. Unfortunately, all 244 drugs identified in these models have failed in clinical trials in elderly patients. Work from my laboratory has suggested that plaque deposits of Aβ rather than causing the dementia is merely a biomarker for a decline in the capacity of the endoplasmic reticulum (ER) in the cells to catalyze the posttranslational processing of 40% of cellular proteins, including those synaptic, membrane proteins required for a functioning memory. This paradigm is based on our observation that in the CSF all Aβ is normally N-glycosylated and bound to ER proteins, ERp57 and calreticulin. These data suggest a new direction for drug discovery in which agents are screened for their ability to increase the levels in cell lines of fluorescently labeled components of the ER posttranslational pathway. The development of these cell lines would permit rapid screening for potential therapeutic agents in plate readers.

Biography:

Marina Zueva, Professor of Pathophysiology, PhD, Dr. Biol. Sci., graduated from the Lomonosov Moscow State University (Department of Physiology of Higher Nervous Activity), received her PhD and Dr. Biol. Sci. degrees from Moscow Helmholtz Research Institute of Eye Diseases. Currently, she is the Head of the Division of Clinical Physiology of Vision at the Moscow Helmholtz Research Institute of Eye Diseases. She is a member of International Society of Clinical Electrophysiology of Vision (ISCEV), European Association on Vision and Eye Research (EVER), European Society of Retina Specialists (EURETINA), the Society for Research on Biological Rhythms (SRBR). She has published over ten peer-reviewed papers in English (over 80 in Russian) and presented over 60 topics at international conferences.

Abstract:

The theory of "fractality of sensations" was recently published, which for the first time substantiates that healthy functions of the brain and visual system are tied intimately to the fractal complexity of the temporal and spatial structure of the environmental visual, auditory and other cues, which accompany the person during his life. It follows from the theory that the loss for various reasons of the complex fractal characteristics of the environment stimuli can contribute to the simplification of network connections and the activity of the brain. It, in turn, can result in the distortion in the timing of CNS maturation (e.g., in amblyopia) and biological rhythms regulation and aggravate the age-related neurodegenerative disorders (e.g., in glaucoma, Alzheimer's diseases). An application of fractal flickering, sound pulses and other fractal rhythms seem to be effective in restoring the function of the brain and visual system, in particular, in patients with neurodegenerative diseases and amblyopia. The artificial fractal cues may underlie new therapeutic paradigms for the reactivation of brain plasticity. It determines the relevance of the elaboration of technologies providing the intermittent fractal stimuli of the complex temporal structure. Possible new directions for experimental and applied research based on the fundamental tenets of this theory must determine benefits of and indications for non-linear stimulation, and for the combined use of fractal stimulation and noise therapy. One should also explore the assumption that exposure to artificial visual and auditory stimuli with regular temporal structure may contribute to the decline in brain functions.

Biography:

John Kennedy is a pioneer in the field of Applied Neuroplasticity. He was contracted by the US Marines in 2006 to create an on-digital neuroplastic mental performance training program to reduce casualties in combat by improving attention, intuition and decision making under stress. He has since helped over 2500 people, in the areas of military, education, business, mental resiliency, improve their quality of life. He speaks regularly at corporate events and parent organizations on the topic of creating neuroplastically enriching environments. He is also the author of the forthcoming book Zombie Thinking™- Why we do what we do and how to change it.

Abstract:

PACE is the core modality of Combat Brain Training™ (CBT) a unique, non-digital neuroplastic training regimen developed at the request of US Military forces to improve intuition and situational awareness. Vetted by USSOCOM, it has proven to be an effective pre-deployment force multiplier for all branches of the Armed Forces including Marines, SEALs, Snipers and Pilots. As Marines returned from combat with severe TBI, CBT was found to significantly accelerate recovery and is currently being integrated into Rush Hospital’s (Chicago) Road Home program for transitioning vets. It provides targeted robust mental stimulation to create long term potentiation in the areas of the brain associated with executive function using analog neuroplastic training tools. These changes solidify in as little as 20 minutes and after the stabilization process ends the synapse is significantly stronger - this process can occur as many times as need be until the synapse no longer receives the stimulation that is greater than it is prepared for, hence progressively accelerated cognitive exertion. The exercise tools look like games and can be performed with family and caregivers so sessions are fun and interactive and carry no stigma usually associated with interventions. In the civilian world it has helped victims of TBI from accidents, athletes suffering from concussions and children with severe LD. Over 2500 people have experienced PACE with 100% reporting significant improvements in real world performance.

Biography:

Abstract:

Background and Objective: Verticalization was reported to improve the level of arousal and awareness in patients with severe acquired brain injury (ABI) and to be safe in ICU. We evaluated the effectiveness of a very early stepping verticalization protocol on their functional and neurological outcome.

Methods: Consecutive patients with Vegetative State or Minimally Conscious State were enrolled in ICU on the third day after an ABI. They were randomized to undergo conventional physiotherapy alone or associated to fifteen 30-minute sessions of verticalization, using a tilt table with robotic stepping device. Once stabilized, patients were transferred to our Neurorehabilitation unit for an individualized treatment. Outcome measures (Glasgow Coma Scale, Coma Recovery Scale revised -CRSr-, Disability Rating Scale –DRS- and Levels of Cognitive Functioning) were assessed on the third day from the injury (T0), at ICU discharge (T1) and at Rehab discharge (T2). Between- and within-group comparisons were performed by the Mann-Whitney U test and Wilcoxon signed-rank test, respectively.

Results: Of the 40 patients enrolled, 31 completed the study without adverse events (15 in the verticalization group and 16 in the conventional physiotherapy). Early verticalization started  12.4±7.3 (mean±SD) days after ABI. The length of stay in ICU was longer for the verticalization group (38.8 ± 15.7 vs 25.1 ± 11.2 days, p=0.01), while the total length of stay (ICU+Neurorehabilitation) was not significantly different (153.2 ± 59.6 vs 134.0 ± 61.0 days, p=0.41). All outcome measures significantly improved in both groups after the overall period (T2 vs T0, p<0.001 all), as well as after ICU stay (T1 vs T0, p<0.004 all) and after Neurorehabilitation (T2 vs T1, p<0.004 all). The improvement was significantly better in the experimental group for CRSr (T2-T0 p=0.033, T1-T0 p=0.006) and (borderline) for DRS (T2-T0 p=0.040, T1-T0 p=0.058).

Conclusions: a stepping verticalization protocol, started since the acute stages, improves the short-term and long-term functional and neurological outcome of ABI patients.

Biography:

Abstract:

Over preliminary avocation to (virtual) experimentation upon the feasibility of regional or overall transmission of Human Brain’s Electromagnetic waves – as an EEG Signal confi guration – to another Person’s Cerebral cortex, But: REMOTELY – like a modulated Signal of compatible Frequency Magnitude, without implement mediation e.g. microchip, cerebral implants or skull electrodes – IN OPEN AIR and ON ANY GPS PARAMETER. Meaning Emission Interaction from Brain to Brain (B-B Interface) means Radio Antennas sensors and Satellite mediated procedures. Primary schedule runs as: EEGgraphic waves properly detected, through specifi c sensitive appliances are gathered to be Transmitted TO OTHER Participant’s Brain. It
follows a with detectable Phase Diff erence Elaboration of those EEGgraphic Signals because these are compatible with Human Brain’s Electrophysiology. Here Not a PC but Cortex is the Decoding matter. Eff ects are impressive and constitute COGNITIVE COMMUNICATION of other’s Cerebral funct resulting in Comprehension of them as a copied Speech Analogon–Parallele,
coinciding technically to the long spoken concept of Telepathy. Th at goes back even to the very early origination of Mental Constructions’ that is to Th ought and Intangible (sensed) Images΄ making of. Furthermore this Brain to Brain Transmittal comprises not only cognitive but also Sensory interpretations. Th e quality of Perception and Interaction from person to person coincides with Reality in some fi elds while simultaneously and at any moment Intangible sensory and cognitive Images – Noetic forms Gestalt* - are realized bilaterally:

Biography:

Abstract:

Neural stem cells (NSC) have  self-renewal and multipotent properties and may serve as an ideal cell source for transplantation to treat neurodegenerative insults such as Parkinson’s, Alzheimer’s, and spinal cord injury (SCI).  Obtaining NSCs from adult human olfactory bulb (OB) would avoid ethical issues associated with the use of embryonic tissue, and provide an easily accessible cell source that would preclude the need for invasive brain surgery.  To assess the therapeutic potential of OBNSCs, we studied the fate of allogenic adult human olfactory bulb neural stem/progenitor cells (OBNSC/NPCs) transplanted into the rat hippocampus treated with ibotenic acid (IBO), striatum of 6-OHDA Parkinsonian rats, and in a rat model of SCI at day 7 post injury. In AD, stereological analysis of engrafted OBNSCs eight weeks post transplantation revealed a 1.89 fold increase with respect to the initial cell population, indicating a marked ability for survival and proliferation. In addition, 54.71_11.38%, 30.18_6.00%, and 15.09_5.38% of engrafted OBNSCs were identified by morphological criteria suggestive of mature neurons, oligodendrocytes and astrocytes respectively. In PD, the grafted cells survived in the lesion environment for more than eight weeks after implantation with no tumor formation. The grafted cells differentiated in vivo into oligodendrocyte-like (25±2.88%), neuron-like (52.63±4.16%), and astrocytic-like (22.36±}1.56%) lineages based on morphological criteria. Transplanted rats exhibited a significant partial correction in cognitive ability (AD) and stepping and placing non-pharmacological behavioral tests (PD), using a pole and rotarod. In SCI, the survival rate was about 30% relevant to initially transplanted cells. 27% of the engrafted cells differentiated along the oligodendrocyte, nearly as many (16%) differentiated into neurons, and about 56% of the cells displayed astrocyte morphology. The study revealed that OBNSCs were able to survive in the lesion  environment for more than eight weeks after implantation; this  was supported by transgenic overexpression of hNGF on engrafted cells. We didn't observe locomotor recovery by BBB test, footprint analysis and grid walk tests three months post-treatment. Taken together, this work demonstrated that human OBNSCs ameliorate the cognitive and motor deficiencies associated with AD and PD rats model rats, and the improvement can probably be attributed primarily to neuronal and glial cell replacement as well as the trophic influence exerted by the secreted NGF. In contrast, we didn't observe locomotor recovery by BBB test, footprint analysis and grid walk tests three months post-treatment in SCI.

Biography:

CDM is an MTech and PhD from Indian Institute of Technology, Kharagpur, India and gained postdoctoral experience in neurobiotechnology under eminent scientists at Ohio State University Medical centre, USA. She has more than 30 publications in reputed journals and sponsored research projects. Presently she is actively engaged in teaching and research and her research interest includes preparation of nanomedicine from natural products to treat neurodegenerative diseases.

Abstract:

New research shows that an overactive immune system plays a powerful role in causing central nervous system inflammation and the destruction of neurons. It is hypothesized that nonsteroidal anti-inflammatory agents that cross the blood brain barrier could halt the release of these damaging immune factors and reduce risk of developing Alzheimer’s disease (AD). Present FDA approved medications for AD can’t reverse the natural course of the disease. A natural antioxidant, turmeric, plays a protective role in AD through immunomodulation. Epidemiological studies in India, where turmeric consumption is widespread, suggest it has the lowest prevalence rates of AD in the world. Preclinical research work has already established the effectiveness of curcumin in lowering Aβ loads, alleviating neuroinflammation, preserving neurones and synapses and preventing hyperphosphorylation of tau proteins. However, because of poor bioavailability of curcumin and rapid biotransformation in blood, translation of curcumin’s effectiveness in clinical settings is not fully observed. Encapsulation of curcumin bioactive compounds in nanopraticles which can cross blood brain barrier plays a significant role in neurorestoration by inhibiting glial proliferation and Aβ plaque formation. Curcumin C3 complex in patients with mild to moderate stage of the disease is being tried to understand the efficacy [through AD Assessment Scale, cognitive subscale (ADASCog), Neuropsychiatric Inventory (NPI), Activities of Daily Living Scale (ADCS-ADL)] the mechanism of action of curcumin (cholesterol levels, CSF isoprostanes, alpha-1-antichymotrypsin, C-reactive protein, tau, Aβ1–40 and Aβ1–42). A 24 week randomized double-blinded, placebo-controlled study of two doses of curcumin in persons with mild-to-moderate AD was promising.

Biography:

John Kennedy is a pioneer in the fi eld of Applied Neuroplasticity. He was contracted by the US Marines in 2006 to create anon-digital neuroplastic mental performance training program to reduce casualties in combat by improving attention, intuition and decision making under stress. He has since helped over 3500 people, in the areas of military, education, business, mental resiliency, improve their quality of life. He speaks regularly at corporate events and parent organizations on the topic of creating neuroplastically enriching environments. He is also the author of the forthcoming book Zombie Thinking™- Why we do what we do and how to change it.

Abstract:

Workshop Details:
Session 1 (required for session 2)
Education:
We will examine the following aspects of Neuroplasticity:
• how zombie systems (unconscious mental processing) are created
• the three primary levels of zombie systems
• how we can recreate our environments to foster positive zombie systems at all levels
Training:
Practical application of what we’ve learned
• Experience Foundational Cognition Targeted Neuroplastic Training (TNT) proven eff ective at improving performance
of 100% of over 3500 people in military, business, education and brain trauma recovery
• Th e only program of its kind in the world, vetted and approved by US Special Operations Command, used by Navy
SEALs, Pilots, Snipers and Marines
• Vetted and approved by Rush Hospital’s Road Home program as an eff ective accelerator of brain trauma recovery
• You will keep the neuroplastic training tools to use on your own aft er the workshop to continue to experience the
benefi ts of improved focus and intuition and better, faster decision making especially under stress

Biography:

Pooneh Heshmati, MD, PhD is a physician and clinical neuroscientist with a background in art, medicine and cognitive neuroscience. Heshmati earned a medical degree from Azad University, and subsequently completed a PhD at the Institute of Cognitive Science Studies. Her research interests are in the areas of memory and emotion, neuropsychological and neurobehavioral medicine, cognitive rehabilitation and brain stimulation.

Heshmati joined the Center for Neurosciences’ Functional Brain Imaging Laboratory as a postdoctoral research trainee. She has experience in both human and animal model research and is currently working on studies in Parkinson’s disease and dystonia

Abstract:

Purpose

SLE patients experience deterioration in cognitive function over time but attribution to disease-related mechanisms is confounded by medication effects, disease flares, hormonal influences and infection. The purpose of this study was to use magnetic resonance diffusion tensor imaging (DTI) to determine whether changes in the anatomical connectivity might begin to account for the cognitive impairment in SLE subjects.

Methods

17 SLE patients with inactive disease and no history of CNS involvement and 14 gender, age-matched healthy control (HC) subjects were imaged using DTI with a 3T MRI scanner (57 slices of 2.5 mm thickness, FOV 240 mm, data acquisition matrix 128 x128 zero filled to 256 x 256, TR 15s).  Five b=0 images and 33 diffusion weighted images with b=800 s/mm2 were acquired.  The DTI images were processed using FSL routines (FMRIB software library: www.fmrib.ox.ac.uk/fsl), and FA and MD maps were calculated. Tracts were reconstructed based on clusters identified by voxel-wise comparison of FDG PET scans using TrackVis software (http://www.trackvis.org/).

Results

Relative to HC, the SLE group displayed a 28% reduction in hippocampal-thalamic (HT) tract count. The basal ganglia-thalamic tract was preserved in the SLE group (% 8.5 difference), whereas hippocampal-parietal tract number was increased (+30%) relative to HC.

Conclusions

This is the first study to show abnormal HT tracts in SLE subjects. Abnormalities in the HT tract have been associated with impaired learning and memory as well as with increased symptoms in individuals at high risk for schizophrenia.

Biography:

Abstract:

Over preliminary avocation to (virtual) experimentation upon the feasibility of regional or overall transmission of Human Brain’s Electromagnetic waves – as an EEG Signal configuration – to another Person’s Cerebral cortex, But: REMOTELY – like a modulated Signal of compatible Frequency Magnitude, without implement mediation e.g. microchip, cerebral implants or skull electrodes – IN OPEN AIR and ON ANY GPS PARAMETER. Meaning Emission Interaction from Brain to Brain (B-B Interface) means Radio Antennas sensors and Satellite mediated procedures. Primary schedule runs as: EEGgraphic waves properly detected, through specific sensitive appliances are gathered to be Transmitted TO OTHER Participant’s Brain. It follows a with detectable Phase Difference Elaboration of those EEGgraphic Signals because these are compatible with Human Brain’s Electrophysiology. Here Not a PC but Cortex is the Decoding matter. Effects are impressive and constitute COGNITIVE COMMUNICATION of other’s Cerebral function resulting in Comprehension of them as a copied Speech Analogon–Parallele, coinciding technically to the long spoken concept of Telepathy. That goes back even to the very early origination of Mental Constructions’ that is to Thought and Intangible (sensed) Images΄ making of. Furthermore this Brain to Brain Transmittal comprises not only cognitive but also Sensory interpretations. The quality of Perception and Interaction from person to person coincides with Reality in some fields while simultaneously and at any moment Intangible sensory and cognitive Images – Noetic forms Gestalt* - are realized bilaterally:

Psychesthetism**Essence in perception and comprehension

At all time Speech interaction simulates open space conversation

Biography:

Joshua A Cuoco completed his MS from Johns Hopkins University. He is currently a second-year medical student at NYIT-COM. He studies the anatomic and functional neuronal diversity in the brain during brain development and in brain pathologies. He has published several papers in the field of neuroscience

Abstract:

Inflammation is a complex biologic response to gross traumatic injury, endogenous ligands (e.g., cell death signals within a slowly degenerating tissue), or exogenous ligands (e.g., bacterial toxins within an acute microbial infection). The inflammatory response is necessary for reestablishing organismal homeostasis. It must be meticulously monitored and tightly regulated as over- or under activation of the inflammatory response can cause morbidity and even mortality. Emerging evidence has begun to depict the molecular mechanisms by which inflammation is regulated via the nervous system; that is, inflammation is controlled by neuroimmunologic circuitry operating in a reflexive continuum. Known as the inflammatory reflex arc, this pathway exhibits an afferent and efferent arc: both of which derive from vagal nerve fibers. The afferent arc is comprised of vagal receptors detecting specific ligands indicating injury. An activated afferent arc will initiate the efferent arc, the cholinergic anti-inflammatory pathway, which regulates immunologically-mediated inflammation. Suboccipital decompression by osteopathic manipulative treatment has been demonstrated to enhance vagal output. Considering this association, we postulate that suboccipital decompression may stimulate the efferent branch of this vagal-mediated reflex, the cholinergic anti-inflammatory pathway, thereby suppressing pro-inflammatory cytokine concentrations. In this poster, we discuss the molecular mechanisms of the vagal-mediated inflammatory reflex arc emphasizing the possibility ofsuppressing inflammation with osteopathic manipulative treatment

Biography:

Abstract:

Historically, a number of studies focusing on mentalising skills in children with ASD (Baron-Cohen, Leslie & Frith, 1985) and in patients diagnosed with schizophrenia (Frith, 1992) claimed that people who received a diagnosis of ASD or schizophrenia tended not to do well in identifying other people’s point of view. In fact, the primary or default perspective the brain activates is always one’s own (Samson, Apperly, Braithwaite, Andrews & Scott, 2010) and in order for anyone to acknowledge somebody else’s perspective, the self-perspective has to be inhibited. In order to investigate the actual presence of impairments in the alter centric perspective recognition in schizophrenia, twenty-five outpatients diagnosed with schizophrenia (Group S) and on anti-psychotic medication for more than ten years and twenty-five healthy controls who had never received a diagnosis of a mental health disorder and who had never received any psychiatric medication (Group C) took part in three experiments. Participants were matched for verbal comprehension IQ, working memory skills and attention. The experiments consisted of a visual computational perspective-taking task, a facial emotions recognition task and a hinting task. Results for the visual computational perspective-taking task showed that people who received a diagnosis of schizophrenia made more mistakes than controls when identifying the avatar’s perspective, not their own perspective. The hinting task results showed that patients had more difficulties than controls in identifying what the hints meant. Facial emotions recognition task results showed no significant differences between patients and controls. Results from the facial emotions recognition task suggest that facial emotions recognition is a separate visual interpretation skill that perhaps is not directly related to being able to acknowledge another person’s perspective.

Biography:

Abstract:

OBJECTIVE: To describe, for the fi rst time, an isolated right pseudoabducens palsy in a young patient with acute left thalamic
infarction revealed by diff usion-weighted magnetic resonance imaging (DWI MRI).
BACKGROUND: Ocular abnormalities are rarely reported in thalamic strokes. When present, impairment of vertical gaze is usually noted, sometimes accompanied by vertical diplopia. Other oculomotor defi cits such as skew deviation or third nerve palsy have also been reported in pure thalamic infarctions. Th e presentation of thalamic stroke with pseudoabducens palsy is
extremely rare and are associated with impairment in vertical eye movements.
CASE PRESENTATION: A 31-year-old right-handed smoker, otherwise healthy, man presented with a 12-hour history of progressively worsening horizontal diplopia and related feeling unsteady on his feet, and mild left -occipital headache. He reported feeling unsteady on his feet because of his double vision. Cranial nerve examination showed horizontal diplopia in
all directions of gaze and was most prominent when focusing on distant objects especially and more on the right gaze. Eye movements were disconjugate when looking to the right; there was no abduction of the right eye. DWI MRI revealed a focus of restricted diff usion in the left thalamus, consistent with acute ischemic infarct, with no lesions in the brainstem or the cerebellum; however, the subthalamic area above the midbrain was possibly involved.
CONCLUSIONS: Th is case supports the hypothesis that a lesion can cause isolated esotropia by interrupting descending inhibitory convergence pathways that traverse the paramedian thalamus and decussate in the subthalamic region to innervate the contralateral third oculomotor nucleus.

Biography:

Ayodeji Egunlusi is a pharmacist who is currently busy with his PhD. He had participated in the young scientist program organised by the Novartis Pharma (Basel). His PhD entails the design and synthesis of novel molecules as potential neuroprotective agents. Few compounds have been synthesised and screened for neuroprotective activities.

Abstract:

Neurodegenerative disorders are debilitating conditions characterised by progressive dysfunction and death of neuronal cells by means of apoptosis, necrosis or autophagic degeneration. Amidst the proposed mechanisms of neurodegeneration, the effects of excitotoxicity via glutamate receptor stimulation on neuronal cells are prominent. Numerous molecules have been synthesised to regulate glutamate receptors but some, such as dizolcipine and phencyclidine, have been marked by undesirable side effects. Uncompetitive blockers such as memantine and amantadine proved to be neuroprotective with fewer side effects and are approved for clinical use. This has led to the development of structurally related polycyclic molecules such as NPG1-01, which exhibit neuroprotective properties through NMDA receptor and VGCC inhibitions with lower side effect profile. In this study, a series of compounds were synrhesised for evalulation of inhibitiion of calcium influx through NMDA receptor channels and voltage-gated calcium channels (VGCC). The structures were confrimed using NMR, IR and MS. Compounds (2, 3, 6, 7 and 10) demonstrated potential ability to attenuate calcium influx through NMDA receptor and/or VGCC. Based on the significant activity of compound 2 & 3, a new series of tricycloundecane derivatives have been proposed. However, the true potential benefit of the already synthesised novel compounds as neuroprotective agents and safety in patients is yet to be established. Additional derivatives have been designed and are in the process of being synthesised. The compounds could serve as lead structures for the development of novel neuroprotective drugs.