Huntingtin gene repeat size variations affect risk of lifetime depression

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Huntingtin gene repeat size variations affect risk of lifetime depression. / Gardiner, Sarah L.; van Belzen, Martine J.; Boogaard, Merel W.; van Roon-Mom, Willeke M. C.; Rozing, Maarten P.; van Hemert, Albert M.; Smit, Johannes H.; Beekman, Aartjan T. F.; van Grootheest, Gerard; Schoevers, Robert A.; Voshaar, Richard C. Oude; Roos, Raymund A. C.; Comijs, Hannie C.; Penninx, Brenda W. J. H.; van der Mast, Roos C.; Aziz, N. Ahmad.

In: Translational Psychiatry, Vol. 7, 1277, 11.12.2017, p. 1-8.

Research output: Contribution to journalReviewResearchpeer-review

Harvard

Gardiner, SL, van Belzen, MJ, Boogaard, MW, van Roon-Mom, WMC, Rozing, MP, van Hemert, AM, Smit, JH, Beekman, ATF, van Grootheest, G, Schoevers, RA, Voshaar, RCO, Roos, RAC, Comijs, HC, Penninx, BWJH, van der Mast, RC & Aziz, NA 2017, 'Huntingtin gene repeat size variations affect risk of lifetime depression', Translational Psychiatry, vol. 7, 1277, pp. 1-8. https://doi.org/10.1038/s41398-017-0042-1

APA

Gardiner, S. L., van Belzen, M. J., Boogaard, M. W., van Roon-Mom, W. M. C., Rozing, M. P., van Hemert, A. M., ... Aziz, N. A. (2017). Huntingtin gene repeat size variations affect risk of lifetime depression. Translational Psychiatry, 7, 1-8. [1277]. https://doi.org/10.1038/s41398-017-0042-1

Vancouver

Gardiner SL, van Belzen MJ, Boogaard MW, van Roon-Mom WMC, Rozing MP, van Hemert AM et al. Huntingtin gene repeat size variations affect risk of lifetime depression. Translational Psychiatry. 2017 Dec 11;7:1-8. 1277. https://doi.org/10.1038/s41398-017-0042-1

Author

Gardiner, Sarah L. ; van Belzen, Martine J. ; Boogaard, Merel W. ; van Roon-Mom, Willeke M. C. ; Rozing, Maarten P. ; van Hemert, Albert M. ; Smit, Johannes H. ; Beekman, Aartjan T. F. ; van Grootheest, Gerard ; Schoevers, Robert A. ; Voshaar, Richard C. Oude ; Roos, Raymund A. C. ; Comijs, Hannie C. ; Penninx, Brenda W. J. H. ; van der Mast, Roos C. ; Aziz, N. Ahmad. / Huntingtin gene repeat size variations affect risk of lifetime depression. In: Translational Psychiatry. 2017 ; Vol. 7. pp. 1-8.

Bibtex

@article{1394ab1ae82542c1b4bbc3867b7a40e2,
title = "Huntingtin gene repeat size variations affect risk of lifetime depression",
abstract = "Huntington disease (HD) is a severe neuropsychiatric disorder caused by a cytosine-adenine-guanine (CAG) repeat expansion in the HTT gene. Although HD is frequently complicated by depression, it is still unknown to what extent common HTT CAG repeat size variations in the normal range could affect depression risk in the general population. Using binary logistic regression, we assessed the association between HTT CAG repeat size and depression risk in two well-characterized Dutch cohorts─the Netherlands Study of Depression and Anxiety and the Netherlands Study of Depression in Older Persons─including 2165 depressed and 1058 non-depressed persons. In both cohorts, separately as well as combined, there was a significant non-linear association between the risk of lifetime depression and HTT CAG repeat size in which both relatively short and relatively large alleles were associated with an increased risk of depression (β = −0.292 and β = 0.006 for the linear and the quadratic term, respectively; both P < 0.01 after adjustment for the effects of sex, age, and education level). The odds of lifetime depression were lowest in persons with a HTT CAG repeat size of 21 (odds ratio: 0.71, 95{\%} confidence interval: 0.52 to 0.98) compared to the average odds in the total cohort. In conclusion, lifetime depression risk was higher with both relatively short and relatively large HTT CAG repeat sizes in the normal range. Our study provides important proof-of-principle that repeat polymorphisms can act as hitherto unappreciated but complex genetic modifiers of depression.",
author = "Gardiner, {Sarah L.} and {van Belzen}, {Martine J.} and Boogaard, {Merel W.} and {van Roon-Mom}, {Willeke M. C.} and Rozing, {Maarten P.} and {van Hemert}, {Albert M.} and Smit, {Johannes H.} and Beekman, {Aartjan T. F.} and {van Grootheest}, Gerard and Schoevers, {Robert A.} and Voshaar, {Richard C. Oude} and Roos, {Raymund A. C.} and Comijs, {Hannie C.} and Penninx, {Brenda W. J. H.} and {van der Mast}, {Roos C.} and Aziz, {N. Ahmad}",
year = "2017",
month = "12",
day = "11",
doi = "10.1038/s41398-017-0042-1",
language = "English",
volume = "7",
pages = "1--8",
journal = "Translational Psychiatry",
issn = "2158-3188",
publisher = "nature publishing group",

}

RIS

TY - JOUR

T1 - Huntingtin gene repeat size variations affect risk of lifetime depression

AU - Gardiner, Sarah L.

AU - van Belzen, Martine J.

AU - Boogaard, Merel W.

AU - van Roon-Mom, Willeke M. C.

AU - Rozing, Maarten P.

AU - van Hemert, Albert M.

AU - Smit, Johannes H.

AU - Beekman, Aartjan T. F.

AU - van Grootheest, Gerard

AU - Schoevers, Robert A.

AU - Voshaar, Richard C. Oude

AU - Roos, Raymund A. C.

AU - Comijs, Hannie C.

AU - Penninx, Brenda W. J. H.

AU - van der Mast, Roos C.

AU - Aziz, N. Ahmad

PY - 2017/12/11

Y1 - 2017/12/11

N2 - Huntington disease (HD) is a severe neuropsychiatric disorder caused by a cytosine-adenine-guanine (CAG) repeat expansion in the HTT gene. Although HD is frequently complicated by depression, it is still unknown to what extent common HTT CAG repeat size variations in the normal range could affect depression risk in the general population. Using binary logistic regression, we assessed the association between HTT CAG repeat size and depression risk in two well-characterized Dutch cohorts─the Netherlands Study of Depression and Anxiety and the Netherlands Study of Depression in Older Persons─including 2165 depressed and 1058 non-depressed persons. In both cohorts, separately as well as combined, there was a significant non-linear association between the risk of lifetime depression and HTT CAG repeat size in which both relatively short and relatively large alleles were associated with an increased risk of depression (β = −0.292 and β = 0.006 for the linear and the quadratic term, respectively; both P < 0.01 after adjustment for the effects of sex, age, and education level). The odds of lifetime depression were lowest in persons with a HTT CAG repeat size of 21 (odds ratio: 0.71, 95% confidence interval: 0.52 to 0.98) compared to the average odds in the total cohort. In conclusion, lifetime depression risk was higher with both relatively short and relatively large HTT CAG repeat sizes in the normal range. Our study provides important proof-of-principle that repeat polymorphisms can act as hitherto unappreciated but complex genetic modifiers of depression.

AB - Huntington disease (HD) is a severe neuropsychiatric disorder caused by a cytosine-adenine-guanine (CAG) repeat expansion in the HTT gene. Although HD is frequently complicated by depression, it is still unknown to what extent common HTT CAG repeat size variations in the normal range could affect depression risk in the general population. Using binary logistic regression, we assessed the association between HTT CAG repeat size and depression risk in two well-characterized Dutch cohorts─the Netherlands Study of Depression and Anxiety and the Netherlands Study of Depression in Older Persons─including 2165 depressed and 1058 non-depressed persons. In both cohorts, separately as well as combined, there was a significant non-linear association between the risk of lifetime depression and HTT CAG repeat size in which both relatively short and relatively large alleles were associated with an increased risk of depression (β = −0.292 and β = 0.006 for the linear and the quadratic term, respectively; both P < 0.01 after adjustment for the effects of sex, age, and education level). The odds of lifetime depression were lowest in persons with a HTT CAG repeat size of 21 (odds ratio: 0.71, 95% confidence interval: 0.52 to 0.98) compared to the average odds in the total cohort. In conclusion, lifetime depression risk was higher with both relatively short and relatively large HTT CAG repeat sizes in the normal range. Our study provides important proof-of-principle that repeat polymorphisms can act as hitherto unappreciated but complex genetic modifiers of depression.

U2 - 10.1038/s41398-017-0042-1

DO - 10.1038/s41398-017-0042-1

M3 - Review

C2 - 29225330

VL - 7

SP - 1

EP - 8

JO - Translational Psychiatry

JF - Translational Psychiatry

SN - 2158-3188

M1 - 1277

ER -

ID: 188414234