^{10th Global Summit on}
Neuroscience and Neuroimmunology

Levi is the pre-Clinical department manager at MD Biosciences Ltd. MD Biosciences is a global industry-leading provider of preclinical services include efficacy and mode of action studies in the inflammation, immunology and CNS therapeutics areas. Dr. Levi holds a Ph.D. in Medical Science from the department of Immunology and Microbiology, Faculty of Medicine, in Ben Gurion University, Israel

In spite of differences between the pathophysiology of EAE and the human Multiple Sclerosis (MS), EAE has become a common animal model in the development therapies for treatment of MS. The Myelin Basic Protein (MBP) induced EAE in rat consists of inflammatory cells infiltration into the spinal cord, cerebellum and brainstem. The paralytic episodes that in this model are thought to be the result of blood–brain barrier breakdown, inflammation, and edema, but not from demyelination. This paralysis initiates approximately 10 days post induction, followed by spontaneously recovers in 5–7 days. Therefore, the therapeutic window is very short. Blood-brain barrier (BBB) disruption and permeability in MBP-EAE animals was assessed by culling animals on study days 2, 6, 9, 11 and 13 for brain harvest, 2 hours following an intrajugular injection of 4% Evan’s blue solution. Following collection, brains were sliced and immersed in formamide at 55°C overnight to extract the Evan’s blue dye. The Evans blue dye content was quantified as μg/g brain tissue. Our data show that while the first clinical signs of the disease were seen on study day 9 following induction with MBP, the Evan’s blue dye was observed in the brain already 2 days following induction (17.80±3.29 μg/g). The dye content in the brain tissue remained high until study day 9 (18.40±2.16 μg/g). Its level markedly decreased on study day 11, and was similar to the level in the naïve brain tissue Mono-nuclear and T-cells infiltration to the brain was observed early following induction with MBP, before the initiation of the first clinical symptoms of the disease. These data show dissociation between BBB permeability and the pick of the disease questioning the therapeutic vs. prophylactic traditional approach.

Marcela Cuestas, from her beginnings as a scientist, has had a great interest in the cellular mechanisms behind the processes of synaptic plasticity related to the formation of memory and learning. Since one of the characteristic features of Alzheimer's disease (AD) is the deterioration of cognitive processes and that, the processes of synaptic plasticity underlie these. She and her group of collaborators decided to evaluate how the synaptic activity of hippocampal neurons changes in Alzheimer's models. Therefore, he has extensive experience in the electrophysiological evaluation of neuronal activity in vivo and in vitro using patch clamping techniques and field registration in Alzheimer's models. Its field of action seeks to contribute, both to the diagnosis of AD, through the typing of patterns of spontaneous synaptic activity; as to the treatment of AD, by identifying new therapeutic targets to mitigate the harmful effects of beta-amyloid accumulation on cognitive function. She hopes to continue making important contributions to the basic knowledge related to the disease and clinical application. As well as continuing to promote the development of Alzheimer's neurophysiology in Colombia.

Alzheimer's disease (AD) is a neurodegenerative disorder related to age and characterized by producing a cognitive deficit, specifically memory loss, and deterioration of learning processes. One of the main features of AD is the extracellular accumulation of beta-amyloid (Aβ), which can form beta-amyloid oligomers (AβO). These AβO applied ex vivo and in vivo act on the mechanisms underlying the learning processes, such as long-term depression (LTD) and long-term potentiation (LTP); facilitating the first (1,2) and deteriorating the second (3,4). In spite of the recent findings that relate the alterations of the neuronal synaptic activity with the deterioration of the cognitive processes, characteristic of AD; there is little or nothing that is known about the synaptic cellular mechanisms that would explain this detriment. Given the determinant role of spontaneous activity in the maturation and maintenance of synapses, homeostasis, and plasticity (5,6,7), it is critical and interesting to study how it changes This type of basal activity in primary culture of hippocampal neurons exposed to different concentrations of AβO. Specifically, how the probability of release of neurotransmitters changes, the sensitivity of postsynaptic receptors, the expression of new postsynaptic receptors and the flow of current through these receptors. In the present work, we applied different concentrations of oligomeric beta-amyloid (AβO) on primary cultures of hippocampal neurons of rat embryos, followed by evaluation of spontaneous electrical activity, specifically excitatory postsynaptic potentials sEPSP through the patch clamp technique whole-cell mode, finding changes in amplitude and frequency of the sEPSP. Understand the effects of AβO on sEPSP, crucial for neuronal functioning and communication; it will allow us to elucidate the synaptic cellular bases behind the cognitive deterioration characteristic of AD, which will facilitate the typing of sEPSP patterns that contribute to improving the diagnosis of AD; as well as, the identification of new therapeutic targets that mitigate the deleterious effects of AβO on cognitive function.

Spinal ischemia-reperfusion injury (IRI) is one of the worrisome issues to the neurosurgeons, as it plays a big role in increasing length of stay and cost of hospitalization. Unfortunately, all the investigations attempted to control the IRI found no clear solution. This is possibly due to many factors such as the presence of a large number of the experimental protocols. In addition, the complete understanding of the IRI mechanism is not fully understood yet. One of the possible complications for the spinal IRI is paraplegia. Incomplete paraplegia has been proven to be effectively treated by neuro-rehabilitation programs .However, no study was found in the literature investigating the effectiveness of the neuro-rehabilitation therapy for this injury. In this case report we discuss a case with spinal IRI led to paraplegia leaving the patient bed bound.This patient underwent an intensive rehabilitation in a dedicated unit. Fortunately, patient was discharged fully independent and ambulatory.