Buchwald J S, Erwin R J, Read S, Van Lancker D, Cummings J L
Department of Physiology, UCLA Medical Center.
Electroencephalogr Clin Neurophysiol. 1989 Sep-Oct;74(5):378-84. doi: 10.1016/0168-5597(89)90005-1.
The human 'P1' middle latency evoked potential is postulated to be generated in the thalamus by a cholinergic component of the ascending reticular activating system. To test the hypothesis that P1 and its generator substrate are abnormal in Alzheimer's disease (AD), a disorder of marked cholinergic deficiency, recordings of middle latency responses to click stimuli were carried out. Comparisons between the AD and age-matched control groups indicated normal auditory brain-stem and Pa responses but a significant decrease in P1 amplitude. This P1 abnormality suggests that the midbrain cholinergic cells in AD may be dysfunctional.
人类“P1”中潜伏期诱发电位被假定为由网状上升激活系统的胆碱能成分在丘脑产生。为了验证阿尔茨海默病（AD，一种明显胆碱能缺乏的疾病）中P1及其产生基质异常这一假设，对点击刺激的中潜伏期反应进行了记录。AD组与年龄匹配的对照组之间的比较表明，听觉脑干和Pa反应正常，但P1波幅显著降低。这种P1异常表明AD患者的中脑胆碱能细胞可能功能失调。
