Twenty-Four-Hour Beta-Endorphin Secretory Pattern in Alzheimer’s Disease

Rolandi, E; Franceschini, R.; Cataldi, A.; Garibaldi, A; Barreca, T

doi:10.1159/000118835

Cited by 12 publications

(5 citation statements)

References 15 publications

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“…Previous evidence regarding the differences in neuroendocrine function between AD and VD patients indicated contrasting results: while neuroendocrine regulation of growth hormone (GH) appeared more damaged in AD than in multi-infarct dementia patients (40), both AD and VD patients showed a similar behavior of plasma b-endorphin and cortisol circadian rhythms and similar abnormalities of dexamethasone suppression test (41,42).…”

Section: Discussionmentioning

confidence: 99%

Allopregnanolone and dehydroepiandrosterone response to corticotropin-releasing factor in patients suffering from Alzheimer's disease and vascular dementia

Bernardi

Lanzone

Cento

et al. 2000

European Journal of Endocrinology

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Objective: Neurosteroids have been suggested to be involved in the regulation of cognitive performances. A major neurosteroid gamma-aminobutyric acid (GABA) agonist is allopregnanolone: the main source of circulating allopregnanolone is the adrenal cortex. Studies indicated that a disturbance of the central regulation of the hypothalamic-pituitary-adrenocortical axis occurs in both senile (Alzheimer's disease: AD) and vascular dementia (VD). Design: The aim of the present study was to evaluate the levels of circulating allopregnanolone, dehydroepiandrosterone (DHEA) and cortisol and their response to corticotropin-releasing factor (CRF) test in AD and VD. Methods: Three groups of 12 subjects were included in the study: AD, VD and age-matched control subjects. CRF test was performed in all subjects and allopregnanolone, DHEA and cortisol levels were measured every 15 min for 2 h. Results: Mean Ϯ S.E.M. allopregnanolone and DHEA basal levels were significantly lower in AD and VD than in controls, while cortisol levels were significantly higher than in controls (P<0.01). Allopregnanolone and DHEA levels increase in response to CRF test in all subjects but the area under curve (AUC) in patients was significantly lower than in controls (P<0.01). Cortisol secretion appeared to be very sensitive in response to CRF stimulation: in fact, cortisol response to CRF test in AD and VD subjects was higher (both as AUC and as % max increase) than in controls (P<0.01). Conclusions:The present study firstly showed that allopregnanolone levels are reduced both in AD and in VD and that dementia has a preserved stimulated response of allopregnanolone to CRF. Overall, however, the total response of allopregnanolone to CRF remains reduced in respect to controls. Further studies are necessary for a better understanding of the role of neurosteroids in the regulation of cognitive function.

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Section: Discussionmentioning

confidence: 99%

Allopregnanolone and dehydroepiandrosterone response to corticotropin-releasing factor in patients suffering from Alzheimer's disease and vascular dementia

Bernardi

Lanzone

Cento

et al. 2000

European Journal of Endocrinology

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“…The recent observation [Scherder and Bouma, 2000] that AD patients complain more of acute than chronic pain reinforces the idea of a delay in pain report because of a loss of past points of reference. These changing states of memory probably involve much more than muscarinic cholinergic and NMDA systems, as different degrees of impairment in a variety of other neurotransmitter systems like benzodiazepine and serotoninergic [Cain et al, 2000] and endogenous opioid systems [Rolandi et al, 1992] have been observed in AD. Recent evidence has also shown that the central muscarinic and the NMDA systems interact in the hippocampus in the modulation of cognitive function [Li et al, 1997[Li et al, , 2001Daniel and Dohanich, 2001].…”

Section: Discussionmentioning

confidence: 99%

Memory Impairment Means Less Pain for Mice

Pickering¹,

Chapuy²,

Eschalier³

et al. 2004

Gerontology

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Background: Clinical observations have reported that individuals with memory deterioration, like in Alzheimer’s disease, display a lesser pain sensibility than patients with no cognitive impairment. Objective: To clarify the link between pain and loss of memory, we studied how memory-impaired mice behave when submitted to hotplate nociceptive tests. Methods: For 5 days (D1–D5), male CD1 mice were injected daily intraperitonealy with saline or scopolamine (s, an anticholinergic drug, 0.2 mg/kg) or ketamine (k, an N-methyl-D-aspartate receptor antagonist (NMDAr), 2.5 mg/kg), at doses leading to memory impairment with no analgesic effect. From D6 to D9, all received saline only. They were placed on the hotplate and removed at the first sign of discomfort, response time being recorded. Results: From D1 to D5, reaction time decreased significantly in controls only and did not change in mice with scopolamine or ketamine. From D6 to D9, response times decreased (p < 0.05 (s) and p < 0.0001 (k)) to reach the steady state of control animals. At D5, response time was significantly prolonged for scopolamine (p < 0.01) and ketamine (p < 0.05), compared to controls. Conclusion: These results show that pain sensibility needs the integrity of the central cholinergic and of the NMDA systems, and that mice with memory impairment display a lesser pain sensibility than normal mice. Further research on the complex interactions of receptors and neurotransmitters involved in pain and cognition could assist in gaining a better understanding of pain and analgesia in patients with memory impairment and in demented individuals.

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“…A link between the /3-endorphin secretory pattern and functional outcome cannot be established with certainty by our study because of the relatively small number of cases. However, if we consider that similar changes in the /3-endorphin secretory pattern occur in multi-infarct dementia, 23 the possibility that /3-endorphin secretion might potentially serve as a marker of motor, cognitive, and behavioral function after stroke may be proposed.…”

Section: Discussionmentioning

confidence: 99%

Twenty-four-hour beta-endorphin secretory pattern in stroke patients.

Franceschini

Gandolfo

Cataldi

et al. 1994

Stroke

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Background and Purpose Abnormalities of hypothalamopituitary-adrenocortical axis function have been observed frequently in stroke patients. The aim of this study was to investigate plasma /S-endorphin and cortisol 24-hour secretory patterns in patients early after stroke and in the convalescent period to evaluate a possible influence of brain damage on hormonal circadian pattern.Methods Patients (n=15; age, 46 to 75 years) were evaluated in the first 24 hours and 10 days after hospital admission for ischemic cerebral stroke and compared with 15 age-and sex-matched normal subjects. Blood samples for /3-endorphin and cortisol determination were drawn every 4 hours from 8 AM to 8 PM and every 2 hours from midnight to 6 AM.Results Mean 24-hour /J-endorphin and cortisol levels, recorded in the acute phase, were significantly (P<.05) higher

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Twenty-Four-Hour Beta-Endorphin Secretory Pattern in Alzheimer’s Disease

Cited by 12 publications

References 15 publications

Allopregnanolone and dehydroepiandrosterone response to corticotropin-releasing factor in patients suffering from Alzheimer's disease and vascular dementia

Allopregnanolone and dehydroepiandrosterone response to corticotropin-releasing factor in patients suffering from Alzheimer's disease and vascular dementia

Memory Impairment Means Less Pain for Mice

Twenty-four-hour beta-endorphin secretory pattern in stroke patients.

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