Lal H, Forster M J
Department of Pharmacology, Texas College of Osteopathic Medicine, Forth Worth 76107-2690.
Neurobiol Aging. 1988 Sep-Dec;9(5-6):733-42. doi: 10.1016/s0197-4580(88)80141-6.
It is suggested that the immune system may play a role in the etiology of age-associated cognitive decline and/or Alzheimer's disease. The relationship between brain-reactive antibodies (BRA) and age-associated cognitive dysfunction is reviewed and discussed. A parallel relationship between BRA increases with age and decline of avoidance learning capacity is described in mouse models. Transfer of immunity from old to young mice was found to accelerate both age-related formation of brain-reactive antibodies and age-related decline of avoidance learning capacity. Short-lived mouse genotypes with accelerated autoimmunity were found to show accelerated age-related declines in their ability to acquire an avoidance response when compared with nonautoimmune mice. Overall, these findings suggest that the immune system could be an important target for development of intervention strategies aimed at extending the intellectually competent period of life. Mice in which autoimmunity is accelerated may be useful as models for the development of such interventions.
有人认为，免疫系统可能在与年龄相关的认知衰退和/或阿尔茨海默病的病因中起作用。本文回顾并讨论了脑反应性抗体（BRA）与年龄相关的认知功能障碍之间的关系。在小鼠模型中描述了BRA随年龄增加与回避学习能力下降之间的平行关系。研究发现，将老年小鼠的免疫转移到年轻小鼠身上，会加速与年龄相关的脑反应性抗体形成以及回避学习能力的年龄相关下降。与非自身免疫小鼠相比，自身免疫加速的短命小鼠基因型在获得回避反应的能力上表现出加速的年龄相关下降。总体而言，这些发现表明，免疫系统可能是旨在延长智力正常生活期的干预策略开发的重要靶点。自身免疫加速的小鼠可用作此类干预措施开发的模型。
