17^th Global Neuroscience Conference October 16-17, 2017 Osaka, Japan

Professor WK Tang was appointed as professor in the Department of Psychiatry, The Chinese University of Hong Kong in 2011. His main research areas are Addictions and Neuropsychiatry in Stroke. Professor Tang has published over 100 papers in renowned journals, and has also contributed to the peer review of 40 journals. He has secured over 20 major competitive research grants. He has served the editorial boards of five scientific journals. He was also a recipient of the Young Researcher Award in 2007, awarded by the Chinese University of Hong Kong.

Introduction: Previous studies reported stroke patients exhibited poststroke behavioral disinhibition (PSBD). The prevalence rates across studies were inconsistent and vary widely (ranged from 5 to 76%). Moreover, the clinical correlates of PSDB were unknown. Therefore, this study aimed to determine the prevalence of PSDB and its correlates with clinical variables, i.e. functional dependence, cognitive functioning, anxiety and depressive symptoms, after 3-month after stroke. Methods: Stroke survivors who had ischemic stroke admitted to the Acute Stroke Unit of the Prince of Wales Hospital from September 2016 to April 2017 were recruited. PSBD was assessed by the disinhibition subscale of the Chinese version of the Neuropsychiatric Inventory (CNPI), which was responded by the caregivers. The stroke survivors’ functional dependence, anxiety and depressive symptoms were assessed by Barthel Index, the anxiety subscale of the Hospital Anxiety Depression Scale, and the Beck Depression Inventory respectively. Results: Twenty-eight stroke survivors were recruited, 9 were excluded due to the absence of caregivers (n = 8) and history of schizophrenia (n = 1). Thus, 19 stroke survivors and their caregivers were assessed. The mean age of the stroke survivors was 67.11 (SD = 6.79) and 11 (57.9%) were male. The types of caregiver were spouse (63.2%), children (26.3%), and others (10.5%). None of the caregivers reported the presence of behavioral disinhibition of the corresponding stroke survivors. Conclusion: PSBD is uncommon amongst ischemic stroke survivors in Hong Kong. Acknowledgement: The project is supported by the Direct Grant for Research 2015/2016 (Round 1) Ref. No. 2015.1.061

Michalina Radomska has received a Master degree in Clinical and Cognitive Psychology from Faculty of Psychology and Educational Sciences at University of Geneva, Switzerland. She is currently working as an assistant and clinical psychologist in Psychopathology and Cognitive Neuropsychology Unit at University of Geneva. She is also pursuing her PhD in psychology in the field of psychological outcomes of Deep Brain Stimulation for Parkinson Disease. Her main research interest lies in the understanding of the relationship between preoperative expectations and postoperative psychological adjustment in PD patients.

Statement of the Problem: Clinical studies in epileptic patients (EP) successfully treated with temporal lobectomy have identified a range of psychosocial postoperative maladjustments. Such postoperative issues have also been reported in patients treated with Deep Brain Stimulation (DBS). Researchers have suggested that presurgery unrealistic or unspecific expectations may lead to adverse outcomes, despite significant improvements in objective measures. Although various assessments of expectations have been used, there is no validated tool clearly focusing on expectations or hopes related to surgical treatment for neurological diseases. The main purpose of this study was thus to develop an instrument assessing presurgery expectations / hopes and to explore its psychometric properties across two clinical populations: patients undergoing epilepsy surgery and patients qualified for the DBS. Methodology: The Treatment Hope and Expectations Questionnaire (THEQ) was elaborated following a thorough review of relevant literatures. It consists in 22 statements exploring four expectations domains (daily living activities, mental and physical health, psychological wellbeing, social-relational life). Each domain is assessed on 3 subscales: realistic expectations, hopes and current state (control measure). The THEQ was completed by 30 DBS and 30 EP before the planned surgery. Findings: The THEQ had good psychometric properties. Paired t-tests conducted on realistic expectations and hope total scores (i.e., cross-domains) revealed that both EP and DBS patients reported significantly higher hopes than realistic expectations. Moreover, the two groups were characterized by high expectations and hopes for the "mental and physical health" domain. Nevertheless, DBS patients had significantly higher expectations and hopes for the “social-relational life” domain as compared to EP. By and large, DBS patients’ expectations and hopes were more attuned towards psychological or interpersonal improvements as compared to EP

Ms. Chih-Yi Chang is the research assistant at Dr. Shang-Hsun Yang’s laboratory in Department of Physiology at National Cheng Kung University (NCKU), Taiwan. She received her bachelor degree at China Medical University in 2012, and master’s degree at NCKU, Tainan, Taiwan in 2014. Her research topics focus on the regulation of microRNAs on HD, and try to understand the regulatory mechanisms and potentially therapeutic directions for this neurodegenerative disease.

MicroRNAs (miRNAs), non-protein-coding RNA molecules, play important roles in several neurobiological processes, including the development and progression of diseases. Previously, we identified that one specific miRNA, miR-196a, provides neuroprotective effects on Huntington’s disease (HD), although the detailed mechanism is still unclear. Based on our bioinformatic analyses, we hypothesize miR-196a might offer neuroprotective functions through improving cytoskeletons of brain cells. Here, we show that miR-196a could enhance neuronal morphology, further ameliorating intracellular transport, synaptic plasticity, neuronal activity, and learning and memory abilities. Additionally, we found that miR-196a could suppress the expression of RAN binding protein 10 (RANBP10) through binding to its 3’ untranslated region, and higher expression of RANBP10 exacerbates neuronal morphology and intracellular transport. Furthermore, miR-196a enhances neuronal morphology through suppressing RANBP10 and increasing the ability of β-tubulin polymerization. Most importantly, we observed higher expression of RANBP10 in the brains of HD transgenic mice, and higher expression of RANBP10 might exacerbate the pathological aggregates in HD. Taken together, we provide evidence that enhancement of neuronal morphology through RANBP10 is one of the neuroprotective mechanisms for miR-196a. Since miR-196a has also been reported in other neuronal diseases, this study might offer insights with regard to the therapeutic use of miR-196a in other neuronal diseases.

Dr. Yi-Chinn Weng received her PhD from Department of Molecular Medicine, University of Texas Health Science Center, San Antonio, and postdoctoral studies from University of California, San Francisco. She has published several research papers in reputed journals including Nature, Proceedings of the National Academy of Sciences, Annals of Neurology, and Journal of Biological Chemistry.

Ischemic stroke is a major cause of death and long-term disability worldwide. Tissue plasminogen activator (tPA) is the only drug approved for pharmacological intervention to reverse acute ischemic stroke, but reestablishment of circulation may paradoxically initiate reperfusion injury. Activated immune cells (neutrophils, macrophages) infiltrate into ischemic brain tissue, release free radicals, proinflammatory cytokines and proteins, thus causing brain edema, disruption of blood-brain barrier (BBB) and neuronal cell death. Therefore, treatments that can inactivate these immune cells and limit stroke-reperfusion injuries are urgently needed. Our recent results demonstrate that neutrophil gelatinase-associated lipocalin (NGAL) was acutely induced in mice and humans after ischemic stroke and is an important mediator of stroke-reperfusion injury. Increased levels of NGAL were observed in mouse serum as early as 1 hour after transient middle cerebral artery occlusion (tMCAo), reaching peak levels at 23 hours. NGAL was also detected in neutrophils infiltrating into the ipsilateral hemisphere, as well as a subset of astrocytes after tMCAo, but not in neurons and microglia. Cerebral infarction, neurological deficits, infiltration of immune cells, proinflammatory molecules and BBB permeability after tMCAo were significantly reduced in NGAL null mice. The plasma concentration of NGAL was markedly elevated in patients with ischemic stroke. During a four-year follow-up, patients with higher levels of NGAL had higher mortality rates. These results demonstrate that NGAL is a neurotoxic factor secreted rapidly in response to cerebral ischemia, suggesting its potential usage as an early stroke biomarker and a novel therapeutic target to reduce stroke-reperfusion injury.

Ting-Ting Yang is the Professor in neuroscience in School of Medicine for international students and a senior fellow of School of Chinese Medicine for Post-Baccalaureate at I-Shou University. She has also been a visiting professor in the atomic bomb disease institute at Nagasaki University. Dr. Yang received master’s level training and doctoral training in cellular and molecular biology at Nagasaki University. The major focus of her ongoing research is the investigation of disease- and treatment-induced changes in gene and protein expression profiles that regulate neuroenergetics and neuroplasticity signaling pathways in Neurodegeneration Disease including Alzheimer's disease and Parkinson's disease et.al. She has received ongoing research funding from the above mentioned. As a scientist she has been a major contributor to progress in the field of neuroscience research for more than 17 years. In addition to research, Dr. Yang teaches neuropathology to B.S./ M.S. students of I-Shou University.

Microglial activation (MA) and dopaminergic (DA) neuron loss are features of aging brain in Parkinson’s disease (PD). Although the etiology of PD remains unclear, age and inflammation are known PD risk factors. Because reduced brain-derived neurotrophic factor (BDNF) are associated with DA neuron loss in the substantia nigra (SN), age- and LPS-related BDNF/TrkB Signaling Pathway for MA and DA neuron loss in PD have been characterized. Infusing recombinant BDNF into the SN of mice at 6-month-old by osmotic mini-pump for 3 months, we found BDNF inhibited LPS-evoked area of MA in SN, striatum, hippocampus. Exposure to LPS induced phosphorylation of p38, JNK, and GSK3, which then increased phosphorylation of NF-кB. Phosphorylated NF-кB translocated into nucleus and bound to CBP and other coactivators. The NF-кB-CBP complex then induced transcription of inflammatory-related genes. Exogenous supplement with BDNF or endogenous up-regulating the expression of BDNF by exercise inhibited MA. Potential suppressive mechanisms of BDNF on MA might depend on three pathways: 1) BDNF induced Erk activation, which then phosphorylates CREB. Activated CREB inhibited NF-κB activity through competition for limited amounts of CBP. Activated CREB was also known to induce transcription of anti-inflammatory genes. Furthermore, activated CREB might also induced a positive feed forward production of BDNF. 2) BDNF actives Akt, which inhibited the activation of GSK3, resulting in a decrease of NF-кB activation and an increase of CREB activation. 3) BDNF upregulated MKP-1, which then reduced the LPS-induced phosphorylation of p38 and JNK.

Mahboubeh Manouchehrabadi is a MS. c, student in Developmental Biology Islamic Azad University of Karaj. She is expert in experimenting in vitro and in vivo models of Parkinson’s disease. In this regard, she has studied the neuroprotective effect of phenolic monoterpene carvacrol in both models.

Parkinson's disease (PD) is a progressive neurodegenerative movement disorder characterized by selective loss of dopaminergic neurons and the presence of lewy bodies. Treatment for PD that prevents neuronal death in the dopaminergic system and abnormal protein deposition in the brain is not yet available. Evidence from human and animal studies has suggested that oxidative damage critically contributes to neuronal loss in PD. This study aimed to evaluate the potential neuroprotective effects of Carvacrol on PC12 cells treated with 6-OHDA, a cellular model of Parkinson's disease. Carvacrol, a naturally occurring monoterpenic phenol and food additive, has been shown to have antimicrobials, antitumor, neuroprotective and antidepressant – like activities. We found that Carvacrol protect against 6-OHDA induced cell death in a dose-dependent manner. Neuroprotection was found to coincide with increasing cell viability and reductions in intracellular reactive oxygen species and lipid peroxidation. This study demonstrate that Carvacrol protected against 6-OHDA induced cell death via inhibition of oxidative stress, suggesting that Carvacrol may be a candidate neuroprotective agent for 6-OHDA induced Parkinsonism, and possibly for other genetic or sporadic forms of PD.

Seiju Kobayashi was born on March 11, 1976 in Japan She is Presently holding a Position as Director for Department of Psychiatry and also a Faculty in Medicine at Institution Nakae Hospital Her working years are 2001-2002 in Department of Neuropsychiatry, Sapporo Medical University School of Medicine, Sapporo, Japan from 2002-2003 at Department of Psychiatry, Goryokai Hospital, from 2003-2004: Department of Neuropsychiatry, Sapporo Medical University School of Medicine, Sapporo, Japan from 2004-2008: Department of Psychiatry, Sunagawa City Medical Center, Sunagawa, Japan from 2008-2016 at Department of Neuropsychiatry, Sapporo Medical University School of Medicine, Sapporo, Japan and presently at Nakae Hospital

Background: Current diagnostic criteria recommend neuroimaging as a diagnostic support tool for the clinical diagnosis of dementia with Lewy bodies (DLB). Because DLB causes characteristic impairments and disabilities, such as neuroleptic hypersensitivity, which may significantly increase morbidity and mortality, its prompt and correct diagnosis is very important. The aim of this study was to evaluate the extent with which diagnostic accuracy can be increased using a combination of brain perfusion SPECT (bp-SPECT), 123 I-metaiodobenzylguanidine myocardial scintigraphy (MIBG scintigraphy), and DAT-SPECT. Taking finances and patient burden into consideration, we compared the tests to determine priority. Methods: Thirty-four patients with probable DLB (75.0 ± 8.3 years old, 14 male: 20 female) underwent bp-SPECT, MIBG myocardial scintigraphy, and DAT-SPECT. Results: Our comparison of three functional imaging techniques indicated that MIBG scintigraphy (79%) or DAT-SPECT (79%) had better sensitivity for characteristic abnormalities in DLB than bp-SPECT (53%). The combination of the three modalities could increase sensitivity for diagnosis of DLB to 100%. Additionally the ratio of patients with rapid eye movement sleep behavior disorder (RBD) was significantly higher in MIBG (+) group than in MIBG (-) group. Conclusions: In the stand-alone diagnostic means, priority should be placed on MIBG scintigraphy or DAT-SPECT for the diagnosis of DLB. However, our results suggest that the combination of bp-SPECT, MIBG scintigraphy, and DAT-SPECT increased accuracy of the clinical diagnosis of DLB.

Statement of the problem: Deep brain stimulation (DBS) has become a leading treatment for alleviating the motor symptoms of Parkinson’s disease (PD). Patients may nevertheless experience psychosocial maladjustment after surgery. Initially conceptualized in epilepsy surgery, the burden of normality (BoN) has been viewed as an applicable model for addressing this issue in DBS for PD; however, there is a lack of empirical data supporting this assumption. Methodology & Theoretical Orientation: We reviewed the literature to identify elements of psychosocial maladjustment in DBS for PD described in the three levels of the BoN; 1) precursory conditions: chronic illness, sense of disablement, and chance for dramatic cure; 2) clinical manifestations of psychosocial maladjustment, and; 3) two mediating variables: pre-treatment expectations and discarding roles associated with pre-DBS PD. Next, we administered a DBS-adapted version of the semi-structured Austin CEP interview – designed to assess the BoN in epilepsy – to 19 patients aged 58.8 ± 10.1 years treated with DBS for PD. Findings: The applicability of the BoN found strong support in the literature for each of the three levels, although no research addressed sick roles. Similarly, patients from the pilot study fulfilled the precursory conditions with a disease duration of 11.3 ± 3.5 years, a low pre-DBS quality of life (SF-36 means: PCS = 38.1 ± 7.2, MCS = 39.8 ± 7.4) and a significant improvement of motor symptoms sustained in the long term (24.5 ± 7.7 months; UPDRS-III: 28.5%, r = .667, p = .003). Qualitative data revealed that psychosocial maladjustment was characterized by psychological, behavioral, affective and sociological symptoms, which appeared to be fostered by unrealistic/ambivalent expectations and difficulties to forgo sick roles. Conclusion & Significance: The BoN is useful to comprehend the post-DBS psychosocial maladjustment experienced by patients with PD, and could constitute a theoretical basis for clinical rehabilitation.

Sunanta Prommin is studying her Master degree at the School of Physical Therapy, Faculty of Associated Medical Sciences, Khon Kaen University, Thailand. She graduated with a Bachelor's degree in Physical therapy programs. Her further project is interested in the effect of an organized play and environmental modification program in orphans.

Several researches demonstrate that infants in orphanage had delayed gross motor development [1-5]. However, these evidences reported delayed gross motor development of orphans when being adopted or while living in orphanages using a cross-sectional assessment. Previous longitudinal study of Darrah and colleagues found that motor development of typically-developing infants are not stable in the rate of emergence of gross motor development. The greatest variability was observed from infants aged 6 to12 months and instability within individual infants over time during the first 12 months [6]. Longitudinal study seems to be a helpful design to provide useful data about gross motor development variability of individual within a group on some behaviors over time. The purpose of this study therefore was to investigate gross motor developmental instability via a longitudinal design while infants are living in the orphanages. Methodology: Six participants aged 6 months were recruited from an orphanage in Northeastern part of Thailand. The gross motor development of each infant was assessed monthly at the age of 6.5 months until 11.5 months using the Alberta Infant Motor Scale (AIMS). Demographic data were reported using descriptive statistics. The AIMS scores were summarized and plotted on the norm reference graph from the study of Canadian infants [7]. The number of times and percentile of infants with scores occurring below designated cut-offs were reported. Findings: Table 1 shows characteristics of participants. Figure 1 shows the variation of individual orphans’ percentile ranks from 6.5 months to 11.5 months, with no systematic pattern of change noted across infants. However, there were observable less instability compared with typically-developing child in Darrah et al’s study (Figure 2). Three orphans showed variability of percentile lower than the 50th percentiles across six assessments. One infant showed two times of scores which was lower than cut-offs percentile (the 5th percentile). The results could be that these participants had biological risk factors such as low birth weight and biological underlying. The lesser variability of gross motor in these orphans could be caused by limited environment in orphanage. Conclusion: Infants who are living in the orphanages tend to have less variability of gross motor percentile. Recommendation: Results of this study implies that orphaned infants need a longitudinal screening for gross motor development especially those who were born with biological risk factors to confirm their gross motor development delay