Lawlor B A, Davis K L
Department of Psychiatry, Mount Sinai School of Medicine, New York, NY.
Biol Psychiatry. 1992 Feb 15;31(4):337-50. doi: 10.1016/0006-3223(92)90227-q.
Although glutamate dysfunction has been implicated in the pathogenesis of Alzheimer's disease (AD), it is unclear which direction a glutamatergic strategy should take in this illness. Increasing glutamate function may enhance excitotoxicity and neuronal death, whereas decreasing activity in this excitatory amino acid pathway may impair memory processes. Pharmacological modulation of the different NMDA and nonNMDA receptor sites, together with the concept of an agonist versus antagonist approach, are discussed in this review. It would appear that a glutamatergic approach may represent a new and exciting option to pursue in the experimental pharmacotherapeutics of AD.
尽管谷氨酸功能障碍与阿尔茨海默病（AD）的发病机制有关，但尚不清楚在这种疾病中谷氨酸能策略应采取何种方向。增强谷氨酸功能可能会增强兴奋性毒性和神经元死亡，而降低这条兴奋性氨基酸途径的活性可能会损害记忆过程。本文综述了对不同NMDA和非NMDA受体位点的药理学调节，以及激动剂与拮抗剂方法的概念。在AD的实验性药物治疗中，谷氨酸能方法似乎可能是一个新的、令人兴奋的选择。
