Brilliant M, Elble R J, Ghobrial M, Struble R G
Center for Alzheimer Disease and Related Disorders, Southern Illinois University School of Medicine, Springfield 62794-9230.
Neurosci Lett. 1992 Dec 14;148(1-2):23-6. doi: 10.1016/0304-3940(92)90795-9.
A4 protein (beta-protein, beta-amyloid) deposits were identified with silver stains in postmortem brainstem sections from 13 patients with Alzheimer disease (AD), 6 patients with mixed Alzheimer disease and Parkinson disease (AD-PD), 5 disease controls, and 2 elderly controls. A rostro-caudal gradient of A4 was found in patients with AD and AD-PD, such that A4 was most prevalent in the midbrain and least prevalent in the medulla. The brainstem of the controls contained little or no A4. The midbrain tectum and tegmentum contained the greatest densities of A4, but the red nucleus and substantia nigra pars reticulata were largely spared. This distribution of A4 suggests that A4 deposition is a function of synaptic connectivity rather than passive diffusion from vascular sources.
在13例阿尔茨海默病（AD）患者、6例阿尔茨海默病与帕金森病混合型（AD-PD）患者、5例疾病对照者及2例老年对照者的死后脑干切片中，通过银染鉴定出A4蛋白（β蛋白，β淀粉样蛋白）沉积。在AD和AD-PD患者中发现A4呈头尾梯度分布，使得A4在中脑最为普遍，而在延髓最少见。对照者的脑干中几乎没有或不存在A4。中脑顶盖和被盖中A4的密度最大，但红核和黑质网状部基本未受累。A4的这种分布表明，A4沉积是突触连接的一种功能，而非来自血管源的被动扩散。
