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The World Journal of Biological Psychiatry ISSN: 1562-2975 (Print) 1814-1412 (Online) Journal homepage: http://www.tandfonline.com/loi/iwbp20 Biological markers for anxiety disorders, OCD and PTSD: A consensus statement. Part II: Neurochemistry, neurophysiology and neurocognition Borwin Bandelow, David Baldwin, Marianna Abelli, Blanca Bolea-Alamanac, Michel Bourin, Samuel R. Chamberlain, Eduardo Cinosi, Simon Davies, Katharina Domschke, Naomi Fineberg, Edna Grünblatt, Marek Jarema, Yong-Ku Kim, Eduard Maron, Vasileios Masdrakis, Olya Mikova, David Nutt, Stefano Pallanti, Stefano Pini, Andreas Ströhle, Florence Thibaut, Matilde M. Vaghi, Eunsoo Won, Dirk Wedekind, Adam Wichniak, Jade Woolley, Peter Zwanzger & Peter Riederer To cite this article: Borwin Bandelow, David Baldwin, Marianna Abelli, Blanca Bolea-Alamanac, Michel Bourin, Samuel R. Chamberlain, Eduardo Cinosi, Simon Davies, Katharina Domschke, Naomi Fineberg, Edna Grünblatt, Marek Jarema, Yong-Ku Kim, Eduard Maron, Vasileios Masdrakis, Olya Mikova, David Nutt, Stefano Pallanti, Stefano Pini, Andreas Ströhle, Florence Thibaut, Matilde M. Vaghi, Eunsoo Won, Dirk Wedekind, Adam Wichniak, Jade Woolley, Peter Zwanzger & Peter Riederer (2016): Biological markers for anxiety disorders, OCD and PTSD: A consensus statement. Part II: Neurochemistry, neurophysiology and neurocognition, The World Journal of Biological Psychiatry, DOI: 10.1080/15622975.2016.1190867 To link to this article: http://dx.doi.org/10.1080/15622975.2016.1190867 Published online: 15 Jul 2016. Submit your article to this journal Article views: 10 View related articles View Crossmark data Citing articles: 1 View citing articles Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=iwbp20 Download by: [Georg-August-Universitaet Goettingen], [Borwin Bandelow] Date: 18 July 2016, At: 05:52 THE WORLD JOURNAL OF BIOLOGICAL PSYCHIATRY, 2016 http://dx.doi.org/10.1080/15622975.2016.1190867 WFSBP CONSENSUS PAPER Biological markers for anxiety disorders, OCD and PTSD: A consensus statement. Part II: Neurochemistry, neurophysiology and neurocognition Borwin Bandelowa , David Baldwinb, Marianna Abellic , Blanca Bolea-Alamanaci, Michel Bourine , Samuel R. Chamberlainf,g , Eduardo Cinosih , Simon Daviesd,i, Katharina Domschkej, Naomi Finebergf , Edna Grunblatt€ j,k,l,m , Marek Jareman , Yong-Ku Kimo , Eduard Maronp,q,t, Vasileios Masdrakisr , Olya Mikovas, David Nuttt , Stefano Pallantiu , Stefano Pinic , Andreas Strohle€ v, Florence Thibautw , Matilde M. Vaghix , Eunsoo Wono , Dirk Wedekinda, Adam Wichniakn, Jade Woolleyb, Peter Zwanzgery,z and Peter Riedererj aDepartment of Psychiatry and Psychotherapy, University of G€ottingen, Germany; bFaculty of Medicine, University of Southampton, Southampton, UK; cDepartment of Clinical and Experimental Medicine, Section of Psychiatry, University of Pisa, Pisa, Italy; dCentre for Addiction and Mental Health, Geriatric Psychiatry Division, University of Toronto, Toronto, Canada; eNeurobiology of Anxiety and Mood Disorders, University of Nantes, Nantes, France; fHertfordshire Partnership University NHS Foundation Trust and University of Hertfordshire, Parkway, UK; gDepartment of Psychiatry, University of Cambridge, Cambridge, UK; hDepartment of Neuroscience Imaging and Clinical Sciences, Gabriele D’Annunzio University, Chieti, Italy; iSchool of Social and Community Medicine, Academic Unit of Psychiatry, University of Bristol, Bristol, UK; jDepartment of Psychiatry Psychosomatics and Psychotherapy, University of Wuerzburg, Wuerzburg, Germany; kDepartment of Child and Adolescent Psychiatry and Psychotherapy, Psychiatric Hospital, University of Zurich, Zurich, Switzerland; lNeuroscience Center Zurich, University of Zurich and the ETH Zurich, Zurich, Switzerland; mZurich Center for Integrative Human Physiology, University of Zurich, Zurich, Switzerland; nThird Department of Psychiatry, Institute of Psychiatry and Neurology, Warszawa, Poland; oDepartment of Psychiatry College of Medicine, Korea University, Seoul, Republic of Korea; pDepartment of Psychiatry, North Estonia Medical Centre, Tallinn, Estonia; qDepartment of Psychiatry, University of Tartu, Estonia; rAthens University Medical School, First Department of Psychiatry, Eginition Hospital, Athens, Greece; sFoundation Biological Psychiatry, Sofia, Bulgaria; tFaculty of Medicine Department of Medicine, Centre for Neuropsychopharmacology, Division of Brain Sciences, Imperial College London, UK; uUC Davis Department of Psychiatry and Behavioural Sciences, Sacramento, CA, USA; vDepartment of Psychiatry and Psychotherapy, Campus Charite Mitte, Charite – University Medica Center Berlin, Berlin, Germany; wFaculty of Medicine Paris Descartes, University Hospital Cochin, Paris, France; xDepartment of Psychology and Behavioural and Clinical Neuroscience Institute, University of Cambridge, UK; ykbo-Inn-Salzach-Klinikum Wasserburg am Inn, Germany; zDepartment of Psychiatry and Psychotherapy, Ludwig- Maximilian-University Munich, Munich, Germany ABSTRACT ARTICLE HISTORY Objective: Biomarkers are defined as anatomical, biochemical or physiological traits that are spe- Received 2 May 2016 cific to certain disorders or syndromes. The objective of this paper is to summarise the current Accepted 3 May 2016 knowledge of biomarkers for anxiety disorders, obsessive-compulsive disorder (OCD) and post- traumatic stress disorder (PTSD). Methods: Findings in biomarker research were reviewed by a task force of international experts KEYWORDS Anxiety disorders; in the field, consisting of members of the World Federation of Societies for Biological Psychiatry neuroimaging; genetic; Task Force on Biological Markers and of the European College of Neuropsychopharmacology neurochemistry; Anxiety Disorders Research Network. neurobiology; review Results: The present article (Part II) summarises findings on potential biomarkers in neurochem- istry (neurotransmitters such as serotonin, norepinephrine, dopamine or GABA, neuropeptides such as cholecystokinin, neurokinins, atrial natriuretic peptide, or oxytocin, the HPA axis, neuro- trophic factors such as NGF and BDNF, immunology and CO2 hypersensitivity), neurophysiology (EEG, heart rate variability) and neurocognition. The accompanying paper (Part I) focuses on neu- roimaging and genetics. Conclusions: Although at present, none of the putative biomarkers is sufficient and specific as a Downloaded by [Georg-August-Universitaet Goettingen], [Borwin Bandelow] at 05:52 18 July 2016 diagnostic tool, an abundance of high quality research has accumulated that should improve our understanding of the neurobiological causes of anxiety disorders, OCD and PTSD. Abbreviations: 5-HIAA: 5-Hydroxyindoleacetic acid; 5-HT: Serotonin; 5-HTP: Hydroxytryptophan; 5- HTT: Serotonin transporter; 5-HTTLPR: Serotonin-transporter-linked polymorphic region; A-SepAD: Adult Separation Anxiety Disorder; ACC: Anterior cingulate cortex; ACTH: Adrenocorticotropic hor- mone or corticotropin; ADRN: Anxiety Disorders Research Network; ANP: Atrial natriuretic peptide; ASLO: Anti-streptolysin O; BDD: Body Dysmorphic Disorder; BDNF: Brain-derived neurotrophic fac- tor; C-SepAD: Childhood Separation Anxiety Disorder; CBT: Cognitive-behavioural therapy; CCK: Cholecystokinin; CNS: Central nervous system; COMT: Catechol-O-methyltransferase; CRH: CONTACT Prof. Dr. Borwin Bandelow [email protected] von-Siebold-Str. 5, Department of Psychiatry and Psychotherapy, University of G€ottingen D-37075 G€ottingen, Germany ß 2016 Informa UK Limited, trading as Taylor & Francis Group 2 B. BANDELOW ET AL. Corticotropin-releasing hormone; CRP: C-reactive protein; CSF: Cerebro-spinal fluid; DHEAS: Dehydroepiandrosterone sulphate; DAT: Dopamine transporter; DSM: Diagnostic and Statistical Manual of Mental Disorders; DST: Dexamethasone suppression test; ECNP: European College of Neuropsychopharmacology; EEG: Electroencephalography; ELISA: Enzyme-linked immunosorbent assay; ERN: Error-related negativity; ERP: Event-related potential; fMRI: Functional magnetic reson- ance imaging; GABA: c-Aminobutyric acid; GABHS: Group A beta haemolytic streptococci ; GAD: Generalized Anxiety Disorder; GWAS: Genome-wide association study; HF: High frequency (high frequency oscillation is a frequency-domain heart rate variability measure); HPA axis: Hypothalamic-pituitary-adrenal axis; HPLC: High-performance liquid chromatography; HRV: Heart rate variability; IL: Interleukin; LF: Low frequency (low frequency oscillation is a frequency-domain heart rate variability measure); MAO: Monoamine oxidase; MDD: Major Depressive Disorder; mPFC: Medial prefrontal cortex; mRNA: Messenger ribonucleic acid; NE: Norepinephrine (noradre- nalin); NET: Norepinephrine transporter; NGF: Nerve growth factor; NK: Neurokinin; OCD: Obsessive-Compulsive Disorder; OC-RD: Obsessive-Compulsive-Related Disorders; OFC: Orbitofrontal cortex; PANDAS: Pediatric autoimmune neuropsychiatric disorder associated with streptococcal infections; PANS: Pediatric acute-onset neuropsychiatric syndrome; PDA: Panic dis- order with or without Agoraphobia; PFC: Prefrontal cortex; POMC: Proopiomelanocortin; PSG: Polysomnography; PTSD: Posttraumatic Stress Disorder; RMSSD: Root mean square of successive differences; SAD: Social Anxiety Disorder; SDNN: Standard deviation of normal sinus intervals; SNRI: Serotonin norepinephrine reuptake inhibitor; SSRI: Selective serotonin reuptake inhibitor; SSRT: Stop signal reaction task; TNF: Tumor necrosis
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    Anatomical and functional evidence for trace amines as unique modulators of locomotor function in the mammalian spinal cord Elizabeth A. Gozal, Emory University Brannan E. O'Neill, Emory University Michael A. Sawchuk, Emory University Hong Zhu, Emory University Mallika Halder, Emory University Chou Ching-Chieh , Emory University Shawn Hochman, Emory University Journal Title: Frontiers in Neural Circuits Volume: Volume 8 Publisher: Frontiers | 2014-11-07, Pages 134-134 Type of Work: Article | Final Publisher PDF Publisher DOI: 10.3389/fncir.2014.00134 Permanent URL: https://pid.emory.edu/ark:/25593/mr95r Final published version: http://dx.doi.org/10.3389/fncir.2014.00134 Copyright information: © 2014 Gozal, O'Neill, Sawchuk, Zhu, Halder, Chou and Hochman. This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits distribution of derivative works, making multiple copies, distribution, public display, and publicly performance, provided the original work is properly cited. This license requires credit be given to copyright holder and/or author, copyright and license notices be kept intact. Accessed September 27, 2021 11:18 AM EDT ORIGINAL RESEARCH ARTICLE published: 07 November 2014 NEURAL CIRCUITS doi: 10.3389/fncir.2014.00134 Anatomical and functional evidence for trace amines as unique modulators of locomotor function in the mammalian spinal cord Elizabeth A. Gozal , Brannan E. O’Neill , Michael A. Sawchuk , Hong Zhu , Mallika Halder , Ching-Chieh Chou and Shawn Hochman* Physiology Department, Emory University, Atlanta, GA, USA Edited by: The trace amines (TAs), tryptamine, tyramine, and β-phenylethylamine, are synthesized Brian R.
  • Treatment for Disease Modification in Chronic Neurodegeneration

    Treatment for Disease Modification in Chronic Neurodegeneration

    cells Review Perspective: Treatment for Disease Modification in Chronic Neurodegeneration Thomas Müller 1,* , Bernhard Klaus Mueller 1 and Peter Riederer 2,3 1 Department of Neurology, St. Joseph Hospital Berlin-Weissensee, Gartenstr. 1, 13088 Berlin, Germany; [email protected] 2 Center of Mental Health, Department of Psychiatry, Psychosomatics and Psychotherapy, University Hospital Würzburg, Margarete-Höppel-Platz 1, 97080 Würzburg, Germany; [email protected] 3 Department of Psychiatry, Southern Denmark University Odense, J.B. Winslows Vey 18, 5000 Odense, Denmark * Correspondence: [email protected] Abstract: Symptomatic treatments are available for Parkinson’s disease and Alzheimer’s disease. An unmet need is cure or disease modification. This review discusses possible reasons for negative clinical study outcomes on disease modification following promising positive findings from experi- mental research. It scrutinizes current research paradigms for disease modification with antibodies against pathological protein enrichment, such as α-synuclein, amyloid or tau, based on post mortem findings. Instead a more uniform regenerative and reparative therapeutic approach for chronic neurodegenerative disease entities is proposed with stimulation of an endogenously existing repair system, which acts independent of specific disease mechanisms. The repulsive guidance molecule A pathway is involved in the regulation of peripheral and central neuronal restoration. Therapeutic antagonism of repulsive guidance molecule A reverses neurodegeneration according to experimental Citation: Müller, T.; Mueller, B.K.; outcomes in numerous disease models in rodents and monkeys. Antibodies against repulsive guid- Riederer, P. Perspective: Treatment for ance molecule A exist. First clinical studies in neurological conditions with an acute onset are under Disease Modification in Chronic Neurodegeneration. Cells 2021, 10, way.