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Author Notes:

Mary L. Woody, M.S., Department of Psychology, Binghamton University (SUNY), Binghamton, NY 13902-6000. mwoody1@binghamton.edu and phone calls may be directed to (607) 777-3304.

We would like to thank Ashley Johnson; Lindsey Stone; Andrea Hanley; Katie Burkhouse; Sydney Meadows; Michael Van Wie; and Devra Alper for their help in conducting assessments for this project; and Kayla Beaucage for her help with genotyping.

Subjects:

Research Funding:

This project was supported by National Institute of Child Health and Human Development grant HD057066; and National Institute of Mental Health grant awarded to B. E. Gibb; 1S10RR023457-01A1; and Shared equipment grants (ShEEP) from the Medical Research Service of the Department of Veteran Affairs to J. E. McGeary.

Keywords:

  • Brooding rumination
  • CRHR1
  • Cognitive vulnerability
  • Endophenotype
  • Intergenerational transmission of depression
  • Major depressive disorder
  • Adolescent
  • Adult
  • Case-Control Studies
  • Child
  • Child of Impaired Parents
  • Depression
  • Depressive Disorder, Major
  • Female
  • Haplotypes
  • Humans
  • Inheritance Patterns
  • Male
  • Mothers
  • Receptors, Corticotropin-Releasing Hormone

Influence of maternal depression on children’s brooding rumination: Moderation by CRHR1 TAT haplotype

Tools:

Journal Title:

Cognition and Emotion

Volume:

Volume 30, Number 2

Publisher:

, Pages 302-314

Type of Work:

Article | Post-print: After Peer Review

Abstract:

There is growing evidence that brooding rumination plays a key role in the intergenerational transmission of major depressive disorder (MDD) and may be an endophenotype for depression risk. However, less is known about the mechanisms underlying this role. Therefore, the goal of the current study was to examine levels of brooding in children of mothers with a history of MDD (n = 129) compared to children of never depressed mothers (n = 126) and to determine whether the variation in a gene known to influence hypothalamic-pituitary-adrenal axis functioning—corticotropin-releasing hormone receptor 1 (CRHR1) —would moderate the link between maternal MDD and children's levels of brooding. We predicted children of mothers with a history of MDD would exhibit higher levels of brooding than children of mothers with no lifetime depression history but that this link would be stronger among children carrying no copies of the protective CRHR1 TAT haplotype. Our results supported these hypotheses and suggest that the development of brooding among children of depressed mothers, particularly children without the protective CRHR1 haplotype, may serve as an important mechanism of risk for the intergenerational transmission of depression.

Copyright information:

© 2015 Taylor & Francis.

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