Kudinova N V, Kudinov A R, Berezov T T
Biomed Khim. 2007 Mar-Apr;53(2):119-27.
During a decade there was a dogma that Alzheimer's amyloid beta (Ap) is produced only upon the disease, and that this protein is neurotoxic for neurons and brain tissue. Current scientific evidence demonstrate that AP is an essential molecule in synaptic plasticity that underlie learning and memory. Therefore, it was hypothesized that the change of AP biology in Alzheimer's disease (as well as in a number of other human pathologies, including cardiovascular disease, Niemann-Pick type C disease and Down syndrome) represents a physiological mechanism serving to compensate the impaired brain structure or function. This review summarizes experimental evidence on Abeta as functional player in synaptic plasticity and neurochemical pathways.
在过去十年里，一直存在一种观点，即阿尔茨海默病的β淀粉样蛋白（Aβ）仅在患病时产生，且这种蛋白质对神经元和脑组织具有神经毒性。目前的科学证据表明，Aβ是突触可塑性中的一种重要分子，而突触可塑性是学习和记忆的基础。因此，有人提出假说，认为在阿尔茨海默病（以及包括心血管疾病、尼曼-匹克C型病和唐氏综合征在内的许多其他人类疾病）中，Aβ生物学特性的改变代表了一种生理机制，用于补偿受损的脑结构或功能。本综述总结了关于Aβ作为突触可塑性和神经化学通路中功能性参与者的实验证据。
