HPA axis

Publication Title: 
Psychoneuroendocrinology

This mini-review refers to recent findings on psychobiological long-term consequences of childhood trauma and adverse living conditions. The continuum of trauma-provoked aftermath reaches from healthy adaptation with high resilience, to severe maladjustment with co-occurring psychiatric and physical pathologies in children, adolescents and adults. There is increasing evidence of a strong interconnectivity between genetic dispositions, epigenetic processes, stress-related hormonal systems and immune parameters in all forms of (mal)-adjustment to adverse living conditions.

Author(s): 
Ehlert, Ulrike
Publication Title: 
Biological Psychiatry

BACKGROUND: Enhanced glucocorticoid receptor (GR) sensitivity is present in people with posttraumatic stress disorder (PTSD), but the molecular mechanisms of GR sensitivity are not understood. Epigenetic factors have emerged as one potential mechanism that account for how trauma exposure leads to sustained PTSD symptoms given that PTSD develops in only a subset of trauma survivors.

Author(s): 
Yehuda, Rachel
Flory, Janine D.
Bierer, Linda M.
Henn-Haase, Clare
Lehrner, Amy
Desarnaud, Frank
Makotkine, Iouri
Daskalakis, Nikolaos P.
Marmar, Charles R.
Meaney, Michael J.
Publication Title: 
The World Journal of Biological Psychiatry: The Official Journal of the World Federation of Societies of Biological Psychiatry

OBJECTIVES: Transmission of parental post-traumatic stress disorder (PTSD) to offspring might be explained by transmission of epigenetic processes such as methylation status of the glucocorticoid receptor (GR) gene (NR3C1).

Author(s): 
Perroud, Nader
Rutembesa, Eugene
Paoloni-Giacobino, Ariane
Mutabaruka, Jean
Mutesa, LÈon
Stenz, Ludwig
Malafosse, Alain
Karege, FÈlicien
Publication Title: 
Neuroscience

Stress, a common if unpredictable life event, can have pronounced effects on physiology and behavior. Individuals show wide variation in stress susceptibility and resilience, which are only partially explained by variations in coding genes. Developmental programing of the hypothalamic-pituitary-adrenal stress axis provides part of the explanation for this variance. Epigenetic approaches have successfully helped fill the explanatory gaps between the influences of gene and environment on stress responsiveness, and differences in the sequelae of stress across individuals and generations.

Author(s): 
Griffiths, B. B.
Hunter, R. G.
Publication Title: 
American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics: The Official Publication of the International Society of Psychiatric Genetics

Stress is a major contributor to anxiety and mood disorders. The recent discovery of epigenetic changes in the brain resulting from stress has enhanced our understanding of the mechanism by which stress is able to promote these disorders. Although epigenetics encompasses chemical modifications that occur at both DNA and histones, much attention has been focused on stress-induced DNA methylation changes on behavior.

Author(s): 
Hing, Benjamin
Gardner, Caleb
Potash, James B.
Publication Title: 
The International Journal of Neuropsychopharmacology

BACKGROUND: Polymorphisms in the FK506 binding protein 5 (FKBP5) gene have been shown to influence glucocorticoid receptor sensitivity, stress response regulation, and depression risk in traumatized subjects, with most consistent findings reported for the functional variant rs1360780. In the present study, we investigated whether the FKBP5 polymorphism rs1360780 and lifetime history of major depression are associated with DNA methylation and FKBP5 gene expression after psychosocial stress.

Author(s): 
Hˆhne, Nina
Poidinger, Maximilian
Merz, Franziska
Pfister, Hildegard
Br¸ckl, Tanja
Zimmermann, Petra
Uhr, Manfred
Holsboer, Florian
Ising, Marcus
Publication Title: 
The Journal of Experimental Biology

Longitudinal epidemiological studies with birth cohorts have shown that physical aggression in humans does not appear suddenly in adolescence as commonly thought. In fact, physically aggressive behaviour is observed as early as 12 months after birth, its frequency peaks around 2-4 years of age and decreases in frequency until early adulthood. However, a minority of children (3-7%) maintain a high frequency of physical aggression from childhood to adolescence and develop serious social adjustment problems during adulthood.

Author(s): 
ProvenÁal, Nadine
Booij, Linda
Tremblay, Richard E.
Publication Title: 
Biological Psychiatry

Altered stress reactivity is a predominant feature of posttraumatic stress disorder (PTSD) and may reflect disease vulnerability, increasing the probability that an individual will develop PTSD following trauma exposure. Environmental factors, particularly prior stress history, contribute to the developmental programming of the hypothalamic-pituitary-adrenal stress axis. Critically, the consequences of stress experiences are transgenerational, with parental stress exposure impacting stress reactivity and PTSD risk in subsequent generations.

Author(s): 
Rodgers, Ali B.
Bale, Tracy L.
Publication Title: 
Stress (Amsterdam, Netherlands)

Clinical and pre-clinical studies have shown that early-life adversities, such as abuse or neglect, can increase the vulnerability to develop psychopathologies and cognitive decline later in life. Remarkably, the lasting consequences of stress during this sensitive period on the hypothalamic-pituitary-adrenal axis and emotional function closely resemble the long-term effects of early malnutrition and suggest a possible common pathway mediating these effects.

Author(s): 
Yam, Kit-Yi
Naninck, Eva F. G.
Schmidt, Mathias V.
Lucassen, Paul J.
Korosi, Aniko
Publication Title: 
Depression and Anxiety

BACKGROUND: Hypothalamic-pituitary-adrenal (HPA) axis functioning has been implicated in the development of stress-related psychiatric diagnoses and response to adverse life experiences. This study aimed to investigate the association between genetic and epigenetics in HPA axis and response to cognitive behavior therapy (CBT). METHODS: Children with anxiety disorders were recruited into the Genes for Treatment project (GxT, N = 1,152). Polymorphisms of FKBP5 and GR were analyzed for association with response to CBT.

Author(s): 
Roberts, Susanna
Keers, Robert
Lester, Kathryn J.
Coleman, Jonathan R. I.
Breen, Gerome
Arendt, Kristian
Blatter-Meunier, Judith
Cooper, Peter
Creswell, Cathy
Fjermestad, Krister
Havik, Odd E.
Herren, Chantal
Hogendoorn, Sanne M.
Hudson, Jennifer L.
Krause, Karen
Lyneham, Heidi J.
Morris, Talia
Nauta, Maaike
Rapee, Ronald M.
Rey, Yasmin
Schneider, Silvia
Schneider, Sophie C.
Silverman, Wendy K.
Thastum, Mikael
Thirlwall, Kerstin
Waite, Polly
Eley, Thalia C.
Wong, Chloe C. Y.
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