Asian Pacific Society Research Articles

Loss of TDP-43 function causes neurodegeneration in the mice brain

Event Abstract Back to Event Loss of TDP-43 function causes neurodegeneration in the mice brain Ming-Che J. Wu1*, Lien-Szu Wu1, Wei-Cheng Cheng1 and C.-K. J. Shen1 1 Academia Sinica, Institute of Molecular Biology, Taiwan Tar-DNA binding protein 43 (TDP-43), a nuclear protein, plays an important role in regulating transcription and mRNA splicing. TDP-43 is the major constituent of proteinaceous inclusion in the cytoplasm of amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD) patients‚Äô diseased neurons, and over hundreds studies have been published on TDP-43 and its role in ALS and FTLD, suggesting that TDP-43 is a critical protein in these neurodegenerative diseases. However, the physiological function of TDP-43 and underlying mechanism to cause neurodegeneration are still elusive. To address these questions, we have showed that targeted depletion of TDP-43 expression in spinal cord motor neurons caused the ALS-phenotypes in mice. Here, we generate conditional knockout mice in which Tardbp gene is inactivated in higher central nervous systems. In comparison to control mice, the conditional knockout mice show behavior and brain pathological alteration. Furthermore, we found that the abnormal electrophysiology in not only the primary culture of mouse cortical neurons with TDP-43 knockdown, but also in the hippocampal CA1 region of the brain slices from conditional TDP-43 knockout mice. In this study, we demonstrate that TDP-43 plays an important role in the higher central nervous system, and provide some molecular mechanism for further studies to investigate the TDP-43 biological function. Keywords: Electrophysiology, neurodegeneration, in vivo, in vitro, Nuclear protein Conference: 14th Meeting of the Asian-Pacific Society for Neurochemistry, Kuala Lumpur, Malaysia, 27 Aug - 30 Aug, 2016. Presentation Type: Poster Presentation Session Topic: 14th Meeting of the Asian-Pacific Society for Neurochemistry Citation: Wu MJ, Wu L, Cheng W and Shen CJ (2016). Loss of TDP-43 function causes neurodegeneration in the mice brain. Conference Abstract: 14th Meeting of the Asian-Pacific Society for Neurochemistry. doi: 10.3389/conf.fncel.2016.36.00158 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 03 Aug 2016; Published Online: 11 Aug 2016. * Correspondence: Mr. Ming-Che J Wu, Academia Sinica, Institute of Molecular Biology, Taipei, Taiwan, mcjameswu@gate.sinica.edu.tw Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Ming-Che J Wu Lien-Szu Wu Wei-Cheng Cheng C.-K. J Shen Google Ming-Che J Wu Lien-Szu Wu Wei-Cheng Cheng C.-K. J Shen Google Scholar Ming-Che J Wu Lien-Szu Wu Wei-Cheng Cheng C.-K. J Shen PubMed Ming-Che J Wu Lien-Szu Wu Wei-Cheng Cheng C.-K. J Shen Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Effects of naloxone and bicuculline on acquisition of passive avoidance task in mitragynine-treated rats

Event Abstract Back to Event Effects of naloxone and bicuculline on acquisition of passive avoidance task in mitragynine-treated rats Farah W. Suhaimi1*, Zurina Hassan1, Visweswaran Navaratnam1, Christian P. Muller2 and Sharif M. Mansor1 1 Universiti Sains Malaysia, Centre for Drug Research, Malaysia 2 Friedrich-Alexander-University Erlangen-Nuremberg, Department of Psychiatry and Psychotherapy, Germany Mitragynine is the psychoactive substance of Mitragyna speciosa Korth (Kratom), an indigenous plant of the Southeast Asian countries. This plant has been traditionally used as a substitute in the self-treatment of opiate addiction, to reduce pain sensitivity as well as to enhance physical endurance. However, reports on Kratom in various countries have suggested considerable abuse potential despite little understanding on health consequences. We previously reported that acute and chronic administrations of mitragynine impaired learning and memory functions in Sprague-Dawley rats. Pharmacological manipulations of the neural systems that modulate the memory processes may elucidate the possible underlying mechanisms of how mitragynine affects the learning and memory functions. Thus, the present study aims to investigate the involvement of the opioidergic and GABAergic systems in mediating the effects of mitragynine on learning and memory functions. Male Sprague-Dawley rats were co-administered with mitragynine (1, 5, or 10 mg/kg) and naloxone, an opioid antagonist (1.0 mg/kg) or bicuculline, a GABAA antagonist (0.125 mg/kg), immediately after training of the passive avoidance task. Both naloxone and bicuculline were able to overcome the effects of mitragynine on memory retrieval as shown by the increased step-through latencies. Taken together, these results suggest the participations of the opioidergic and GABAergic systems in modulating the effects of mitragynine in learning and memory functions. Acknowledgements Higher Education Centre of Excellence (HICoE) special funding (304.CDADAH.650527.K134) and International Research Collaboration Fund (IReC) (1002.CDADAH.910410) Keywords: Learning, Memory, in vivo, GABAergic system, Psychoactive substance Conference: 14th Meeting of the Asian-Pacific Society for Neurochemistry, Kuala Lumpur, Malaysia, 27 Aug - 30 Aug, 2016. Presentation Type: Poster Presentation Session Topic: 14th Meeting of the Asian-Pacific Society for Neurochemistry Citation: Suhaimi FW, Hassan Z, Navaratnam V, Muller CP and Mansor SM (2016). Effects of naloxone and bicuculline on acquisition of passive avoidance task in mitragynine-treated rats. Conference Abstract: 14th Meeting of the Asian-Pacific Society for Neurochemistry. doi: 10.3389/conf.fncel.2016.36.00118 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 04 Aug 2016; Published Online: 11 Aug 2016. * Correspondence: Dr. Farah W Suhaimi, Universiti Sains Malaysia, Centre for Drug Research, Minden, Penang, Malaysia, sfarahwahida@usm.my Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Farah W Suhaimi Zurina Hassan Visweswaran Navaratnam Christian P Muller Sharif M Mansor Google Farah W Suhaimi Zurina Hassan Visweswaran Navaratnam Christian P Muller Sharif M Mansor Google Scholar Farah W Suhaimi Zurina Hassan Visweswaran Navaratnam Christian P Muller Sharif M Mansor PubMed Farah W Suhaimi Zurina Hassan Visweswaran Navaratnam Christian P Muller Sharif M Mansor Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Possible involvement of alterations in tumor necrosis factor beta secretions in the metformin-induced suppression of the proliferation in P19 cells

Event Abstract Back to Event Possible involvement of alterations in tumor necrosis factor beta secretions in the metformin-induced suppression of the proliferation in P19 cells Nobuyuki Kuramoto1*, N Nitta1, H Higashi1 and T Kinjo1 1 Setsunan University, Laboratory of Molecular Pharmacology, Faculty of Pharmaceutical Sciences, Japan Neural stem/progenitor cells (NPCs), which are defined by their ability to self-renew and differentiate into 3 major cell types including neurons, astrocytes, and oligodendrocytes, play a key role in the development and maturation of the central nervous system. P19 embryonic carcinoma cells resemble NPCs. It has been reported that 5’-AMP-activated protein kinase (AMPK) acts not only as an efficient sensor for cellular ATP level, but as a regulator for cellular proliferation and differentiation. Here, we measured cytokine expressions in P19 cells under the condition of the metformin-induced suppression of the proliferation. P19 cells were cultured in alpha minimum essential medium in a 5% CO2 humidified chamber at 37°C. After plating P19 cells at a concentration of 3.0×105 cells/mL, at every 12 h, cell viability was measured by abilities of MTT reduction and gene expression was semi-quantified by RT-PCR. P19 cells grew and reached confluence within 48 h after the plating. Metformin suppressed the proliferation of P19 cells in a concentration-dependent manner. Among several cytokines, gene expression of tumor necrosis factor (TNF)-beta increased by metformin in a concentration dependent manner. It was therefore suggested that metformin-induced suppression of the proliferation in P19 cells might involve the alteration of the gene expressions and secretions of TNF-beta. Keywords: Cytokines, Gene Expression, in vitro, neural progenitor cells, P19 cells Conference: 14th Meeting of the Asian-Pacific Society for Neurochemistry, Kuala Lumpur, Malaysia, 27 Aug - 30 Aug, 2016. Presentation Type: Poster Presentation Session Topic: 14th Meeting of the Asian-Pacific Society for Neurochemistry Citation: Kuramoto N, Nitta N, Higashi H and Kinjo T (2016). Possible involvement of alterations in tumor necrosis factor beta secretions in the metformin-induced suppression of the proliferation in P19 cells. Conference Abstract: 14th Meeting of the Asian-Pacific Society for Neurochemistry. doi: 10.3389/conf.fncel.2016.36.00115 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 04 Aug 2016; Published Online: 11 Aug 2016. * Correspondence: Prof. Nobuyuki Kuramoto, Setsunan University, Laboratory of Molecular Pharmacology, Faculty of Pharmaceutical Sciences, Hirakata, Osaka, 573-0101, Japan, kuramoto@pharm.setsunan.ac.jp Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Nobuyuki Kuramoto N Nitta H Higashi T Kinjo Google Nobuyuki Kuramoto N Nitta H Higashi T Kinjo Google Scholar Nobuyuki Kuramoto N Nitta H Higashi T Kinjo PubMed Nobuyuki Kuramoto N Nitta H Higashi T Kinjo Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

The effects of acute ethanol challenge on amygdala protein and gene expression of mglu5 and pkc epsilon during ethanol withdrawal induced anxiety in rats

Event Abstract Back to Event The effects of acute ethanol challenge on amygdala protein and gene expression of mglu5 and pkc epsilon during ethanol withdrawal induced anxiety in rats Jaya Kumar1, 2*, Hermizi Hapidin3, Yvonne Tee Get Bee3 and Zalina Ismail2 1 Universiti Kebangsaan Malaysia, Department of Physiology, UKM Medical Centre, Malaysia 2 Universiti Sains Malaysia, BRAINetwork Centre for Neurocognitive Sciences, Malaysia 3 Universiti Sains Malaysia, School of Health Sciences, Malaysia Cessation from prolonged and excessive ethanol intake can lead to hyperexcitability of glutamatergic neurotransmission in the amygdala, which induces an anxiety-like syndrome. Most alcoholics that suffer from such symptoms frequently depend on habitual drinking as self-medication to alleviate their symptoms. Metabotropic glutamate receptors 5 (mGlu5) and Protein Kinase C (PKC) epsilon have been related to ethanol consumption and anxiety-related behaviours. mGlu5 signalling has been associated with PKC activities and the epsilon isoform of PKC has been suggested as a crucial signalling target for modulation of ethanol consumption by mGlu5. This study explores the changes in mGlu5 and PKC epsilon at protein and gene-levels in the amygdala following acute ethanol challenge during EW induced anxiety in rats. Male Wistar rats were fed a modified liquid diet containing low fat cow milk, sucrose, and maltodextrin, with a gradual introduction of 2.4%, 4.8% and 7.2% ethanol for 20 days. Six hours into EW, the rats were intraperitoneally injected with normal saline and ethanol (2.5?g/kg, 20% v/v), and exposed to open field and elevated plus maze tests. Then, amygdala tissue was dissected from the rat brain for Western blot and gene expression studies. EW-induced anxiety was accompanied by a significant increment of mGlu5, total PKC epsilon and phosphorylated PKC epsilon protein levels and also of mRNA of mGlu5 (GRM5) in the amygdala. Acute administration of ethanol significantly attenuated EW-induced anxiety as well as an EW-induced increase in GRM5. The acute challenge of ethanol to EW rats had little effect on the phosphorylated and total protein levels of PKC epsilon in the amygdala. Our results show that amygdala PKC epsilon may not be directly involved in the development of anxiety following EW. Keywords: Amygdala, hyperexcitability, PKC, mGlu5, ethanol challenge Conference: 14th Meeting of the Asian-Pacific Society for Neurochemistry, Kuala Lumpur, Malaysia, 27 Aug - 30 Aug, 2016. Presentation Type: YIC05: Young Investigator Colloquium 5 Topic: 14th Meeting of the Asian-Pacific Society for Neurochemistry Citation: Kumar J, Hapidin H, Tee Get Bee Y and Ismail Z (2016). The effects of acute ethanol challenge on amygdala protein and gene expression of mglu5 and pkc epsilon during ethanol withdrawal induced anxiety in rats. Conference Abstract: 14th Meeting of the Asian-Pacific Society for Neurochemistry. doi: 10.3389/conf.fncel.2016.36.00069 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 04 Aug 2016; Published Online: 11 Aug 2016. * Correspondence: Dr. Jaya Kumar, Universiti Kebangsaan Malaysia, Department of Physiology, UKM Medical Centre, Cheras, Kuala Lumpur, Malaysia, jayakumar@ukm.edu.my Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Jaya Kumar Hermizi Hapidin Yvonne Tee Get Bee Zalina Ismail Google Jaya Kumar Hermizi Hapidin Yvonne Tee Get Bee Zalina Ismail Google Scholar Jaya Kumar Hermizi Hapidin Yvonne Tee Get Bee Zalina Ismail PubMed Jaya Kumar Hermizi Hapidin Yvonne Tee Get Bee Zalina Ismail Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Role of epigenetic modulation in hypobaric hypoxia induced memory impairment

Event Abstract Back to Event Role of epigenetic modulation in hypobaric hypoxia induced memory impairment Rahul Kumar1, Vishal Jain2, Neetu Kushwah1, Aastha Dheer1, Dipti Prasad1 and Shashi B. Singh1* 1 Defense Institute of Physiology and Allied Sciences (DIPAS) DRDO, Neurobiology Department, India 2 Defense Institute of Physiology and Allied Sciences (DIPAS) DRDO, Neurophysiology Department, India Long term memory formation requires a series of cellular as well as molecular adaptation that control the gene expression at the transcription level. However, epigenetic mechanisms such as histone acetylation, methylation, phosphorylation and DNA methylation have emerge critical regulators of transcription during memory consolidation process. Epigenetic mechanism controls gene expression bidirectional i.e. either enhance or repress gene expression. In addition, histone acetylation has been the main mechanism of epigenetics and play important role in memory formation as well as reconsolidation. Stressful environmental conditions such as hypobaric hypoxia (HH) leads to change in learning and memory. Present study is designed to explore global as well as specific histone modifications, mainly acetylation in different brain regions during different duration of HH exposure. Sprague Dawley rats (220 to 230 gm) were exposed to different duration of HH i.e. 1, 3, 7 and 14 days in an animal decompression chamber at an altitude of 25,000 feet. After exposure, rats were sacrificed and hippocampus and cortex were isolated. Activity of histone acetylase (HAT), histone deacetylase (HDAC) and DNA methyl transferase (DNMT) was analyzed using kits. Further specific histone acetylation sites i.e. H2BK5Acetylation, H3K9Acetylation and H4K14Acetylation were also studied in different brain regions. Results from the present study revealed the correlation between expressions of HDAC and HIF-1 alpha which further control other hypoxia responsive genes in both the brain regions. Gradual increased expression of HDAC on HH exposure causes repression of learning and memory related genes. In addition, the decline in H2BK5Ac expression may also account for inactivation of transcription of memory responsive gene leading to decline in memory. In brief, it can be concluded that epigenetic modification at histone acetylation sites may account for HH mediated memory impairment. Keywords: Memory, epigenetic, in vivo, histone acetylation, hypobaric hypoxia Conference: 14th Meeting of the Asian-Pacific Society for Neurochemistry, Kuala Lumpur, Malaysia, 27 Aug - 30 Aug, 2016. Presentation Type: Poster Presentation Session Topic: 14th Meeting of the Asian-Pacific Society for Neurochemistry Citation: Kumar R, Jain V, Kushwah N, Dheer A, Prasad D and Singh SB (2016). Role of epigenetic modulation in hypobaric hypoxia induced memory impairment. Conference Abstract: 14th Meeting of the Asian-Pacific Society for Neurochemistry. doi: 10.3389/conf.fncel.2016.36.00191 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 04 Aug 2016; Published Online: 11 Aug 2016. * Correspondence: Dr. Shashi B Singh, Defense Institute of Physiology and Allied Sciences (DIPAS) DRDO, Neurobiology Department, New Delhi, North Delhi, India, drshashisingh@gmail.com Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Rahul Kumar Vishal Jain Neetu Kushwah Aastha Dheer Dipti Prasad Shashi B Singh Google Rahul Kumar Vishal Jain Neetu Kushwah Aastha Dheer Dipti Prasad Shashi B Singh Google Scholar Rahul Kumar Vishal Jain Neetu Kushwah Aastha Dheer Dipti Prasad Shashi B Singh PubMed Rahul Kumar Vishal Jain Neetu Kushwah Aastha Dheer Dipti Prasad Shashi B Singh Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Copper and iron changes in Parkinson's disease brain; implications for aetiology and potential for novel treatments

Event Abstract Back to Event Copper and iron changes in Parkinson's disease brain; implications for aetiology and potential for novel treatments Katherine Davies1, Benjamin Trist2, Veronica Cottam2, Dominic J. Hare3, Sylvain Bohic4, Asuncion Carmona5, Richard Ortega5 and Kay L. Double2* 1 Neuroscience Research Australia, Australia 2 The University of Sydney, School of Medical Sciences, Sydney Medical School, Australia 3 Florey Institute of Neuroscience and Mental Health, University of Technology Sydney, and The University of Melbourne , Australia 4 Universite Grenoble Alpes, Inserm, France 5 and Centre National de la Recherche Scientifique, University of Bordeaux, France We have used sensitive, high resolution biophysical imaging methods to investigate biometals changes at the single cell level in the Parkinson’s disease brain. Consistent with a large body of bulk tissue reports, we identified increased intraneuronal Fe in the degenerating substantia nigra in this disorder, a change not present in non-degenerating brain regions. We have suggested that Fe and dopamine form a potent biochemical redox couple, thus the accumulation of Fe within the dopaminergic substantia nigra in the Parkinson’s disease brain may contribute to the selective vulnerability of this brain region. We also identified significantly decreased Cu levels in these same neurons, associated with altered cellular Cu transport pathways. Decreased intraneuronal Cu was also present in the substantia nigra in incidental Lewy body disease prior to the onset of neuronal loss, suggesting this change occurs early in the disease process. The decrease in Cu in these vulnerable neurons is associated with alterations in cuproproteins. Regional changes in cuproproteins in the Parkinson’s disease brain may contribute to the accumulation of intraneuronal Fe in this disorder, but also to mechanisms of degeneration linked to dysfunction of the cuproprotein superoxide dismutase 1. We suggest that normalisation of brain Fe and Cu levels in Parkinson’s disease brain represents a tractable target for neuroprotective therapy. Keywords: Copper, Iron, Substantia Nigra, Parkinson, neurodegeneration Conference: 14th Meeting of the Asian-Pacific Society for Neurochemistry, Kuala Lumpur, Malaysia, 27 Aug - 30 Aug, 2016. Presentation Type: Symposium 3: Metals in the Aetiology and Treatment of Neurodegenerative Diseases Topic: 14th Meeting of the Asian-Pacific Society for Neurochemistry Citation: Davies K, Trist B, Cottam V, Hare DJ, Bohic S, Carmona A, Ortega R and Double KL (2016). Copper and iron changes in Parkinson's disease brain; implications for aetiology and potential for novel treatments. Conference Abstract: 14th Meeting of the Asian-Pacific Society for Neurochemistry. doi: 10.3389/conf.fncel.2016.36.00015 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 26 Jul 2016; Published Online: 11 Aug 2016. * Correspondence: Prof. Kay L Double, The University of Sydney, School of Medical Sciences, Sydney Medical School, Sydney, NSW, Australia, kay.double@sydney.edu.au Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Katherine Davies Benjamin Trist Veronica Cottam Dominic J Hare Sylvain Bohic Asuncion Carmona Richard Ortega Kay L Double Google Katherine Davies Benjamin Trist Veronica Cottam Dominic J Hare Sylvain Bohic Asuncion Carmona Richard Ortega Kay L Double Google Scholar Katherine Davies Benjamin Trist Veronica Cottam Dominic J Hare Sylvain Bohic Asuncion Carmona Richard Ortega Kay L Double PubMed Katherine Davies Benjamin Trist Veronica Cottam Dominic J Hare Sylvain Bohic Asuncion Carmona Richard Ortega Kay L Double Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

PDGF-A activated signaling pathways and molecular mediators in glioma growth and migration

Event Abstract Back to Event PDGF-A activated signaling pathways and molecular mediators in glioma growth and migration Juhi Singh1*, Kedarlal Sharma1 and Prakash P. Pillai1 1 The Maharaja Sayajirao University of Baroda, Division of Neurobiology, Department of Zoology, Faculty of Science, India Gliomas contribute to 50% of the brain tumors characterised by its highly invasiveness, aggressive tumorigenicity and resistance to chemotherapy and radiation. The molecular mechanisms governing these characteristics involve numerous physiological and genetic alterations. One of the common genetic alteration or defect observed in gliomas is the presence of PDGF (Platelet Derived Growth Factor) autocrine loop marked by the co-expression of the PDGF and its receptor. PDGFR amplification in glioblastoma has been frequently linked to its abnormal proliferation and metastasis. Stimulation of PDGFR by its ligand results in the activation of several signalling pathways such as ERK1/2, PI3K and ROCK pathways causing aberrant growth, proliferation and migration. However, the role of PDGF mediated intracellular signalling in glioma growth and migration has not been much explored. The objective of the present study focuses on the intracellular pathways involved in PDGF receptor inhibition mediated suppression of Rat C6 glioma growth and migration. To study the effect of PDGFR inhibition on MAPK-ERK and ROCK signalling, pERK and pMLC levels were determined in C6 cells exposed to PDGFR inhibitor or PDGF-A. We found reduction in pERK and pMLC levels in PDGFR inhibitor group compared to control and PDGF-A treated group and it suggested MAPK-ERK and ROCK signalling act downstream of PDGFR. Further, growth and migration of C6 cells were studied and found to be reduced in PDGFR inhibitor, MEK inhibitor and ROCK inhibitor compared to control and PDGF-A treated groups. Also, PDGFR inhibition lled to up-regulation of BDNF (Brain Derived Neurotrophic factor), MeCP2 (Methyl CpG binding Protein 2) and GFAP (Glial Fibrillary Acidic Protein) expressions which were found to be associated in regulation of glioma progression. Thus, the study suggests PDGFR inhibition regulates the growth and migration by modulating ERK-ROCK signalling which can be a future potential target for the treatment for glioma. Keywords: Migration, therapy, molecular genetics, Signalling pathway, Glioma growth Conference: 14th Meeting of the Asian-Pacific Society for Neurochemistry, Kuala Lumpur, Malaysia, 27 Aug - 30 Aug, 2016. Presentation Type: Poster Presentation Session Topic: 14th Meeting of the Asian-Pacific Society for Neurochemistry Citation: Singh J, Sharma K and Pillai P (2016). PDGF-A activated signaling pathways and molecular mediators in glioma growth and migration. Conference Abstract: 14th Meeting of the Asian-Pacific Society for Neurochemistry. doi: 10.3389/conf.fncel.2016.36.00198 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 04 Aug 2016; Published Online: 11 Aug 2016. * Correspondence: Ms. Juhi Singh, The Maharaja Sayajirao University of Baroda, Division of Neurobiology, Department of Zoology, Faculty of Science, Vadodara, Gujarat, India, juhivsingh@gmail.com Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Juhi Singh Kedarlal Sharma Prakash P. Pillai Google Juhi Singh Kedarlal Sharma Prakash P. Pillai Google Scholar Juhi Singh Kedarlal Sharma Prakash P. Pillai PubMed Juhi Singh Kedarlal Sharma Prakash P. Pillai Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Detection of active site conformation changes of gamma-secretase, a key enzyme associated with Alzheimer disease, with small molecules

Event Abstract Back to Event Detection of active site conformation changes of gamma-secretase, a key enzyme associated with Alzheimer disease, with small molecules Natalya Gertsik1, 2, Yue-Ming Li1, 3 and De-Ming Chau4* 1 Memorial Sloan-Kettering Cancer Center, Molecular Pharmacology and Chemistry Program, United States 2 Weill Graduate School of Medical Sciences of Cornell University, Biochemistry and Molecular Biology Program, United States 3 Weill Graduate School of Medical Sciences of Cornell University, Program of Pharmacology, United States 4 Universiti Putra Malaysia, Department of Biomedical Science, Faculty of Medicine & Health Sciences, Malaysia Gamma-secretase is a membrane-bound aspartyl-protease that cleaves many membrane substrates including Amyloid Precursor Protein (APP), Notch, E-cadherin, Her4 and CD44. APP is a particularly notable substrate because of its association with Alzheimer disease. Together, gamma-secretase and beta-secretase cleave APP to produce amyloid beta peptides that aggregate in the brain as cytotoxic beta-amlyoid plaques, which is one of the hallmarks of Alzheimer disease. Many small molecules are being developed to target gamma-secretase as a therapeutic strategy for Alzheimer disease. However, studying the effects of these molecules on the active site conformation of gamma-secretase is challenging due to the complexity of this enzyme. In our study, we have developed new biochemical techniques to probe the active site structure of gamma-secretase. We are able to show that different gamma-secretase inhibitors and modulators, when bind to gamma-secretase, affect the active site structure of gamma-secretase differently. More importantly, we discovered that these small molecules, which were developed to target gamma-secretase, also affect the active site structure of Signal Peptide Peptidase, a similar membrane-bound aspartyl-protease. This discovery has major implication on the development of gamma-secretase inhibitors as therapeutic drugs for Alzheimer disease due to potential off-target effects. Keywords: neurodegeneration, Alzheimer’s disease, therapeutic, molecule, Gamma secretase Conference: 14th Meeting of the Asian-Pacific Society for Neurochemistry, Kuala Lumpur, Malaysia, 27 Aug - 30 Aug, 2016. Presentation Type: Poster Presentation Session Topic: 14th Meeting of the Asian-Pacific Society for Neurochemistry Citation: Gertsik N, Li Y and Chau D (2016). Detection of active site conformation changes of gamma-secretase, a key enzyme associated with Alzheimer disease, with small molecules. Conference Abstract: 14th Meeting of the Asian-Pacific Society for Neurochemistry. doi: 10.3389/conf.fncel.2016.36.00137 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 04 Aug 2016; Published Online: 11 Aug 2016. * Correspondence: Dr. De-Ming Chau, Universiti Putra Malaysia, Department of Biomedical Science, Faculty of Medicine & Health Sciences, Serdang, Selangor, Malaysia, chau.deming@gmail.com Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Natalya Gertsik Yue-Ming Li De-Ming Chau Google Natalya Gertsik Yue-Ming Li De-Ming Chau Google Scholar Natalya Gertsik Yue-Ming Li De-Ming Chau PubMed Natalya Gertsik Yue-Ming Li De-Ming Chau Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

The non-canonical effects of N-acetyl-d-glucosamine kinase on the formation of neuronal dendrites and axons

Event Abstract Back to Event The non-canonical effects of N-acetyl-d-glucosamine kinase on the formation of neuronal dendrites and axons M A. Islam1 and Il Soo Moon1* 1 Dongguk University Graduate School of Medicine, Department of Anatomy, Republic of Korea Previously, we reported that N-acetylglucosamine kinase (NAGK) plays an enzyme activity-independent, non-canonical role in the dendritogenesis of hippocampal neurons in culture. To elucidate the molecular mechanism, we conducted yeast two-hybrid screening to search for NAGK-binding proteins and found a specific interaction between NAGK and dynein light-chain roadblock type 1 (DYNLRB1). A proximity ligation assay (PLA) of NAGK-dynein followed by tubulin ICC showed the localization of PLA signals on microtubule fibers at dendritic branch points. NAGK-dynein PLA combined with Golgi ICC showed the colocalization of PLA signals with somal Golgi facing the apical dendrite and with Golgi outposts in dendritic branch points and distensions. NAGK-Golgi PLA followed by tubulin or DYNLRB1 ICC showed that PLA signals colocalized with DYNLRB1 at dendritic branch points and at somal Golgi, indicating a tripartite interaction between NAGK, dynein and Golgi. Finally, the ectopic introduction of a small peptide derived from the C-terminal amino acids 74-96 of DYNLRB1 resulted in the stunting of hippocampal dendrites in culture. Our data indicate that the NAGK-dynein-Golgi tripartite interaction at dendritic branch points functions to regulate dendritic growth and/or branching. Other non-canonical functions of NAGK in cell division and migration will also be presented. Keywords: Cell Division, Hippocampus, cell migration, Neuron, in vitro Conference: 14th Meeting of the Asian-Pacific Society for Neurochemistry, Kuala Lumpur, Malaysia, 27 Aug - 30 Aug, 2016. Presentation Type: Free Paper Session 2: Molecular Mechanisms of the Nervous System Topic: 14th Meeting of the Asian-Pacific Society for Neurochemistry Citation: Islam MA and Moon I (2016). The non-canonical effects of N-acetyl-d-glucosamine kinase on the formation of neuronal dendrites and axons. Conference Abstract: 14th Meeting of the Asian-Pacific Society for Neurochemistry. doi: 10.3389/conf.fncel.2016.36.00106 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 04 Aug 2016; Published Online: 11 Aug 2016. * Correspondence: Prof. Il Soo Moon, Dongguk University Graduate School of Medicine, Department of Anatomy, Gyeongju, Republic of Korea, moonis@dongguk.ac.kr Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers M A Islam Il Soo Moon Google M A Islam Il Soo Moon Google Scholar M A Islam Il Soo Moon PubMed M A Islam Il Soo Moon Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Blood-brain barrier permeability studies of Centella asiatica extract as potential neuroprotective agent

Event Abstract Back to Event Blood-brain barrier permeability studies of Centella asiatica extract as potential neuroprotective agent Nur Aziah Hanapi1, Siti Rafidah Yusof1, Mohd Ilham Adenan2 and Tengku Sifzizul Tengku Muhammad3* 1 Universiti Sains Malaysia, Centre for Drug Research, Malaysia 2 Universiti Teknologi Mara , Atta-ur-Rahman Institute for Natural Product Discovery, Malaysia 3 Universiti Malaysia Terengganu , Institute of Marine Biotechnology , Malaysia Centella asiatica (CA) plant has been used to treat eczema, asthma, ulcers, psychiatric disorders, leprosy and to promote wound healing. Notably, it has also been used in the treatment of neurodegenerative diseases such as Alzheimer’s disease (AD). Centella asiatica extract (CAE) was found to boost the competency of rats in performing several tasks including passive avoidance test and Morris water maze. In AD transgenic mouse model, the use of CAE was reported to diminish the deposition of amyloid ß (Aß) in hippocampus and improved the behavioural deficits of mice. The bioactivities of CAE could be contributed by its bioactive triterpenes which include asiaticoside, asiatic acid, madecassoside and madecassic acid. Based on the central nervous system bioactivities, CA bioactive compounds are assumed to be able to cross the blood-brain barrier (BBB). Nevertheless, research on effects of CAE on the BBB function and BBB permeability of CAE is still lacking. Therefore, this study aimed to investigate the effects of CAE on primary brain endothelial cells (PBECs) which make up the BBB and its ability to cross the BBB. MTT assay was carried out to study the cytotoxicity effect of CAE towards the PBECs. The effect of CAE on PBEC tight junction function was determined by conducting real-time transendothelial electrical resistance (TEER). The permeability assay was conducted to determine the ability of CAE to cross the BBB. Results showed that CAE was not toxic towards the PBECs at all concentrations tested up to 100 µg/ml, and the BBB tight junction function is maintained in presence of the CAE. Our study reveals that CAE showed no adverse effects on the PBECs and showed promise to be developed further as a potential therapeutic agent for neurodegenerative disorders. Keywords: Blood-Brain Barrier, Permeability, Neuroprotection, neurodegeneration, natural product Conference: 14th Meeting of the Asian-Pacific Society for Neurochemistry, Kuala Lumpur, Malaysia, 27 Aug - 30 Aug, 2016. Presentation Type: Poster Presentation Session Topic: 14th Meeting of the Asian-Pacific Society for Neurochemistry Citation: Hanapi N, Yusof S, Adenan M and Tengku Muhammad T (2016). Blood-brain barrier permeability studies of Centella asiatica extract as potential neuroprotective agent. Conference Abstract: 14th Meeting of the Asian-Pacific Society for Neurochemistry. doi: 10.3389/conf.fncel.2016.36.00142 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 04 Aug 2016; Published Online: 11 Aug 2016. * Correspondence: Dr. Tengku Sifzizul Tengku Muhammad, Universiti Malaysia Terengganu, Institute of Marine Biotechnology, Kuala Terengganu, Terengganu, Malaysia, TengkuSifzizul.TengkuMuhammad@frontiersin.org Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Nur Aziah Hanapi Siti Rafidah Yusof Mohd Ilham Adenan Tengku Sifzizul Tengku Muhammad Google Nur Aziah Hanapi Siti Rafidah Yusof Mohd Ilham Adenan Tengku Sifzizul Tengku Muhammad Google Scholar Nur Aziah Hanapi Siti Rafidah Yusof Mohd Ilham Adenan Tengku Sifzizul Tengku Muhammad PubMed Nur Aziah Hanapi Siti Rafidah Yusof Mohd Ilham Adenan Tengku Sifzizul Tengku Muhammad Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Pathogen-inspired glycolipid probes reveal membrane heterogeneity and dynamics

Event Abstract Back to Event Pathogen-inspired glycolipid probes reveal membrane heterogeneity and dynamics Rachel Kraut1, 2*, Sarah Lehnert1, 3, Umit H. Yildiz3, Manoj Manna1, 4, Natalie Haustein1, Jagadish Sankaran1, 5, Artur Matysik6, Kamila Oglecka3, Bo Liedberg3 and Thorsten Wohland4 1 Nanyang Technological University, School of Biological Sciences, Singapore 2 TU Dresden, Biotec, Germany, Germany 3 Nanyang Technological University, School of Materials Science and Engineering, Singapore 4 National University of Singapore, Department of Chemistry, Centre for BioImaging Sciences, Singapore 5 National University of Singapore, Mechanobiology Institute, Singapore 6 Nanyang Technological University, Singapore Centre on Environmental Life Sciences Engineering, Singapore Many pathogens and bacterial toxins use glycosphingolipids to invade cells. We take advantage of this phenomenon to design toxin-derived peptides that interact with glycosphingolipid-containing domains at the plasma membrane. The peptide probes are able to trace the diffusion dynamics of domains in live cells, and their compositional heterogeneity in synthetic membrane systems such as supported lipid bilayers. We compared the diffusion dynamics of CtxB and the novel ganglioside-binding probes SBD from Alzheimer’s Aß, and TeNT46 from Tetanus in live cells using TIRF-Fluorescence Correlation Spectroscopy (FCS). All three probes displayed slow, bimodal diffusion typical for ordered domains, but their lipid preferences differed. FCS on cells and Imaging Surface Plasmon Resonance on hybrid bilayers showed that cholesterol and sphingomyelin affected binding and diffusion of SBD, TeNT46, and CtxB differently, and that toxin-bound domains are immobilized without the probe necessarily being bound by cholesterol. A new parameter, ΔCCF (difference in Cross-Correlation Function), showed that the probes' anisotropic diffusion coefficient distributions—i.e. heterogeneity—like the diffusion itself, was sensitive to sphingolipid and cytoskeletal disruption. However, ΔCCF detected heterogeneity to which conventional FCS is blind, revealing two distinguishable levels of membrane organization: short-range diffusion detectable by FCS, vs. longer-scale heterogeneity detectable by ΔCCF. This work may be of long-term interest for the design anti-pathogen decoys, for example using vesicular engineered lipid targets. Keywords: Glycosphingolipids, membrane dynamics, cell invasion, Membrane heterogeneity, pathogen-inspired glycolipid Conference: 14th Meeting of the Asian-Pacific Society for Neurochemistry, Kuala Lumpur, Malaysia, 27 Aug - 30 Aug, 2016. Presentation Type: Symposium 12: Glycolipids and the Regulation of Complex Networks in Neural Membranes Topic: 14th Meeting of the Asian-Pacific Society for Neurochemistry Citation: Kraut R, Lehnert S, Yildiz UH, Manna M, Haustein N, Sankaran J, Matysik A, Oglecka K, Liedberg B and Wohland T (2016). Pathogen-inspired glycolipid probes reveal membrane heterogeneity and dynamics. Conference Abstract: 14th Meeting of the Asian-Pacific Society for Neurochemistry. doi: 10.3389/conf.fncel.2016.36.00052 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 26 Jul 2016; Published Online: 11 Aug 2016. * Correspondence: Dr. Rachel Kraut, Nanyang Technological University, School of Biological Sciences, Singapore, Singapore, rachel.kraut@biotec.tu-dresden.de Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Rachel Kraut Sarah Lehnert Umit H Yildiz Manoj Manna Natalie Haustein Jagadish Sankaran Artur Matysik Kamila Oglecka Bo Liedberg Thorsten Wohland Google Rachel Kraut Sarah Lehnert Umit H Yildiz Manoj Manna Natalie Haustein Jagadish Sankaran Artur Matysik Kamila Oglecka Bo Liedberg Thorsten Wohland Google Scholar Rachel Kraut Sarah Lehnert Umit H Yildiz Manoj Manna Natalie Haustein Jagadish Sankaran Artur Matysik Kamila Oglecka Bo Liedberg Thorsten Wohland PubMed Rachel Kraut Sarah Lehnert Umit H Yildiz Manoj Manna Natalie Haustein Jagadish Sankaran Artur Matysik Kamila Oglecka Bo Liedberg Thorsten Wohland Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Alteration in dopaminergic neurotransmission following exposure to immobilization stress on the neurobehavioral toxicity of lambda-cyhalothrin in rats

Event Abstract Back to Event Alteration in dopaminergic neurotransmission following exposure to immobilization stress on the neurobehavioral toxicity of lambda-cyhalothrin in rats Rajendra K. Shukla1, 2*, Richa Gupta1, Lalit P. Chandravanshi1, Yogesh K. Dhuriya1, Pranay Srivastava1, Mohammad H. Siddiqui3, Ajay Kumar2, Aditya B. Pant1 and Vimay K. Khanna1 1 CSIR-Indian Institute of Toxicology Research, Developmental Toxicology Laboratory, System Toxicology and Health Risk Assessment Group , India 2 Integral University, Department of Biochemistry, Integral Institute of Medical Sciences & Research, India 3 Integral University, Department of Bioengineering, Faculty of Engineering, India Impact of stress in exacerbating the toxicity of environmental chemicals has been suggested whereas the effect and mechanism associated are not clearly understood. Therefore the present study has been carried out to investigate the influence of immobilization stress (IMS), a psychological stressor on the neurobehavioral toxicity of lambda-cyhalothrin (LCT), a new generation type-II synthetic pyrethroid with extensive applications in outdoor and indoor including public health programmes. Rats subjected to IMS (15 min/day) for 28 days or exposed to LCT (3.0 mg/kg body weight, p.o.) for 3 days (day 26, 27 and 28) had no significant effect on DA-D2 receptors, neurotransmitter levels of DA, DOPAC and HVA and immunoreactivity of tyrosine hydroxylase in corpus striatum, plasma corticosterone levels, blood-brain barrier permeability associated with motor activity as compared to controls. Marginal changes were observed in the activity of mitochondrial complexes, expression of selective anti-apoptotic (Bcl2) and pro-apoptotic (Bax, Caspase-3) proteins in the corpus striatum of rats exposed to either IMS or those exposed to LCT as compared to controls. Pre-exposure to IMS for 28 days followed by LCT exposure for 3 days in rats resulted in increased plasma corticosterone levels, blood-brain barrier permeability and decrease motor activity, DA-D2 receptors, expression of tyrosine hydroxylase and alteration in levels of DA, DOPAC and HVA in corpus striatum as compared to rats exposed to IMS or LCT alone. It was interesting to note that pre-exposure to IMS followed by LCT treatment also caused a marked decrease in mitochondrial dysfunctions associated with decreased the expression of anti-apoptotic while pro-apoptotic and stress marker proteins was enhanced in corpus striatum of these rats as compared to those exposed to IMS or LCT alone. The results exhibit that psychological stresses contribute in the LCT induced dopaminergic alterations associated with mitochondrial dysfunctions. Keywords: Dopamine, neurotransmission, Neurotoxicity, in vivo, Neurobehaviour Conference: 14th Meeting of the Asian-Pacific Society for Neurochemistry, Kuala Lumpur, Malaysia, 27 Aug - 30 Aug, 2016. Presentation Type: O03: Postgraduate Travel Awardees Oral Session 3 Topic: 14th Meeting of the Asian-Pacific Society for Neurochemistry Citation: Shukla RK, Gupta R, Chandravanshi LP, Dhuriya YK, Srivastava P, Siddiqui MH, Kumar A, Pant AB and Khanna VK (2016). Alteration in dopaminergic neurotransmission following exposure to immobilization stress on the neurobehavioral toxicity of lambda-cyhalothrin in rats. Conference Abstract: 14th Meeting of the Asian-Pacific Society for Neurochemistry. doi: 10.3389/conf.fncel.2016.36.00094 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 04 Aug 2016; Published Online: 11 Aug 2016. * Correspondence: Mr. Rajendra K Shukla, CSIR-Indian Institute of Toxicology Research, Developmental Toxicology Laboratory, System Toxicology and Health Risk Assessment Group, Lucknow, Uttar Pradesh, India, razshukla@gmail.com Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Rajendra K Shukla Richa Gupta Lalit P Chandravanshi Yogesh K Dhuriya Pranay Srivastava Mohammad H Siddiqui Ajay Kumar Aditya B Pant Vimay K Khanna Google Rajendra K Shukla Richa Gupta Lalit P Chandravanshi Yogesh K Dhuriya Pranay Srivastava Mohammad H Siddiqui Ajay Kumar Aditya B Pant Vimay K Khanna Google Scholar Rajendra K Shukla Richa Gupta Lalit P Chandravanshi Yogesh K Dhuriya Pranay Srivastava Mohammad H Siddiqui Ajay Kumar Aditya B Pant Vimay K Khanna PubMed Rajendra K Shukla Richa Gupta Lalit P Chandravanshi Yogesh K Dhuriya Pranay Srivastava Mohammad H Siddiqui Ajay Kumar Aditya B Pant Vimay K Khanna Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

6z, a novel 5HT3 receptor antagonist reverses depression-like behavior in streptozotocin-induced diabetic mice by normalizing serotonin deficiency and HPA-axis hyperactivity.

Event Abstract Back to Event 6z, a novel 5HT3 receptor antagonist reverses depression-like behavior in streptozotocin-induced diabetic mice by normalizing serotonin deficiency and HPA-axis hyperactivity. Deepali Gupta1* and Radhakrishnan Mahesh1 1 Birla Institute of Technology and Science, Department of Pharmacy, India Individuals with diabetes are three times more likely to have depression than without it. The impairment of brain serotonin activity and hypothalamic-pituitary-adrenal (HPA)-axis hyperactivity has been linked with the pathogenesis of depression in diabetes, while antagonism of 5HT3 receptors (5HT3Rs) has been shown to facilitate serotonin neurotransmission and normalize HPA-axis hyperactivity in animal models of depression. In addition, 5HT3Rs have been implicated in regulation of glucose homeostasis and energy metabolism. We earlier reported that 6z (N-(Benzo [d]thiazol-2-yl)-3-methoxyquinoxalin-2-carboxamide), a novel 5HT3R antagonist posses potential antidepressant activity in preclinical models of depression. In extension to that, the present study was aimed at investigating the antidepressant-like effects of 6z, in depression associated with diabetes. Mice with 8 weeks of streptozotocin (STZ)-induced diabetes were given vehicle/ 6z (1 and 2 mg/kg, i.p.)/ fluoxetine (10 mg/kg, i.p.) for 21 days and then subjected to neurobehavioral models including forced swim test (FST), tail suspension test (TST), hole board test (HBT) and light-dark test (LDT). 24 hrs after the last behavioral assay mice were decapitated, and blood and brains were collected for biochemical analysis. Results showed that STZ-induced diabetic mice exhibited a significant despair behavior (increased duration of immobility) in FST and TST, and reduced exploratory behavior indicated by reduced head dipping activity and exposure to bright chamber in HBT and LDT respectively. This was accompanied by reduced serotonin levels in discrete brain regions and elevated plasma corticosterone levels (a marker of HPA-axis hyperactivity). 6z (1 and 2 mg/kg), similar to fluoxetine reversed diabetes-induced behavioral and biochemical perturbations. It suggests that 6z was able to reverse diabetes-induced depression-like behavior mice and its antidepressant effect was associated with normalization of serotonin deficits and HPA-axis hyperactivity. Keywords: Depression, in vivo, diabetes, hypothalamic-pituitary-adrenal (HPA)-axis hyperactivity, neurobehavioural test Conference: 14th Meeting of the Asian-Pacific Society for Neurochemistry, Kuala Lumpur, Malaysia, 27 Aug - 30 Aug, 2016. Presentation Type: O02: Postgraduate Travel Awardees Oral Session 2 Topic: 14th Meeting of the Asian-Pacific Society for Neurochemistry Citation: Gupta D and Mahesh R (2016). 6z, a novel 5HT3 receptor antagonist reverses depression-like behavior in streptozotocin-induced diabetic mice by normalizing serotonin deficiency and HPA-axis hyperactivity.. Conference Abstract: 14th Meeting of the Asian-Pacific Society for Neurochemistry. doi: 10.3389/conf.fncel.2016.36.00086 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 04 Aug 2016; Published Online: 11 Aug 2016. * Correspondence: Ms. Deepali Gupta, Birla Institute of Technology and Science, Department of Pharmacy, Pilani, Rajasthan, India, deepaligupta2010@gmail.com Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Deepali Gupta Radhakrishnan Mahesh Google Deepali Gupta Radhakrishnan Mahesh Google Scholar Deepali Gupta Radhakrishnan Mahesh PubMed Deepali Gupta Radhakrishnan Mahesh Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Electrical stimulation rescues dopaminergic degeneration in dorsal raphe nucleus and enhanced hippocampal neurogenesis of vulnerable depressive rats

Event Abstract Back to Event Electrical stimulation rescues dopaminergic degeneration in dorsal raphe nucleus and enhanced hippocampal neurogenesis of vulnerable depressive rats Sharafuddin Khairuddin1*, Wei Ling Lim2, William Wai Lun Fung1, Yasin Temel3 and Lee Wei Lim1 1 The University of Hong Kong, School of Biomedical Sciences, Li Ka Shing Faculty of Medicine, Hong Kong (SAR) 2 Sunway University, School of Biological Sciences, Malaysia 3 Maastricht University, Departments of Neuroscience and Neurosurgery, Netherlands Electrical stimulation is a potential treatment for patients with depression. In this study, we investigate the effects of high-frequency stimulation (HFS) on various depressive-like behaviours using the stress resilience and vulnerable rat depression models. Our results demonstrated that animals with 3 weeks chronic unpredictable stress (CUS) induced exhibition of reduced sucrose consumption in 51% of animals, thus separating the resilience and vulnerable group of CUS-induced model. CUS vulnerable sham animals demonstrated anxiety-like behaviour, decreased motivation and increased immobility compared to that of the resilience group, implicating high susceptibility of vulnerable individuals to the CUS procedure. Interestingly, vmPFC HFS significantly reduced anxiety response, increased hedonia and motivation levels for food intake in the vulnerable group compared to the resilience group. HFS in ventromedial prefrontal cortex (vmPFC) and lateral habenula also showed reduced behavioural despair in both CUS vulnerable and resilience groups. In histochemistry, our results demonstrate that vmPFC HFS rescued the stress-induced dopamine neuron degeneration in the dorsal raphe nucleus, as well as increased hippocampal neurogenesis in stress vulnerable animals. In conclusion, these results suggest that vmPFC HFS effectively restores depressive-like behaviours by mechanisms of dorsal raphe dopaminergic neurons restoration and enhanced hippocampal neuroplasticity in the vulnerable CUS-induced model. Keywords: Dopamine, Hippocampus, Neurogenesis, dorsal raphe nucleus, in vivo Conference: 14th Meeting of the Asian-Pacific Society for Neurochemistry, Kuala Lumpur, Malaysia, 27 Aug - 30 Aug, 2016. Presentation Type: O01: Postgraduate Travel Awardees Oral Session 1 Topic: 14th Meeting of the Asian-Pacific Society for Neurochemistry Citation: Khairuddin S, Lim W, Fung W, Temel Y and Lim L (2016). Electrical stimulation rescues dopaminergic degeneration in dorsal raphe nucleus and enhanced hippocampal neurogenesis of vulnerable depressive rats. Conference Abstract: 14th Meeting of the Asian-Pacific Society for Neurochemistry. doi: 10.3389/conf.fncel.2016.36.00078 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 04 Aug 2016; Published Online: 11 Aug 2016. * Correspondence: Dr. Sharafuddin Khairuddin, The University of Hong Kong, School of Biomedical Sciences, Li Ka Shing Faculty of Medicine, Hong Kong, Hong Kong, Hong Kong (SAR), sharafkdin@gmail.com Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Sharafuddin Khairuddin Wei Ling Lim William Wai Lun Fung Yasin Temel Lee Wei Lim Google Sharafuddin Khairuddin Wei Ling Lim William Wai Lun Fung Yasin Temel Lee Wei Lim Google Scholar Sharafuddin Khairuddin Wei Ling Lim William Wai Lun Fung Yasin Temel Lee Wei Lim PubMed Sharafuddin Khairuddin Wei Ling Lim William Wai Lun Fung Yasin Temel Lee Wei Lim Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Role of reactive astrocytes and gliotransmitters in neurodegenerative diseases

Event Abstract Back to Event Role of reactive astrocytes and gliotransmitters in neurodegenerative diseases Changjoon J. Lee1* 1 Brain Science Institute, KIST, Center for Neuroscience and Functional Connectomics, Republic of Korea Brain is composed of not only neurons but also glia. It has been recently established that in addition to neurons, glial cells can release various transmitters (termed gliotransmitters), such as GABA, glutamate, and d-serine. The functional significance of these gliotransmitters is beginning to unravel as the detailed mechanisms of release have become available. We have recently demonstrated the role of GABA, synthesized via MAO-B and released through GABA-permeable Best1 channel from reactive astrocytes, in neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. During the course of these studies, we have developed various molecular tools, mouse and rat models, and neural probes to address specific questions in animal models of neurodegenerative diseases. These newly developed targets and tools will prove useful in developing novel therapeutics for various neurodegenerative diseases that currently have no cure for. Keywords: Astrocytes, Alzheimer, GABA, neurodegeneration, MAO-B Conference: 14th Meeting of the Asian-Pacific Society for Neurochemistry, Kuala Lumpur, Malaysia, 27 Aug - 30 Aug, 2016. Presentation Type: Plenary Lecture 4 Topic: 14th Meeting of the Asian-Pacific Society for Neurochemistry Citation: Lee CJ (2016). Role of reactive astrocytes and gliotransmitters in neurodegenerative diseases. Conference Abstract: 14th Meeting of the Asian-Pacific Society for Neurochemistry. doi: 10.3389/conf.fncel.2016.36.00004 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 26 Jul 2016; Published Online: 11 Aug 2016. * Correspondence: Prof. Changjoon J Lee, Brain Science Institute, KIST, Center for Neuroscience and Functional Connectomics, Seoul, Seoul, Republic of Korea, cjl@kist.re.kr Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Changjoon J Lee Google Changjoon J Lee Google Scholar Changjoon J Lee PubMed Changjoon J Lee Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Neuroprotective capability of dental pulp stem cells in an in vitro model of Parkinson's disease

Event Abstract Back to Event Neuroprotective capability of dental pulp stem cells in an in vitro model of Parkinson's disease Nareshwaran Gnanasegaran1, 2*, Vijayendran Govindasamy2 and Noor Hayaty Abu Kasim1 1 University of Malaya, Department of Restorative Dentistry, Faculty of Dentistry, , Malaysia 2 Hygieia Therapeutics Sdn. Bhd., cGMP-compliant Stem Cells Laboratory, Malaysia Dental pulp stem cells (DPSCs) have been popular since the past decade and extensive amount of work have been carried out to understand them. Their inherent propensity towards neuronal lineage coupled with the fact that they are of neural crest origin has allowed huge emphasis to be placed on DPSCs as a treatment modality for cell replacement therapy (CRT) especially in neurodegenerative diseases. However apart from differentiating into cell lineage of interest, the transplanted cells must also withstand the harsh conditions in that specific microenvironment upon transplantation. In this study, neuroprotective and immunomodulatory capacities of DPSCs were evaluated in an in vitro model of Parkinson’s disease (PD). By using IMR-32 and EOC2 cell lines, we first identified the optimum MPTP concentration to simulate ideal PD model. Following to this, both cell lines were co-cultured with DPSCs and assessed in terms of cell count, viability, DNA damage and levels of inflammatory cytokines. As expected, viability and cell count of both cell lines displayed decrements in dose-dependent manner. However when DPSCs were introduced, the attenuation of neurotoxicity, especially in DNA damage was significant as compared to control (p< 0.05). Additionally, inflammatory cytokines such as ILs, IFN-γ and TNFs were deferentially expressed with the introduction of DPSCs. To conclude, this study has demonstrated the neuroprotective and immunomodulatory properties of DPSCs and these findings are expected to increase our understanding in the application of DPSCs in CRT particularly in those related to neurological concerns. Keywords: Neuroprotection, stem cell, Parkinson’s disease, neurodegeneration, in vitro Conference: 14th Meeting of the Asian-Pacific Society for Neurochemistry, Kuala Lumpur, Malaysia, 27 Aug - 30 Aug, 2016. Presentation Type: O01: Postgraduate Travel Awardees Oral Session 1 Topic: 14th Meeting of the Asian-Pacific Society for Neurochemistry Citation: Gnanasegaran N, Govindasamy V and Abu Kasim N (2016). Neuroprotective capability of dental pulp stem cells in an in vitro model of Parkinson's disease. Conference Abstract: 14th Meeting of the Asian-Pacific Society for Neurochemistry. doi: 10.3389/conf.fncel.2016.36.00082 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 04 Aug 2016; Published Online: 11 Aug 2016. * Correspondence: Mr. Nareshwaran Gnanasegaran, University of Malaya, Department of Restorative Dentistry, Faculty of Dentistry,, Lembah Pantai, Kuala Lumpur, Malaysia, naresh_waran_28@hotmail.com Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Nareshwaran Gnanasegaran Vijayendran Govindasamy Noor Hayaty Abu Kasim Google Nareshwaran Gnanasegaran Vijayendran Govindasamy Noor Hayaty Abu Kasim Google Scholar Nareshwaran Gnanasegaran Vijayendran Govindasamy Noor Hayaty Abu Kasim PubMed Nareshwaran Gnanasegaran Vijayendran Govindasamy Noor Hayaty Abu Kasim Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

The role of oxidative stress in bipolar disorder: Is DNA damage a potential biomarker of disease severity?

The role of oxidative stress in bipolar disorder: Is DNA damage a potential biomarker of disease severity?

Revealing the deep complexity of the human transcriptome with targeted sequencing

Event Abstract Back to Event Revealing the deep complexity of the human transcriptome with targeted sequencing Timothy Mercer1*, I Deveson1 and M Brunck1 1 Garvan Institute of Medical Research, Genomics and Epigenetics Division, Australia The human genome encodes an unknown diversity of protein-coding and noncoding RNAs. This diversity and the wide range of gene expression limit the capacity of RNA sequencing to resolve the transcriptome and, as a result, current reference catalogs provide an incomplete profile of human gene content. Here, we target RNA sequencing to human chromosome 21 and syntenic regions of the mouse genome to provide a complete and unbiased cross-section that indicates the size, structure and composition of the mammalian transcriptome. We find that the majority of transcripts are noncoding RNAs that are not represented in current catalogs. These noncoding RNA populations have diverged between human and mouse, and orthologs are rare. Noncoding exons, in contrast to coding exons, are near-universally alternatively spliced to generate an inexhaustible diversity of isoforms. This noncoding isoform diversity is regulated by local cis-elements that are sufficient to recapitulate human alternative splicing profiles in a mouse cell. Our results indicate the full breadth, diversity and plasticity of information encoded in the mammalian genome and reveal distinctions in the organization, splicing and evolution of its coding and noncoding content. Keywords: Gene Expression, RNA, noncoding RNA, human transcriptome, targeted sequencing Conference: 14th Meeting of the Asian-Pacific Society for Neurochemistry, Kuala Lumpur, Malaysia, 27 Aug - 30 Aug, 2016. Presentation Type: Symposium 4: The Living Chemistry of RNA Topic: 14th Meeting of the Asian-Pacific Society for Neurochemistry Citation: Mercer T, Deveson I and Brunck M (2016). Revealing the deep complexity of the human transcriptome with targeted sequencing. Conference Abstract: 14th Meeting of the Asian-Pacific Society for Neurochemistry. doi: 10.3389/conf.fncel.2016.36.00019 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 26 Jul 2016; Published Online: 11 Aug 2016. * Correspondence: Dr. Timothy Mercer, Garvan Institute of Medical Research, Genomics and Epigenetics Division, Darlinghurst, Sydney, Australia, t.mercer@garvan.org.au Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Timothy Mercer I Deveson M Brunck Google Timothy Mercer I Deveson M Brunck Google Scholar Timothy Mercer I Deveson M Brunck PubMed Timothy Mercer I Deveson M Brunck Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

A novel curcumin derivative, f-methyl-curcumin-1 (fmec1), is a potential diagnostic and therapeutic agent for Alzheimer's disease.

Event Abstract Back to Event A novel curcumin derivative, f-methyl-curcumin-1 (fmec1), is a potential diagnostic and therapeutic agent for Alzheimer's disease. Ikuo Tooyama1*, Daijiro Yanagisawa1 and Nor Faeizah Ibrahim1 1 Shiga University of Medical Science, Molecular Neuroscience Research Center, Japan Curcumin has various beneficial pharmacological properties such as anti-tumor, anti-oxidative, and anti-inflammatory effects. Also, some recent reports of in vitro and in vivo experiments suggest favorable effects of curcumin in preventing or treating Alzheimer’s disease (AD) pathology. However, the first clinical trial of curcumin on patients with AD showed no effects. Therefore, more effective curcumin analogues may be needed. We recently developed a novel curcumin derivative, 1,7-Bis(4’-hydroxy-3’-trifluoromethoxyphenyl)-4-methoxycarbonylethyl-1,6-heptadiene-3,5-dione (FMeC1) as a fluorine-19 MRI probe to detect amyloid deposition. We present here the effects of our new compounds on Aβ aggregation in vitro and AD pathology in a mouse model of AD. APPswe/PS1dE9 double transgenic mice were fed with a standard lab chow diet with or without curcumin, FMeC1, or FMeC2 (500 ppm which is equivalent to ~1.25 mg/day or 83 mg/kg body weight) for 6 months from 9 months of age. FMeC1-treated mice showed a reduction in insoluble Aβ deposits and glial activation together with reduced cognitive deficits, compared to animals receiving a control diet or with curcumin or FMeC2 in their diet. Quartz crystal microbalance analysis showed that curcumin and FMeC1 bound not only to Aβ aggregates but also to Aβ oligomers, which are responsible for neuronal and synaptic dysfunction in AD. Both curcumin and FMeC1 modulated the formation of Aβ aggregates, but only FMeC1 significantly attenuated the cell toxicity of Aβ. Keywords: Curcumin, Oxidative Stress, Alzheimer, neurodegeneration, antioxidant Conference: 14th Meeting of the Asian-Pacific Society for Neurochemistry, Kuala Lumpur, Malaysia, 27 Aug - 30 Aug, 2016. Presentation Type: Symposium 7: New Insights on Oxidative Stress in Neurodegenerative Diseases and Therapeutic Potential of Anti- Oxidants as a Drug for the Pre-Emptive Medicine Topic: 14th Meeting of the Asian-Pacific Society for Neurochemistry Citation: Tooyama I, Yanagisawa D and Ibrahim N (2016). A novel curcumin derivative, f-methyl-curcumin-1 (fmec1), is a potential diagnostic and therapeutic agent for Alzheimer's disease.. Conference Abstract: 14th Meeting of the Asian-Pacific Society for Neurochemistry. doi: 10.3389/conf.fncel.2016.36.00031 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 26 Jul 2016; Published Online: 11 Aug 2016. * Correspondence: Prof. Ikuo Tooyama, Shiga University of Medical Science, Molecular Neuroscience Research Center, Otsu, Shiga, Japan, kinchan@belle.shiga-med.ac.jp Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Ikuo Tooyama Daijiro Yanagisawa Nor Faeizah Ibrahim Google Ikuo Tooyama Daijiro Yanagisawa Nor Faeizah Ibrahim Google Scholar Ikuo Tooyama Daijiro Yanagisawa Nor Faeizah Ibrahim PubMed Ikuo Tooyama Daijiro Yanagisawa Nor Faeizah Ibrahim Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Antipsychotic-like effect of Mitragyna speciosa in mice.

Event Abstract Back to Event Antipsychotic-like effect of Mitragyna speciosa in mice. Kamini Vijeepallam1*, Murali Naidu2 and Vijayapandi Pandy1 1 University of Malaya, Department of Pharmacology, Faculty of Medicine , Malaysia 2 University of Malaya, Department of Anatomy, Faculty of Medicine , Malaysia Aim: The present study aimed to investigate the antipsychotic-like effect of methanolic extract of Mitragyna speciosa leaves (MMS) on apomorphine-induced climbing behaviour in mice. Method: Experiments were performed using swiss albino male mice (bodyweight 25-30g). In acute study, MMS at different doses 50, 75, 100, 125, 250 and 500 mg/kg, were administered orally one hour prior to apomorphine (5mg/kg, i.p) injection respectively. Immediately after injection of apomorphine, the mice were placed into cylindrical individual cages (12 cm in diameter and 17 cm in height) with the floor and wall consisting of vertical metal bars and recorded for climbing time and climbing behaviour. The climbing behaviour was scored as 0 = four paws on the floor, 2 = two paws on the wall of the cage, 4 = four paws on the wall of the cage. Data were analysed by using Graph Pad Prism version 5.0 Result: The results revealed that the acute oral treatment of MMS (50, 75, 100, 125, 250 and 500 mg/kg) showed an inverted bell-shaped dose-response in apomorphine-induced cage climbing behaviour in mice. Conclusion: In conclusion, this investigation provides first evidence that MMS exhibits anti-psychotic like behaviour in mice. Further studies are underway in our laboratory to unravel the exact mechanism of action of MMS for its antipsychotic-like activity. Keywords: Apomorphine, antipsychotic, in vivo, behaviour, natural product Conference: 14th Meeting of the Asian-Pacific Society for Neurochemistry, Kuala Lumpur, Malaysia, 27 Aug - 30 Aug, 2016. Presentation Type: Poster Presentation Session Topic: 14th Meeting of the Asian-Pacific Society for Neurochemistry Citation: Vijeepallam K, Naidu M and Pandy V (2016). Antipsychotic-like effect of Mitragyna speciosa in mice.. Conference Abstract: 14th Meeting of the Asian-Pacific Society for Neurochemistry. doi: 10.3389/conf.fncel.2016.36.00205 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 04 Aug 2016; Published Online: 11 Aug 2016. * Correspondence: Dr. Kamini Vijeepallam, University of Malaya, Department of Pharmacology, Faculty of Medicine, Kuala Lumpur, Wilayah Persekutuan, Malaysia, kamini88@hotmail.com Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Kamini Vijeepallam Murali Naidu Vijayapandi Pandy Google Kamini Vijeepallam Murali Naidu Vijayapandi Pandy Google Scholar Kamini Vijeepallam Murali Naidu Vijayapandi Pandy PubMed Kamini Vijeepallam Murali Naidu Vijayapandi Pandy Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.