MECHANISMS OF NEURONAL DEATH IN BRAIN AGING AND ALZHEIMERS-DISEASE - ROLE OF ENDOCRINE-MEDIATED CALCIUM DYSHOMEOSTASIS

被引：112

作者：

LANDFIELD, PW ^{[1
]}

THIBAULT, O ^{[1
]}

MAZZANTI, ML ^{[1
]}

PORTER, NM ^{[1
]}

KERR, DS ^{[1
]}

机构：

[1] UNIV OTAGO, DEPT PSYCHOL, DUNEDIN, NEW ZEALAND

来源：

JOURNAL OF NEUROBIOLOGY | 1992年 / 23卷 / 09期

关键词：

BRAIN AGING; GLUCOCORTICOIDS; CALCIUM REGULATION; HIPPOCAMPUS; NEURON DEATH; CALCIUM POTENTIALS; CALCIUM CURRENTS; ALZHEIMERS DISEASE;

D O I：

10.1002/neu.480230914

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

This paper reviews evidence that brain aging and Alzheimer's disease (AD) are somehow closely related and that the hippocampus (CA1) is highly vulnerable to cell loss under both conditions. In addition, two current lines of evidence on the mechanisms of hippocampal cell loss with aging are considered, including studies of neuronal calcium dysregulation and studies of cumulative glucocorticoid (GC) neurotoxicity. Moreover, recent electro-physiological studies have shown that excess glucocorticoid activation of hippocampal neurons increases the influx of calcium through voltage-activated calcium channels. Second messenger systems may mediate the steroid modulation of calcium channels. Therefore, it is hypothesized that excess glucocorticoid activation and neuronal calcium dysregulation may be two phases of a single process that increases the susceptibility of neurons to neuro-degeneration during aging and Alzheimer's disease.

引用

页码：1247 / 1260

页数：14

共 115 条

[1] EPILEPTIFORM BURST AFTERHYPERPOLARIZATION - CALCIUM-DEPENDENT POTASSIUM POTENTIAL IN HIPPOCAMPAL CA1-PYRAMIDAL CELLS [J].