Mufson E J, Li J M, Sobreviela T, Kordower J H
Department of Neurological Sciences, Rush Alzheimer's Disease Center, Rush Presbyterian St Luke's Medical Center, Chicago, IL 60612, USA.
Neuroreport. 1996 Dec 20;8(1):25-9. doi: 10.1097/00001756-199612200-00006.
In situ hybridization for TrkA mRNA was combined with quantitative optical densitometry to evaluate whether the expression of this gene is altered within cholinergic basal forebrain neurons (CBF) in Alzheimer's disease (AD). TrkA mRNA within individual nucleus basalis neurons was significantly reduced (66%) in AD cases relative to aged controls. Reverse transcription polymerase chain reaction quantitative analyses confirmed that TrkA mRNA levels decreased markedly in AD. In contrast, expression of the gene coding for for the low affinity p75NTR was not significantly altered in AD relative to aged controls. These data indicate that there is a selective defect in trkA gene expression in AD, supporting the hypothesis that the degeneration of CBF neurons seen in this disease results from impaired nerve growth factor trophic support.
将TrkA mRNA的原位杂交与定量光密度测定相结合，以评估该基因的表达在阿尔茨海默病（AD）的胆碱能基底前脑神经元（CBF）中是否发生改变。与老年对照组相比，AD病例中单个基底核神经元内的TrkA mRNA显著减少（66%）。逆转录聚合酶链反应定量分析证实，AD中TrkA mRNA水平显著降低。相比之下，与老年对照组相比，编码低亲和力p75NTR的基因在AD中的表达没有显著改变。这些数据表明，AD中trkA基因表达存在选择性缺陷，支持了该疾病中所见的CBF神经元退化是由神经生长因子营养支持受损导致的这一假说。
