TY - JOUR
T1 - Loss of the cortisol response to naltrexone in Alzheimer's disease
AU - Pomara, Nunzio
AU - Stanley, Michael
AU - Rhiew, H. Benjamin
AU - Bagne, Curtis A.
AU - Deptula, Dennis
AU - Galloway, Matthew P.
AU - Tanimoto, Kenji
AU - Verebey, Karl
AU - Tamminga, Carol A.
PY - 1988/4/1
Y1 - 1988/4/1
N2 - The administration of a single dose of the opiate antagonist naltrexone (NT) was accompanied by significant elevations in plasma cortisol in normal elderly subjects: in contrast, the cortisol response to NT was absent in individuals of comparable age with Alzheimer' s disease (AD). The differential effect of AD on the cortisol response was not accompanied by a significant group difference in plasma prolactin in response to NT administration. Furthermore, this differential cortisol response to NT was not associated with any evident differences in age, sex ratio, plasma levels of naltrexone or its major metabolite β-naltrexol, or with differences in measures of nonspecific stress, such as plasma free MHPG, pulse, or blood pressure, between the two groups. The absence of the well-characterized cortisol response to NT in AD, together with other reports of abnormal responses to other pharmacological challenges, suggests that neuroendocrine abnormalities might be an important concomitant and possibly a central contributor to the pathophysiology of Alzheimer's disease.
AB - The administration of a single dose of the opiate antagonist naltrexone (NT) was accompanied by significant elevations in plasma cortisol in normal elderly subjects: in contrast, the cortisol response to NT was absent in individuals of comparable age with Alzheimer' s disease (AD). The differential effect of AD on the cortisol response was not accompanied by a significant group difference in plasma prolactin in response to NT administration. Furthermore, this differential cortisol response to NT was not associated with any evident differences in age, sex ratio, plasma levels of naltrexone or its major metabolite β-naltrexol, or with differences in measures of nonspecific stress, such as plasma free MHPG, pulse, or blood pressure, between the two groups. The absence of the well-characterized cortisol response to NT in AD, together with other reports of abnormal responses to other pharmacological challenges, suggests that neuroendocrine abnormalities might be an important concomitant and possibly a central contributor to the pathophysiology of Alzheimer's disease.
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U2 - 10.1016/0006-3223(88)90057-1
DO - 10.1016/0006-3223(88)90057-1
M3 - Article
C2 - 3285899
AN - SCOPUS:0023838671
SN - 0006-3223
VL - 23
SP - 726
EP - 733
JO - Biological Psychiatry
JF - Biological Psychiatry
IS - 7
ER -