Hölscher C
Department of Human Anatomy and Physiology, University College Dublin, Ireland.
Neurobiol Dis. 1998 Sep;5(3):129-41. doi: 10.1006/nbdi.1998.0193.
Alzheimer's disease (AD) is a form of dementia in which patients develop neurodegeneration and complete loss of cognitive abilities and die prematurely. No treatment is known for this condition. Evidence points toward beta-amyloid as one of the main causes for cytotoxic processes. The cascade of biochemical events that lead to neuronal death appears to be interference with intracellular calcium homeostasis via activation of calcium channels, intracellular calcium stores, and subsequent production of free radicals by calcium-sensitive enzymes. The glutamatergic system seems to be implicated in mediating the toxic processes. Several strategies promise amelioration of neurodegenerative developments as judging from in vitro experiments. Glutamate receptor-selective drugs, antioxidants, inhibitors of nitric oxide synthase, calcium channel antagonists, receptor or enzyme inhibitors, and growth factors promise help. Especially combinations of drugs that act at different levels might prolong patients' health.
阿尔茨海默病（AD）是一种痴呆症，患者会出现神经退行性变，认知能力完全丧失，并过早死亡。目前尚无针对这种疾病的治疗方法。有证据表明β-淀粉样蛋白是细胞毒性过程的主要原因之一。导致神经元死亡的一系列生化事件似乎是通过激活钙通道、细胞内钙库以及随后由钙敏感酶产生自由基来干扰细胞内钙稳态。谷氨酸能系统似乎参与介导毒性过程。从体外实验判断，有几种策略有望改善神经退行性病变的发展。谷氨酸受体选择性药物、抗氧化剂、一氧化氮合酶抑制剂、钙通道拮抗剂、受体或酶抑制剂以及生长因子有望提供帮助。特别是作用于不同水平的药物组合可能会延长患者的健康期。
