Alzheimer's disease is often characterized by an increase of plasma cortisol without clinical evidence of hypercorticism. The objective of our study was to evaluate whether the measurement of several hormonal parameters could better characterize the patients with Alzheimer's disease. 25 consecutive inpatients with Alzheimer's disease, and 35 subjects comparable for age and sex were studied. The diagnosis was done according to the criteria DSM IV and by neuropsychological tests, EEG, CT-scan and MR-imaging; in most cases also SPECT was performed. The following hormonal parameters were done: plasma cortisol, dehydroepiandrosterone sulphate (DHEAS), the cortisol/ DHEAS ratio and the number of Type I and Type I I corticosteroid receptors in mooonuclear leukocytes. Steroids were measured by enzyme immunoassay and corticosteroid receptors by radioreceptor assay after separation of mononuclear leukocytes by Percoll gradient. Results: in patients with Alzheimer's disease plasma cortisol was higher than in controls (28.4 + 7.9 vs 17.6 + 4.4 ug/dl, p < 0.001). Plasma DHEAS, the ration cortisol/DHEAS and the number of Type I receptors in mononuclear leukocytes were indeed significan@ lower than in controls (respectively 59.4 + 42.4 vs 143.3 + 84.9 ug/dl; 2.2 + 1.6 vs 9.0 + 5.7 and 1434 + 514 vs 2025 + 578 receptors per cell). Ah inverse significant correlation between DHEAS/cortisol ratio and age and between Type II receptors and age was evident only in heahhy controls and not in Alzheimer's disease. These data support the hypothesis of a disregulation of the adrenal pituitaric axis in Alzheimer's disease. The correlation between DHEAS/cortisol and age and Type II receptors and age in controls is consistent with a progression of the physiological aging process, which lacks in Alzheimer's disease. The abnormality of these hormonal at the level of target tissues and the follow up of these parameters could be useful to distinguish physiological and pathological aging process.

Endocrine parameters in Alzheimer disease: their implication in early diagnosis

ARMANINI, DECIO
2001

Abstract

Alzheimer's disease is often characterized by an increase of plasma cortisol without clinical evidence of hypercorticism. The objective of our study was to evaluate whether the measurement of several hormonal parameters could better characterize the patients with Alzheimer's disease. 25 consecutive inpatients with Alzheimer's disease, and 35 subjects comparable for age and sex were studied. The diagnosis was done according to the criteria DSM IV and by neuropsychological tests, EEG, CT-scan and MR-imaging; in most cases also SPECT was performed. The following hormonal parameters were done: plasma cortisol, dehydroepiandrosterone sulphate (DHEAS), the cortisol/ DHEAS ratio and the number of Type I and Type I I corticosteroid receptors in mooonuclear leukocytes. Steroids were measured by enzyme immunoassay and corticosteroid receptors by radioreceptor assay after separation of mononuclear leukocytes by Percoll gradient. Results: in patients with Alzheimer's disease plasma cortisol was higher than in controls (28.4 + 7.9 vs 17.6 + 4.4 ug/dl, p < 0.001). Plasma DHEAS, the ration cortisol/DHEAS and the number of Type I receptors in mononuclear leukocytes were indeed significan@ lower than in controls (respectively 59.4 + 42.4 vs 143.3 + 84.9 ug/dl; 2.2 + 1.6 vs 9.0 + 5.7 and 1434 + 514 vs 2025 + 578 receptors per cell). Ah inverse significant correlation between DHEAS/cortisol ratio and age and between Type II receptors and age was evident only in heahhy controls and not in Alzheimer's disease. These data support the hypothesis of a disregulation of the adrenal pituitaric axis in Alzheimer's disease. The correlation between DHEAS/cortisol and age and Type II receptors and age in controls is consistent with a progression of the physiological aging process, which lacks in Alzheimer's disease. The abnormality of these hormonal at the level of target tissues and the follow up of these parameters could be useful to distinguish physiological and pathological aging process.
2001
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11577/1365262
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