Price D L, Koo E H, Sisodia S S, Martin L J, Koliatsos V E, Muma N A, Walker L C, Cork L C
Neuropathology Laboratory, Johns Hopkins University School of Medicine, Baltimore, MD.
Prog Brain Res. 1990;86:297-308. doi: 10.1016/s0079-6123(08)63186-6.
Alzheimer's disease (AD), the most common type of adult-onset dementia, is characterized by a variety of brain abnormalities, including degeneration of certain populations of nerve cells, alterations in the neuronal cytoskeleton, and the abnormal deposition of amyloid within brain parenchyma. Pathogenetic processes that lead to these brain abnormalities are difficult to study in humans. Recently, investigators have begun to utilize animal models to examine some of the mechanisms that cause cellular/molecular alterations in transmitter systems, cytoskeletal elements, and APP. These investigations have helped to clarify issues related to the lesions that occur in aged humans and individuals with AD.
阿尔茨海默病(AD)是成人期最常见的痴呆类型,其特征是多种脑异常,包括特定神经细胞群的退化、神经元细胞骨架的改变以及淀粉样蛋白在脑实质内的异常沉积。导致这些脑异常的发病机制在人类中很难研究。最近,研究人员开始利用动物模型来研究导致递质系统、细胞骨架成分和淀粉样前体蛋白(APP)发生细胞/分子改变的一些机制。这些研究有助于阐明与老年人类和AD患者中出现的病变相关的问题。