This title appears in the Scientific Report : 2011 
The neuronal transporter gene SLC6A15 confers risk to major depression.
Kohli, M.A.
Lucae, S. / Saemann, P.G. / Schmidt, M.V. / Demirkan, A. / Hek, K. / Czamara, D. / Alexander, M. / Salyakina, D. / Ripke, S. / Hoehn, D. / Specht, M. / Menke, A. / Hennings, J. / Heck, A. / Wolf, C. / Ising, M. / Schreiber, S. / Szisch, M. / Müller, M.B. / Uhr, M. / Bettecken, T. / Becker, A. / Schramm, J. / Rietschel, M. / Maier, W. / Bradley, B. / Ressler, K.J. / Noethen, M.M. / Cichon, S. / Craig, I.W. / Breen, G. / Lewis, C.M. / Hofman, A. / Tiemeier, H. / Van Duijn, C.M. / Holsboer, F. / Müller-Myhsok, B. / Binder, E.B.
Strukturelle und funktionelle Organisation des Gehirns; INM-1
Neuron, 70 (2011) S. 252 - 265
[Cambridge, Mass.] Cell Press 2011
252 - 265
10.1016/j.neuron.2011.04.005
21521612
Journal Article
Connectivity and Activity
Funktion und Dysfunktion des Nervensystems
Neuron 70
Adult
Amino Acid Transport Systems, Neutral: genetics
Analysis of Variance
Animals
Aspartic Acid: analogs & derivatives
Aspartic Acid: metabolism
Chromosomes, Human, Pair 12: genetics
Depressive Disorder, Major: epidemiology
Depressive Disorder, Major: genetics
Depressive Disorder, Major: pathology
Disease Models, Animal
Female
Gene Expression Regulation: physiology
Gene Frequency
Genetic Predisposition to Disease
Genome-Wide Association Study
Genotype
Germany
Great Britain
Hippocampus: metabolism
Hippocampus: pathology
Humans
Linkage Disequilibrium
Magnetic Resonance Imaging: methods
Magnetic Resonance Spectroscopy: methods
Male
Meta-Analysis as Topic
Mice
Middle Aged
Nerve Tissue Proteins: genetics
Polymorphism, Single Nucleotide: genetics
RNA, Messenger: metabolism
Risk Factors
Stress, Psychological: metabolism
Stress, Psychological: pathology
Tritium: diagnostic use
Amino Acid Transport Systems, Neutral
Nerve Tissue Proteins
RNA, Messenger
SLC6A15 protein, human
Tritium
Aspartic Acid
N-acetylaspartate
J
Please use the identifier: http://dx.doi.org/10.1016/j.neuron.2011.04.005 in citations.

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520 |a Major depression (MD) is one of the most prevalent psychiatric disorders and a leading cause of loss in work productivity. A combination of genetic and environmental risk factors probably contributes to MD. We present data from a genome-wide association study revealing a neuron-specific neutral amino acid transporter (SLC6A15) as a susceptibility gene for MD. Risk allele carrier status in humans and chronic stress in mice were associated with a downregulation of the expression of this gene in the hippocampus, a brain region implicated in the pathophysiology of MD. The same polymorphisms also showed associations with alterations in hippocampal volume and neuronal integrity. Thus, decreased SLC6A15 expression, due to genetic or environmental factors, might alter neuronal circuits related to the susceptibility for MD. Our convergent data from human genetics, expression studies, brain imaging, and animal models suggest a pathophysiological mechanism for MD that may be accessible to drug targeting. 
650 2 |2 MeSH  |a Adult 
650 2 |2 MeSH  |a Amino Acid Transport Systems, Neutral: genetics 
650 2 |2 MeSH  |a Analysis of Variance 
650 2 |2 MeSH  |a Animals 
650 2 |2 MeSH  |a Aspartic Acid: analogs & derivatives 
650 2 |2 MeSH  |a Aspartic Acid: metabolism 
650 2 |2 MeSH  |a Chromosomes, Human, Pair 12: genetics 
650 2 |2 MeSH  |a Depressive Disorder, Major: epidemiology 
650 2 |2 MeSH  |a Depressive Disorder, Major: genetics 
650 2 |2 MeSH  |a Depressive Disorder, Major: pathology 
650 2 |2 MeSH  |a Disease Models, Animal 
650 2 |2 MeSH  |a Female 
650 2 |2 MeSH  |a Gene Expression Regulation: physiology 
650 2 |2 MeSH  |a Gene Frequency 
650 2 |2 MeSH  |a Genetic Predisposition to Disease 
650 2 |2 MeSH  |a Genome-Wide Association Study 
650 2 |2 MeSH  |a Genotype 
650 2 |2 MeSH  |a Germany 
650 2 |2 MeSH  |a Great Britain 
650 2 |2 MeSH  |a Hippocampus: metabolism 
650 2 |2 MeSH  |a Hippocampus: pathology 
650 2 |2 MeSH  |a Humans 
650 2 |2 MeSH  |a Linkage Disequilibrium 
650 2 |2 MeSH  |a Magnetic Resonance Imaging: methods 
650 2 |2 MeSH  |a Magnetic Resonance Spectroscopy: methods 
650 2 |2 MeSH  |a Male 
650 2 |2 MeSH  |a Meta-Analysis as Topic 
650 2 |2 MeSH  |a Mice 
650 2 |2 MeSH  |a Middle Aged 
650 2 |2 MeSH  |a Nerve Tissue Proteins: genetics 
650 2 |2 MeSH  |a Polymorphism, Single Nucleotide: genetics 
650 2 |2 MeSH  |a RNA, Messenger: metabolism 
650 2 |2 MeSH  |a Risk Factors 
650 2 |2 MeSH  |a Stress, Psychological: metabolism 
650 2 |2 MeSH  |a Stress, Psychological: pathology 
650 2 |2 MeSH  |a Tritium: diagnostic use 
650 7 |0 0  |2 NLM Chemicals  |a Amino Acid Transport Systems, Neutral 
650 7 |0 0  |2 NLM Chemicals  |a Nerve Tissue Proteins 
650 7 |0 0  |2 NLM Chemicals  |a RNA, Messenger 
650 7 |0 0  |2 NLM Chemicals  |a SLC6A15 protein, human 
650 7 |0 10028-17-8  |2 NLM Chemicals  |a Tritium 
650 7 |0 56-84-8  |2 NLM Chemicals  |a Aspartic Acid 
650 7 |0 997-55-7  |2 NLM Chemicals  |a N-acetylaspartate 
650 7 |2 WoSType  |a J 
915 |0 StatID:(DE-HGF)0010  |a JCR/ISI refereed 
914 1 |y 2011 
500 |a This work has been funded by the Excellence Foundation for the Advancement of the Max Planck Society, the Bavarian Ministry of Commerce, and the Federal Ministry of Education and Research (BMBF) in the framework of the National Genome Research Network (NGFN2 and NGFN-Plus, FKZ 01GS0481 and 01GS08145 (Moods)). The Dutch studies are supported by the Netherlands Organization of Scientific Research (NWO Investments #175.010.2005.011, 911- 03-012), the Netherlands Genomics Initiative (NGI)/Netherlands Organization for Scientific Research (NWO project #050-060-810), the Hersenstichting, and the Centre for Medical Systems Biology (CMSB). The Atlanta cohort was sponsored by RO1 MH071537-01A1. The RADIANT study was supported by the UK MRC (G0701420). This study makes use of data generated by the Wellcome Trust Case-Control Consortium 2 (for author contributions see http://www.wtccc.org.uk). Funding for the project was provided by the Wellcome Trust under award 085475. This study was also supported by NeuroNova (a nonprofit Company for advancement of Genomics). The authors would like to thank G. Ernst-Jansen, G. Gajewsky, J. Huber, E. Kappelmann, S. Sauer, S. Damast, M. Koedel, M. Asmus, A. Sangl, and H. Pfister for their excellent technical support. We further are grateful to R. Hemauer, R. Borschke, and E. Schreiter for excellent MRI data aquisition. We acknowledge the work of Yurii S. Aulchenko, A. Cecile, J.W. Janssens, Maksim Struchalin, and Ben A. Oostra for the ERF study. E.B.B. currently receives grant support from NIMH, the Behrens-Weise Foundation, and PharmaNeuroBoost. F.H. is founder and shareholder of Affectis Pharmaceuticals and HolsboerMaschmeyer NeuroChemie GmbH. Over the past two years, B.M.-M. has been a consultant for Affectis. C.M.v.D. discloses her affiliation to the Centre for Medical Systems Biology (CMSB). Within the last 3 years, K.J.R. has received research funding support from NIMH, NIDA, Lundbeck, Burroughs Wellcome Foundation, and NARSAD, and he has an unrelated agreement with Extinction Pharmaceuticals for NMDA-based therapeutics. Patent applications: A.M., EBB., and F.H. are inventors of means and methods for diagnosing predisposition for treatment emergent suicidal ideation (TESI), international application number PCT/EP2009/061575. EBB., F.H., B.M.-M., and M.U. are inventors of (1) FKBP5, a novel target for antidepressant therapy, international publication number WO 2005/054500; and (2) polymorphisms in ABCB1 associated with a lack of clinical response to medicaments, international application number PCT/EP2005/005194. 
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