ePoster Presentation
Biography
Biography Nikova Aleksandrina Sasheva started her Residency in Neurosurgery in September 2018. She is currently pursuing her PhD in the Department of Neurosurgery at Democritus University of Thrace, Greece. Since May 2018 she is a Mentor for \"Fundamental neuroscience for neuroimaging\" (a course) designed by Johns Hopkins University.
Abstract
Introduction: MCI syndrome is conceptualized as a transition state between normal cognition and dementia, including impairments not only in cognitive domains but also, in gait function. Gait dysfunction in a-MCI patients, is represented with worse rhythm, pace and variability scores but is purely correlated with balance in many researches. A research protocol was conducted to evaluate gait and balance in Greek a-MCI patients. Methodology & Participants: MMSE (Mini Mental State Examination) and Tinetti Scale was applied in (N=17) patients who were diagnosed with mild cognitive impairment (MCI), in the outpatient clinic in the Department of Neurology of the Democritus University of Thrace in Greece. Results: A Pearson’s (r) correlation coefficient was conducted. There was evidence to accept a null hypothesis between the parameters: Tinetti score (M=18,47, SD=5,591) & MMSE: (M=25,29 SD= 1,359) r=.129, p=.622, MMSE & Gait score:(M=8,65, SD= 2,178) r=.143, p=.292, MMSE & Balance score: (M=9,88, SD=3,806) r=.116, p=.658. On the other hand, we found a strong negative association between Tinetti score & age in patients with MCI (M=77,12, SD=7,705) r=.486, p<.05. Conclusions: Higher age was associated with lower level of gait and balance skills in mild cognitive impairment patients. Further research is needed to be implemented in larger Greek MCI patients’ groups.
Biography
Martina Valencia is a part of the research team at the Neuroscience Laboratory of the Pontifical Catholic University of ValparaÃso, Chile and has her expertise in university teaching in subjects such as neurophysiology, research methodology and history of science. In parallel and more than seven years ago, she carried out research on the effect of prenatal stress on neurodevelopment. To achieve this goal, the work is based on a problem that occurs in the obstetric clinic: the use of antenatal and postnatal synthetic glucocorticoids in the prevention of chronic lung disease in premature infants and their adverse side effects at the level of the Central Nervous System, such as, neurodevelopmental delay and various behavioral and brain changes observed in the progeny. She has built this model after years of experience in research, evaluation, teaching and administration both in hospital and education institutions.
Abstract
Postnatal synthetic glucocorticoids (GCs) are widely used in the prevention of chronic lung disease in premature infants and their pharmacologic use is associated with neuro developmental delay and various behavioral and brain changes. Using classic Golgi staining methods, we previously showed that the administration of GCs betamethasone (BET), in equivalent doses to those given in cases of human premature birth, generates long term alterations in Purkinje cell (PC) dendritic development in the cerebellar cortex. On the other hand, the brain-derived neurotrophic factor (BDNF) and the tyrosine kinase B receptor (TrkB) are involved in cerebellar PC dendritic development and maintenance and are located predominantly in the cerebellar molecular layer where PC dendritogenesis occurs. Therefore, we hypothesized that reductions in protracted lower PC dendritic arborization could be due, atleast in part, to changes in dendritic expression of BDNF and TrkB. On the other hand, previous studies demonstrated that animals that experience stress, either via chronic maternal stress or exogenous GCs administration, exhibited a significant alteration in the neurotrophic factors regulation and behavioral changes associated with anxious behaviors. For these reasons, in the present study, we evaluated whether postnatal administration of betamethasone alters the immunohistochemical (IHC) expression of BDNF and TrkB in the cerebellar cortex along with anxiety behaviours in infants, adolescent and adult rats. Consistent with our previous studies, we observed that animals postnatal exposed to betamethasone showed long term alterations in the IHC expression of BDNF and TrkB in adolescent and adult rats. Additionally, these protracted molecular changes were accompanied by an increase of anxiety like behaviors in the elevated plus maze and marble burying test in adolescent and adult rats. Recent Publications 1. Pascual R, Santander O, Cuevas I and Valencia M (2017) Prenatal glucocorticoid administration persistently increased the immunohistochemical expression of type-1 metabotropic glutamate receptor and Purkinje cell dendritic growth in the cerebellar cortex of the rat. Romanian Journal of Morphology and Embryology. 58(1):67-72. 2. Pascual R, Valencia M and Bustamante C (2015) Antenatal betamethasone produces protracted changes in anxiety-like behaviors and in the expression of microtubule-associated protein 2, brain-derived neurotrophic factor and the tyrosine kinase B receptor in the rat cerebellar cortex. International Journal of Developmental Neuroscience. 43:78-85. 3. Pascual R, Valencia M and Bustamante C (2015) Purkinje cell dendritic atrophy induced by prenatal stress is mitigated by early environmental enrichment. Neuropediatrics. 46(1):37-43. 4. Pascual R, Valencia M, Larrea S and Bustamante C (2014) Single course of antenatal betamethasone produces delayed changes in morphology and calbindin-d28k expression in a rat\'s cerebellar Purkinje cells. Acta Neurobiologiae Experimentalis. 74(4):415-423. 5. Bustamante C et al. (2014) Effects of a single course of prenatal betamethasone on dendritic development in dentate gyrus granular neurons and on spatial memory in rat offspring. Neuropediatrics. 45(6):354-361.
Biography
Huwon Kim pursued his MD and PhD in Neurology from Chonnam National University. He is currently a Clinician majoring in Neurology at the Chosun University Hospital, Republic of South Korea. He is one of the principal investigators of National Dementia Research Project, GwangJu. He served as a Research Fellow at the Samsung Medical Center (2000-2001); worked in the Neurology Clinic at Iksan Hospital, Iksan City (2001-2002). He has published more than 15 papers and has presented his talk on several occasions in domestic and international conferences.
Abstract
Background: The white matter hyper intensities (WMHs) are high signal lesions seen on T2 or FLAIR MRI (Fluid-attenuated inversion recovery) images. It is known to be a normal aging process but also as a marker of small vascular disease and severe WHMs are thought to cause cerebral cortical and subcortical atrophy. But WMHs are also founded in the MRIs of normal aging polulation. We aim to understand the effect of WMHs in normal aged subjects as an aging process, especially on the cortical thickness and cognition. Methodology: Total 392 elderly individuals were recruited from the community based study pool of individuals registered in a National Research Center for Dementia, Gwangju, Korea. They have no focal neurological deficits and no history of severe medical illnesses and cerebrovascular accidents and their basic or instrumental daily activities were all normal. They were assessed with a series of questionnaires and comprehensive neuropsychological (NP) assessment using the Seoul Neuropsychological Screening Battery, blood sampling and MRI imaging and last interview by well-trained doctors. They were divided into two groups [cognitively normal (CN; 223) and minimally cognitive impairment (MCI; 169)] according to neuropsychological test z score over/under – 1.5 according to the age, education and gender specific norms. White matter hyperintensities (WMHs) were assessed by visual scoring with a scale by Fazekas et al. into 4 groups (0, 1, 2, 3). Cortical thickness of various cortical areas and hippocampal and ventricular volumes were measured automatically based on 3D MPRAGE (three-dimension magnetization prepared rapid gradient echo) images using Free surfer software. Results: At the demographic and clinical characteristics in CN group age, sex, smoking history was statistically significant. At MCI groups age, height, K-MMSE, monthly income, hypertension, ApoE4 were the significant. At cognitive profiles, WMHs did not affect on any of cognitive domains in cognitive normal group. But in MCI groups, WMHs affects on many cognitive domains, visuospatial (RCFT copy), memory (SVLT/RCFT immediate/delayed recall), and frontal executive function (Stroop test). At cortical thickness, hippocampal and brain volume, WMHs affected atrophy on multiple areas of frontal dominant areas, but the effect on hippocampal atrophy were equivocal. Conclusions: The older, low-educated, smaller, hypertensive and depressive females seem to be more susceptible to WMHs. When cognitive normal, WMHs did not affect cognitive profiles but when cognition decline, WMHs seem to aggravate visuospatial memory and frontal cognitive profiles. As WMH increases, so does the brain decreases but hippocampal atrophy seems not closely related with WMHs. The particular cortical areas vulnerable to increasing WM hyperintensities are fusiform, lingual, insular cortices of frontal lobe and some areas of temporal lobe and cingulate gyrus. We suppose WMHs slow progress in aging phenomenon causes cortical atrophy and cognitive decline, but their effects were not evident until the decompensation develops.