Rodríguez-Santiago Benjamín, Nunes Virginia
Medical and Molecular Genetics Center-Institut de Recerca Oncologica, IDIBELL, Hospital Duran i Reynals, Gran Via s/n, L'Hospitalet del Llobregat 08907, Barcelona, Spain.
Neurobiol Dis. 2005 Mar;18(2):296-304. doi: 10.1016/j.nbd.2004.10.004.
Accumulation of mitochondrial defects is hypothesised to play a role in the complex pathophysiology of the sporadic form of Alzheimer's disease (SAD). Changes in expression of mtDNA encoded genes have been reported in SAD. However no conclusive results were obtained by using different methodologies and analysing distinct transcripts in a variety of brain areas. Here, we measured the expression of five mitochondrial-encoded genes in three brain areas and in lymphocytes from patients and controls by performing reverse transcription followed by quantitative real-time PCR. The analysis of gene expression was also performed by carrying out classic dot-blot experiments to evaluate the two techniques. SAD and control samples showed similar gene expression levels. Estimation of the transcription rate was also measured. No differences were observed when comparing patients and controls. Selective differences in transcription rates were observed only when samples were pooled by tissue, lymphocytes being the tissue with the highest rates.
线粒体缺陷的积累被认为在散发性阿尔茨海默病(SAD)复杂的病理生理学中起作用。已有报道称SAD患者的线粒体DNA编码基因表达发生了变化。然而,使用不同方法并分析多个脑区的不同转录本并未得出确凿结果。在此,我们通过逆转录后进行定量实时PCR,测量了患者和对照组三个脑区以及淋巴细胞中五个线粒体编码基因的表达。还通过经典的点杂交实验进行基因表达分析以评估这两种技术。SAD组和对照组样本显示出相似的基因表达水平。同时也测量了转录速率。比较患者和对照组时未观察到差异。仅在按组织汇集样本时观察到转录速率的选择性差异,淋巴细胞是转录速率最高的组织。