8^th Global Summit on
Neuroscience and Neuroimmunology

Anastasia-Ervina Sela is a student at the 4th year of Nursing at the Technological Educational Institute of Athens.

Dementia is one of the most serious complications of Traumatic Brain Injury. This disease can be mainly caused by road accidents and falls, clearly because the effect of the force on the brain is stronger and the changes in brain function are more radical. A retrospective cohort study, which was approved by the University of California, San Francisco and Human Research Committee and was performed from January 1, 2005, through December 31, 2011 (follow-up, 5-7 years), found that among 51799 patients with trauma, 4361 developed dementia compared with 6610 patients with non-TBI trauma. The correlation of Traumatic Brain Injury and Dementia is evident especially in the larger age groups of the population. In addition, several epidemiological studies suggest that Traumatic Brain Injury (TBI) is a risk factor for Dementia, particularly for Alzheimer’s Disease (AD), although a significant association has not always been detected. There is evidence that in mild and severe Traumatic Brain Injuries most patients have emerged after years Dementia in contrast to those patients who just had a minor injury. In conclusion, Traumatic Brain Injury can be associated to a significant degree with the risk of developing Dementia especially to the people with increased risk. Given the high rates of TBI to the general population serious Dementia prevention measures should be taken in such incidents and clearly to carry out more studies and even longer in order to fully understand the mechanisms that affect between traumatic brain injury and dementia.

The central nervous system has historically been considered immune-privileged; however this privileged position mostly consists of adaptive immune responses with restricted access of infiltrating lymphocytes into the brain parenchyma, while cells of the innate immune system — microglia — are abundant in the brain. Microglia is also considered a key player in many neuroinflammatory conditions. Microglial cells respond to infectious agents such as LPS with reactive phenotype and changes in expression of certain markers such as Iba1. Reactive microglia are also found in the brain during neuroinflammatory processes in depression, bipolar disorder, post-traumatic stress disorder (PTSD). We used animal model of PTSD in order to test how chronic stress affects the neurogenesis, reactivity of microglial cells as well as their density in the dentate gyrus of the hippocampus and whether hippocampal volume is changing during PTSD. According to our results, 10 days after stress onset the number of Iba1+ microglial cells in the dentate gyrus of the hippocampus increased substantially compared to the control group (Mann–Whitney, p=0,028). However we did not see any inflammatory foci, i.e. microglial nodules. The intensity of Iba1+ staining of as well as the size and shape of cells did not differ from the control group. The hippocampal volume did not change significantly. We propose that neurotoxic or neuroprotective role of microglia cells can change depending on the microenvironment, such as in presence of certain cytokines, interleukins, hormones that lead to corresponding changes in the molecular profiles of glial cells. The particular mechanisms of microglia activation and its role in neurogenesis is discussed.

Ahmed Ali Hussein completed a master's degree at the age of 26 years in microbiology and immunology from the University of Qadisiyah - College of Science had gotten a master's degree in 2016. It has been published of a number of research's in local and international journals, I have a book about immunology title " Medical Immunology ". I was assigned to supervise a number of undergraduate graduate studies for the purpose of obtaining a diploma degree, and I also provided a lot of advice to postgraduate students (Masters and PhD) in the field of immunology.

There are several sites in the body that do not develop immune responses to pathogens, tumor cells, or histoincompatible tissue transplants, these sites, include the brain, eye, testis, ovary, and placenta, so-called because of mechanisms of immune tolerance that operate to protect the tissues from immune-mediated damage. The central nervous system complying the brain and spinal cord is an essential organ for survival, because the inflammation in these sites can lead to loss of organ function. The blood-brain barrier plays an important role in maintaining the separation of CNS from the systemic immune system but the presence of the blood-brain barrier, does not, on its own, provide immune privilege. Activated immune cells secret molecules that are neurotoxic and the encasement of the brain in the skull does not permit excessive infiltration of immune cells. Neurons are highly susceptible to damage by inflammatory responses and have limited ability to regenerate. Since the brain lacks a lymphatic system, and the immunoregulatory mechanisms in the brain circumvent damage to neurons and supporting cells such as oligodendrocytes and astrocytes. Mechanisms known to operate in the protection of neurons from attack by CD8 + cytotoxic T cells involve lack of expression of HLA class Ia A, B and C receptors by neurons. Astrocytes express cell surface FasL which promotes apoptosis in activated T cells by engagement with Fas. (Figure 1). Another mechanisms known to operate in the protection of neurons from attack by natural killer cells is the induced expression of HLA class Ib G receptors that bind to NK inhibitory receptors such as KIR. Astrocytes upregulate surface PD-L1 receptors which promotes apoptosis in activated T cells by engagement of PD-1 receptors. In addition, microglial cells inhibit T cell proliferation by mediating depletion of tryptophan with IDO (indolamine 2,3-dioxygenase).