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Depression: HELP
Articles by Martine J. van Belzen
Based on 2 articles published since 2008
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Between 2008 and 2019, M. J. van Belzen wrote the following 2 articles about Depression.
 
+ Citations + Abstracts
1 Review Huntingtin gene repeat size variations affect risk of lifetime depression. 2017

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 / Oude Voshaar, Richard C / Roos, Raymund A C / Comijs, Hannie C / Penninx, Brenda W J H / van der Mast, Roos C / Aziz, N Ahmad. ·Departments of Neurology, Leiden University Medical Centre, Leiden, The Netherlands. · Departments of Human Genetics, Leiden University Medical Centre, Leiden, The Netherlands. · Departments of Clinical Genetics, and Leiden University Medical Centre, Leiden, The Netherlands. · Department of Public Health, Section of Social Medicine, University of Copenhagen, Copenhagen, Denmark. · Departments of Psychiatry, Leiden University Medical Centre, Leiden, The Netherlands. · Department of Psychiatry, and EMGO Institute for Health and Care Research and Neuroscience Campus Amsterdam, VU University Medical Center/GGZ inGeest, Amsterdam, The Netherlands. · Department of Psychiatry, University Medical Centre Groningen, Groningen, The Netherlands. · Department of Psychiatry, Collaborative Antwerp Psychiatric Research Institute (CAPRI), University of Antwerp, Antwerp, Belgium. · Departments of Neurology, Leiden University Medical Centre, Leiden, The Netherlands. N.A.Aziz@lumc.nl. · Department of Neurodegenerative Disease, UCL Huntington's Disease Centre, University College London Institute of Neurology, London, United Kingdom. N.A.Aziz@lumc.nl. ·Transl Psychiatry · Pubmed #29225330.

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.

2 Article Large normal-range TBP and ATXN7 CAG repeat lengths are associated with increased lifetime risk of depression. 2017

Gardiner, S L / van Belzen, M J / Boogaard, M W / van Roon-Mom, W M C / Rozing, M P / van Hemert, A M / Smit, J H / Beekman, A T F / van Grootheest, G / Schoevers, R A / Oude Voshaar, R C / Comijs, H C / Penninx, B W J H / van der Mast, R C / Roos, R A C / Aziz, N A. ·Department of Neurology, Leiden University Medical Centre, Leiden, The Netherlands. · Department of Human Genetics, Leiden University Medical Centre, Leiden, The Netherlands. · Department of Clinical Genetics, Leiden University Medical Centre, Leiden, The Netherlands. · Centre for Healthy Ageing/Department of Public Health, Section of Social Medicine, University of Copenhagen, Copenhagen, Denmark. · Department of Psychiatry, Leiden University Medical Centre, Leiden, The Netherlands. · Department of Psychiatry, Amsterdam Public Health Research Institute and Neuroscience Campus Amsterdam, VU University Medical Centre/GGZ inGeest, Amsterdam, The Netherlands. · Department of Psychiatry, University of Groningen, University Medical Centre Groningen, Research School Cognitive Behavioural Neuroscience, Groningen, The Netherlands. · Department of Psychiatry, Collaborative Antwerp Psychiatric Research Institute (CAPRI), University of Antwerp, Antwerp, Belgium. ·Transl Psychiatry · Pubmed #28585930.

ABSTRACT: Depression is one of the most prevalent and debilitating psychiatric disorders worldwide. Recently, we showed that both relatively short and relatively long cytosine-adenine-guanine (CAG) repeats in the huntingtin gene (HTT) are associated with an increased risk of lifetime depression. However, to what extent the variations in CAG repeat length in the other eight polyglutamine disease-associated genes (PDAGs) are associated with depression is still unknown. We determined the CAG repeat sizes of ATXN1, ATXN2, ATXN3, CACNA1A, ATXN7, TBP, ATN1 and AR 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 individuals-aged 18-93 years. The association between PDAG CAG repeat size and the risk for depression was assessed via binary logistic regression. We found that the odds ratio (OR) for lifetime depression was significantly higher for individuals with >10, compared with subjects with ≤10, CAG repeats in both ATXN7 alleles (OR=1.90, confidence interval (CI) 1.26-2.85). For TBP we found a similar association: A CAG repeat length exceeding the median in both alleles was associated with an increased risk for lifetime depression (OR=1.33, CI 1.00-1.76). In conclusion, we observed that carriers of either ATXN7 or TBP alleles with relatively large CAG repeat sizes in both alleles had a substantially increased risk of lifetime depression. Our findings provide critical evidence for the notion that repeat polymorphisms can act as complex genetic modifiers of depression.