Mufson E J, Conner J M, Kordower J H
Department of Neurological Sciences, Rush Alzheimer's Disease Center, Rush Presbyterian-St Luke's Medical Center, Chicago, IL 60612, USA.
Neuroreport. 1995 May 9;6(7):1063-6. doi: 10.1097/00001756-199505090-00028.
NGF immunohistochemistry was combined with quantitative optical densitometry to evaluate whether retrogradely transported NGF is altered within cholinergic basal forebrain (CBF) neurons in Alzheimer's disease (AD). In normal aged humans, almost all CBF neurons stained for NGF. Although fewer in total number, remaining CBF perikarya in AD displayed diminished (32%) or undetectable NGF immunoreactivity. Based upon these data we hypothesize that there is a defect in retrograde transport of NGF in AD which may be due to a abnormal production and/or utilization of the trk receptor. This defect may be a primary event mediating the degeneration of CBF neurons in AD.
将神经生长因子（NGF）免疫组织化学与定量光密度测定相结合，以评估在阿尔茨海默病（AD）中，逆向转运的NGF在胆碱能基底前脑（CBF）神经元内是否发生改变。在正常老年人中，几乎所有CBF神经元都有NGF染色。虽然总数较少，但AD中剩余的CBF神经元胞体显示NGF免疫反应性降低（32%）或无法检测到。基于这些数据，我们推测AD中NGF的逆向转运存在缺陷，这可能是由于trk受体的产生和/或利用异常所致。这种缺陷可能是介导AD中CBF神经元变性的主要事件。
