Neuropeptide precursor VGF is genetically associated with social anhedonia and underrepresented in the brain of major mental illness: Its downregulation by DISC1

Adriana Ramos; Carmen Rodríguez-Seoane; Isaac Rosa; Svenja V. Trossbach; Alfredo Ortega-Alonso; Liisa Tomppo; Jesper Ekelund; Juha Veijola; Marjo Riitta Järvelin; Jana Alonso; Sonia Veiga; Akira Sawa; William Hennah; Ángel García; Carsten Korth; Jesús R. Requena

doi:10.1093/hmg/ddu303

Neuropeptide precursor VGF is genetically associated with social anhedonia and underrepresented in the brain of major mental illness: Its downregulation by DISC1

Adriana Ramos, Carmen Rodríguez-Seoane, Isaac Rosa, Svenja V. Trossbach, Alfredo Ortega-Alonso, Liisa Tomppo, Jesper Ekelund, Juha Veijola, Marjo Riitta Järvelin, Jana Alonso, Sonia Veiga, Akira Sawa, William Hennah, Ángel García, Carsten Korth, Jesús R. Requena

School of Medicine

Research output: Contribution to journal › Article › peer-review

12 Scopus citations

Abstract

In a large Scottish pedigree, disruption of the gene coding for DISC1 clearly segregates with major depression, schizophrenia and related mental conditions. Thus, study of DISC1mayprovidea clue to understand the biology of major mental illness. A neuropeptide precursor VGF has potent antidepressant effects and has been reportedly associated with bipolar disorder. Here we show that DISC1 knockdown leads to a reduction of VGF, in neurons. VGF is also downregulated in the cortices from sporadic cases with major mental disease. A positive correlation of VGF single-nucleotide polymorphisms (SNPs) with social anhedonia was also observed. We now propose that VGF participates in a common pathophysiology of major mental disease.

Original language	English (US)
Pages (from-to)	5859-5865
Number of pages	7
Journal	Human molecular genetics
Volume	23
Issue number	22
DOIs	https://doi.org/10.1093/hmg/ddu303
State	Published - Nov 15 2014

ASJC Scopus subject areas

Molecular Biology
Genetics
Genetics(clinical)

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Ramos, A., Rodríguez-Seoane, C., Rosa, I., Trossbach, S. V., Ortega-Alonso, A., Tomppo, L., Ekelund, J., Veijola, J., Järvelin, M. R., Alonso, J., Veiga, S., Sawa, A., Hennah, W., García, Á., Korth, C., & Requena, J. R. (2014). Neuropeptide precursor VGF is genetically associated with social anhedonia and underrepresented in the brain of major mental illness: Its downregulation by DISC1. Human molecular genetics, 23(22), 5859-5865. https://doi.org/10.1093/hmg/ddu303

Ramos, A, Rodríguez-Seoane, C, Rosa, I, Trossbach, SV, Ortega-Alonso, A, Tomppo, L, Ekelund, J, Veijola, J, Järvelin, MR, Alonso, J, Veiga, S, Sawa, A, Hennah, W, García, Á, Korth, C & Requena, JR 2014, 'Neuropeptide precursor VGF is genetically associated with social anhedonia and underrepresented in the brain of major mental illness: Its downregulation by DISC1', Human molecular genetics, vol. 23, no. 22, pp. 5859-5865. https://doi.org/10.1093/hmg/ddu303

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title = "Neuropeptide precursor VGF is genetically associated with social anhedonia and underrepresented in the brain of major mental illness: Its downregulation by DISC1",

abstract = "In a large Scottish pedigree, disruption of the gene coding for DISC1 clearly segregates with major depression, schizophrenia and related mental conditions. Thus, study of DISC1mayprovidea clue to understand the biology of major mental illness. A neuropeptide precursor VGF has potent antidepressant effects and has been reportedly associated with bipolar disorder. Here we show that DISC1 knockdown leads to a reduction of VGF, in neurons. VGF is also downregulated in the cortices from sporadic cases with major mental disease. A positive correlation of VGF single-nucleotide polymorphisms (SNPs) with social anhedonia was also observed. We now propose that VGF participates in a common pathophysiology of major mental disease.",

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AU - Veijola, Juha

AU - Järvelin, Marjo Riitta

AU - Alonso, Jana

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Neuropeptide precursor VGF is genetically associated with social anhedonia and underrepresented in the brain of major mental illness: Its downregulation by DISC1

Abstract

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