Hormonal mediation of the memory disorder in depression

Reus, Victor I.

doi:10.1002/ddr.430040505

Cited by 35 publications

(11 citation statements)

References 71 publications

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“…There have been many reports about associations between memory performances and plasma glucocorticoid concentrations in Alzheimer's dementia, schizophrenia, and depression (Cohen et al, 1982;Reus, 1984;Hatzinger et al, 1995;Newcomer et al, 1998;Dong et al, 2004). Corticosterone, one of the glucocorticoids, is the most abundantly circulating hormone in the rat (Garcia-Bueno et al, 2007) and is produced by the stress-responsive hypothalamic-pituitary-adrenal axis (Newcomer et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

“…NCAMs, membrane-bound glycoproteins of the immunoglobulin superfamily of adhesion molecules, play critical roles in morphogenesis, behavioral plasticity, and regeneration of the nervous system as well as in cell-cell interactions (Cremer et al, 1997;Schachner, 1997;Kiss et al, 2001;Sandi, 2004;Tsoory et al, 2008). Some researchers have reported associations between memory performance and depression (Cohen et al, 1982;Reus, 1984). Accordingly, it was emphasized that some antidepressants may be therapeutically effective against stress, improving cognitive functions and decreasing corticosterone levels (Shah et al, 2003;Wesolowska et al, 2006;Wright et al, 2006).…”

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confidence: 96%

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BT‐11 improves stress‐induced memory impairments through increment of glucose utilization and total neural cell adhesion molecule levels in rat brains

Shin

Won²,

Heo

et al. 2008

J of Neuroscience Research

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In Oriental medicine, roots of Polygala tenuifolia Willdenow have been known to be an important herb that exhibits sedative effects in insomnia, palpitation with anxiety, restlessness, and disorientation in humans. We previously reported that BT-11, extracted from those roots, improved scopolamine-induced amnesia in rats and inhibited acetylcholinesterase activities in vitro. Therefore, we proposed that BT-11 could remedy stress-induced memory deficits in rats. In this study, the stress-induced memory impairments in rats were significantly reversed almost to the control level by BT-11 treatment. To seek an active component of BT-11 that plays an important role in antipsychotic effects, we compared BT-11 with 3,4,5-trimethoxycinnamic acid (TMCA), which is a constituent of those root extracts. However, the effects of TMCA were less or were not consistent with those of BT-11 in some of tests. In particular, BT-11 reversed the stress-induced reduction of glucose utilization by [(18)fluorodeoxyglucose]FDG-PET and the levels of neural cell adhesion molecule (NCAM) in rat brains to the control levels, whereas TMCA did not. Therefore, BT-11 improved stress-induced memory impairments through increment of glucose utilization and total NCAM levels in rat brains. In conclusion, BT-11 may be strongly effective against stress-induced amnesia in rats, through the combined effects of TMCA and other active components of BT-11.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 96%

BT‐11 improves stress‐induced memory impairments through increment of glucose utilization and total neural cell adhesion molecule levels in rat brains

Shin

Won²,

Heo

et al. 2008

J of Neuroscience Research

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“…Whilst it is possible that this disturbance arises quite simply as a result of lack of energy availability due to the drastically reduced food intake, it is also possible that the starvation-induced glucocorticoid alterations may play a role. There is evidence that glucocorticoids modulate central nervous system functions involved in stimulus perception and information processing (Carpenter and Gruen 1982;Reus 1984;Rubinow et al 1984;Wolkowitz et al 1990;Starkman et al 1992;Newcomer et al 1994;Lupien et al 1994;McEwan and Sapolsky 1995). Recent evidence suggests that these effects may be mediated, in part, through the hippocampus (Diamond et al 1989(Diamond et al , 1992(Diamond et al , 1994Pavlides et al 1993;McEwan and Sapolsky 1995).…”

Section: Introductionmentioning

confidence: 99%

Basal activity of the hypothalamic-pituitary-adrenal axis and cognitive function in anorexia nervosa

Seed

Dixon

McCluskey

et al. 2000

European Archives of Psychiatry and Clinical Neurosciences

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Anorexia nervosa is associated with abnormalities in neuroendocrine function including sustained hypercortisolism, which has been shown elsewhere to be associated with impairment of function in learning, memory and attention. Cognitive impairment has also been observed in anorexia nervosa. These effects may be mediated in part through cortisol effects on the hippocampus, which is dense with glucocorticoid receptors. We investigated the association between cortisol levels and cognitive function in anorexia nervosa by measuring both 24-hour urinary cortisol counts and performance on tasks of learning, memory and attention in patients suffering from the disorder. Cortisol secretion was shown to be significantly higher in the patient group than in a matched control group and patients were also shown to be impaired in memory and attention. However, no correlations were found between the cognitive deficits and cortisol measures. It is suggested that more sensitive profiling of cortisol levels throughout the circadian cycle may be useful in future studies of cognitive function in anorexia nervosa.

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“…HPA axis hyperactivity, usually measured by nonsuppression of plasma cortisol in the dexamethasone suppression test (DST), has been related to specific clinical features including anorexia, lethargy and sleep disturbance (Miller and Nelson, 1987). Some authors have also suggested a specific relationship with cognitive impairment (Reus, 1984;Oxenkrug and Gershon, 1986) and this work reviews the evidence in support of this hypothesis.…”

mentioning

confidence: 94%

The contribution of hypercortisolaemia to the cognitive decline of geriatric depression

Mitchell

1995

Int J Geriat Psychiatry

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SUMMARYCognitive impairment in depression is well recognized but poorly understood. A subset of depressed patients exhibit a syndrome of severe neuropsychological deficits which may be partially reversible upon episode resolution. This has been called depressive pseudodementia, the dementia syndrome of depression and depression induced cognitive impairment. The epidemiology, clinical features, natural history and prognosis of this condition support the notion of an underlying organic aetiology. The most plausible neurobiological candidate involved in the pathogenesis is hyperactivity of the hypothalamo-pituitary-adrenal (HPA) axis. The homeostatic regulation of the HPA axis becomes increasingly vulnerable to disruption in geriatric depression and perhaps particularly in depressive dementia. Hypercortisolaemia has been correlated with cognitive impairment in depression as well as in other related psychiatric conditions. The mechanism of this abnormality may involve hippocampal dysfunction. Further longitudinal studies are needed to clarify the role of the HPA axis in the cognitive decline of depressive illness.

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Hormonal mediation of the memory disorder in depression

Cited by 35 publications

References 71 publications

BT‐11 improves stress‐induced memory impairments through increment of glucose utilization and total neural cell adhesion molecule levels in rat brains

BT‐11 improves stress‐induced memory impairments through increment of glucose utilization and total neural cell adhesion molecule levels in rat brains

Basal activity of the hypothalamic-pituitary-adrenal axis and cognitive function in anorexia nervosa

The contribution of hypercortisolaemia to the cognitive decline of geriatric depression

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