INDIVIDUAL-DIFFERENCES IN HYPOTHALAMIC-PITUITARY-ADRENAL ACTIVITY IN LATER LIFE AND HIPPOCAMPAL AGING

被引:86
作者
MEANEY, MJ
ODONNELL, D
ROWE, W
TANNENBAUM, B
STEVERMAN, A
WALKER, M
NAIR, NPV
LUPIEN, S
机构
[1] DOUGLAS HOSP, AGING RES PROGRAM, MONTREAL, PQ H4H 1R3, CANADA
[2] MCGILL UNIV, DEPT PSYCHIAT, MONTREAL, PQ, CANADA
[3] MCGILL UNIV, DEPT NEUROL & NEUROSURG, MONTREAL, PQ, CANADA
关键词
GLUCOCORTICOID RECEPTOR; MINERALOCORTICOID RECEPTOR; NEURON LOSS; AGING; HIPPOCAMPUS;
D O I
10.1016/0531-5565(94)00065-B
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
Variation in magnitude of cognitive decline in later life is a central feature of human aging. The more severe forms of dementias, such as Alzheimer's disease, clearly define one end of the spectrum. However, among those showing no obvious signs of clinical dementia there are considerable individual differences. Thus, although evidence for learning, memory, and language loss appears in some individuals as early as 50-55 years of age, many people continue to function alertly well into their 90s. These individuals exemplify what Rowe and Kahn (1987) have termed ''successful'' aging. The wide variability in CNS aging, often a nuisance factor in studies, are becoming a major focus for brain aging research (e.g., Gage et al., 1984; Gallager and Pelleymounter, 1988; Aitken and Meaney, 1990; Issa et al., 1990). Our studies over the past few years have added support to the idea that individual differences in hypothalamic-pituitary-adrenal (HPA) activity can account for part of the variation seen in neurological function among the elderly. In this article we discuss the evidence for the idea that adrenal glucocorticoids can compromise hippocampal function and, thus, produce cognitive impairments, as well as the potential mechanisms for these effects.
引用
收藏
页码:229 / 251
页数:23
相关论文
共 125 条
[1]   TEMPORALLY GRADED, AGE-RELATED IMPAIRMENTS IN SPATIAL MEMORY IN THE RAT [J].
AITKEN, DH ;
MEANEY, MJ .
NEUROBIOLOGY OF AGING, 1989, 10 (03) :273-276
[3]   GLUCOCORTICOID ENDANGERMENT OF HIPPOCAMPAL-NEURONS IS NMDA-RECEPTOR DEPENDENT [J].
ARMANINI, MP ;
HUTCHINS, C ;
STEIN, BA ;
SAPOLSKY, RM .
BRAIN RESEARCH, 1990, 532 (1-2) :7-12
[4]  
BAXTER JD, 1987, ENDOCRINOL METAB, P385
[5]  
BENNETT MC, 1991, PSYCHOBIOLOGY, V19, P301
[6]  
BENSTON J, 1978, J COMPUT ASSIST TOMO, V2, P16
[7]   CORTICOTROPIN-RELEASING FACTOR-LIKE IMMUNOREACTIVITY IN SENILE DEMENTIA OF THE ALZHEIMER TYPE - REDUCED CORTICAL AND STRIATAL CONCENTRATIONS [J].
BISSETTE, G ;
REYNOLDS, GP ;
KILTS, CD ;
WIDERLOV, E ;
NEMEROFF, CB .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1985, 254 (21) :3067-3069
[8]  
BODNOFF SR, 1995, J NEUROSCI, V15, P61
[9]   ROLES OF TYPE-I AND TYPE-II CORTICOSTEROID RECEPTORS IN REGULATION OF BASAL ACTIVITY IN THE HYPOTHALAMO-PITUITARY-ADRENAL AXIS DURING THE DIURNAL TROUGH AND THE PEAK - EVIDENCE FOR A NONADDITIVE EFFECT OF COMBINED RECEPTOR OCCUPATION [J].
BRADBURY, MJ ;
AKANA, SF ;
DALLMAN, MF .
ENDOCRINOLOGY, 1994, 134 (03) :1286-1296
[10]   THE ANTIDEPRESSANTS FLUOXETINE, IDAZOXAN AND PHENELZINE ALTER CORTICOTROPIN-RELEASING HORMONE AND TYROSINE-HYDROXYLASE MESSENGER-RNA LEVELS IN RAT-BRAIN - THERAPEUTIC IMPLICATIONS [J].
BRADY, LS ;
GOLD, PW ;
HERKENHAM, M ;
LYNN, AB ;
WHITFIELD, HJ .
BRAIN RESEARCH, 1992, 572 (1-2) :117-125