Adrenal secretion and major depression in 8- to 16-year-olds, II. Influence of co-morbidity at presentation

Herbert, J.; Goodyer, Ian; Altham, P. M. E.; Pearson, J; Secher, Sandra M.; Shiers, H. M.

doi:10.1017/s0033291700034656

Cited by 54 publications

(24 citation statements)

References 15 publications

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“…The present work stands as a first attempt to study early steroid abnormalities and their consequences on neural development in humans. This work is important to follow because of studies indicating a contribution of early steroid abnormalities to the development of mood and anxiety disorders (Goodyer, Herbert, Tamplin, & Altham, 2000a, 2000bHerbert et al, 1996). A third shortcoming is that despite the use of an age-and sex-matched control group, the healthy group does not permit to control for the effects of a chronic illness on brain development.…”

Section: Discussionmentioning

confidence: 99%

Emotional Memory in Early Steroid Abnormalities: An fMRI Study of Adolescents With Congenital Adrenal Hyperplasia

Mazzone

Mueller

Maheu

et al. 2011

Developmental Neuropsychology

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Hormonal imbalances during development may have long-lasting effects. Using functional magnetic resonance imaging (fMRI), we compared 14 youths with Congenital Adrenal Hyperplasia (CAH), a genetic disorder of hormonal dysfunction, with 22 healthy controls on memory encoding of emotional faces. Patients remembered fewer faces than controls, particularly fearful faces. FMRI data to successfully encoded fearful faces revealed that males with CAH showed significant activations in amygdala, hippocampus, and anterior cingulate relative to unaffected males, while females with CAH demonstrated deactivations relative to unaffected females in these regions. Findings indicate that steroid abnormalities during development can have important effects on neural correlates of emotional memory.A growing body of research documents the influence of steroid hormones, such as glucocorticoids and androgens, on development (Hertsgaard,

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Section: Discussionmentioning

confidence: 99%

Emotional Memory in Early Steroid Abnormalities: An fMRI Study of Adolescents With Congenital Adrenal Hyperplasia

Mazzone

Mueller

Maheu

et al. 2011

Developmental Neuropsychology

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“…DHEA(S) levels also are reduced by intercurrent stressful events such as an episode of major depressive disorder (2,3) or systemic disease (4,5). Recent evidence shows that DHEA and DHEAS have direct actions on the brain, acting as allosteric modulators of ␥-aminobutyric acid type A receptors (6), interacting with voltagegated Ca 2ϩ channels in CA1 hippocampal neurons (7), reducing aggression, and improving memory in mice (8,9).…”

mentioning

confidence: 99%

Dehydroepiandrosterone (DHEA) and DHEA-sulfate (DHEAS) protect hippocampal neurons against excitatory amino acid-induced neurotoxicity

Kimonides

Khatibi²,

Svendsen³

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

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411

237

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DHEA, together with DHEAS, is the most abundant steroid in the blood of young adult humans. Levels in humans decline with age and during certain types of illness or stress. We have found that DHEA(S) can prevent or reduce the neurotoxic actions in the hippocampus of the glutamate agonists N-methyl-D-aspartic acid (NMDA) both in vitro and in vivo or ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and kainic acid in vitro. Pre-treatment with DHEA (10-100 nM for 6-8 h) protected primary hippocampal cultures from embryonic day 18 (E18) embryos against NMDA-induced toxicity (0.1, 1, 10, and 50 mM). DHEA added either with NMDA (1 mM) or 1 h later had lesser, but still significant, protective actions. DHEAS also reduced NMDAinduced toxicity (1 mM), although the lowest effective dose of DHEAS (100 nM) was higher than that of DHEA (10 nM). DHEA (100 nM) protected cultured neurons against the neurotoxic actions of either AMPA (25 M) or kainic acid (1 mM) as well. In vivo, s.c. pellets of DHEA, which resulted in plasma levels that resembled those in young adult humans, protected hippocampal CA1͞2 neurons against unilateral infusions of 5 or 10 nmol of NMDA. Because the release of glutamate has been implicated in the neural damage after cerebral ischemia and other neural insults, these results suggest that decreased DHEA levels may contribute significantly to the increased vulnerability of the aging or stressed human brain to such damage. Levels of DHEA, together with DHEAS, peak at Ϸ20 years of age in humans and then decline ineluctably to reach values of 20-30% at Ϸ70-80 years of age (1). DHEA(S) levels also are reduced by intercurrent stressful events such as an episode of major depressive disorder (2, 3) or systemic disease (4, 5). Recent evidence shows that DHEA and DHEAS have direct actions on the brain, acting as allosteric modulators of ␥-aminobutyric acid type A receptors (6), interacting with voltagegated Ca 2ϩ channels in CA1 hippocampal neurons (7), reducing aggression, and improving memory in mice (8, 9). The functional and clinical significance of age-related or stressinduced declines in DHEA or DHEAS for neural function is not understood. Both age and stress are associated with neuronal vulnerability to degeneration (10). We have found that DHEA or DHEAS can prevent or reduce the neurotoxic actions of the glutamate agonist N-methyl-D-aspartic acid (NMDA) in the hippocampus both in vitro and in vivo, as well as that of two other glutamate receptor agonists, ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and kainic acid in vitro. Because the release of glutamate has been implicated in the neural damage after cerebral ischemia and other neural insults (11-13), these results suggest that decreased DHEA(S) levels may contribute significantly to the increased vulnerability of the aging or stressed human brain to such damage.

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“…Greater understanding of these effects may contribute to the development of more advanced treatment algorithms, and a fuller understanding of physiological factors involved in poor prognostic outcome. This is of particular importance because HPA axis abnormalities have been implicated in developmental models of mood disorders [116][117][118][119][120][121][122].…”

Section: Modulation Of Cognition By Cortisol: Is Hypothalamo-pituitarmentioning

confidence: 99%

Cognition in mania and depression: Psychological models and clinical implications

Chamberlain

Sahakian²

2004

Curr Psychiatry Rep

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Affective disorders, including bipolar disorder and major depressive disorder, are highly prevalent throughout the world and are extremely disabling. Diagnostic and Statistical Manual criteria and psychological models strongly implicate cognitive dysfunctions as being integral to our understanding of these disorders. We review the findings from studies that have used neurocognitive tests and functional imaging techniques to explore abnormal cognition in affective disorders. In particular, we highlight the evidence for cognitive dysfunctions that persist into full clinical remission, and the recent trend toward the use of "hot" processing tasks, involving emotionally charged stimuli, as a means of differentiating between the cognitive underpinnings of mania and depression. The clinical relevance of these developments is discussed.

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Adrenal secretion and major depression in 8- to 16-year-olds, II. Influence of co-morbidity at presentation

Cited by 54 publications

References 15 publications

Emotional Memory in Early Steroid Abnormalities: An fMRI Study of Adolescents With Congenital Adrenal Hyperplasia

Emotional Memory in Early Steroid Abnormalities: An fMRI Study of Adolescents With Congenital Adrenal Hyperplasia

Dehydroepiandrosterone (DHEA) and DHEA-sulfate (DHEAS) protect hippocampal neurons against excitatory amino acid-induced neurotoxicity

Cognition in mania and depression: Psychological models and clinical implications

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