期刊
NEURON
卷 70, 期 2, 页码 252-265出版社
CELL PRESS
DOI: 10.1016/j.neuron.2011.04.005
关键词
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资金
- Excellence Foundation for the Advancement of the Max Planck Society
- Bavarian Ministry of Commerce
- Federal Ministry of Education and Research (BMBF) [FKZ 01GS0481, 01GS08145]
- Netherlands Organization of Scientific Research (NWO) [175.010.2005.011, 911- 03-012]
- Netherlands Genomics Initiative (NGI)/Netherlands Organization for Scientific Research (NWO) [050-060-810]
- Hersenstichting
- Centre for Medical Systems Biology (CMSB)
- UK MRC [G0701420]
- Wellcome Trust [085475]
- NeuroNova
- NIMH
- Behrens-Weise Foundation
- PharmaNeuroBoost
- NIDA
- Lundbeck
- Burroughs Wellcome Foundation
- NARSAD
- [RO1 MH071537-01A1]
- Medical Research Council [G0701420, G0701003, G9817803B] Funding Source: researchfish
- MRC [G0701003, G0701420] Funding Source: UKRI
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 down-regulation 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.
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