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Enhanced production of amyloid precursor protein mRNA by peripheral mononuclear blood cell in Alzheimer's disease
Author(s) -
Jiang Sanduo,
Zhang Mingyuan,
Ren Daming,
Tang Guomei,
Lin Sicui,
Qian Yiping,
Zhang Ye,
Jiang Kaida,
Li Fei,
Wang Dongxiang
Publication year - 2003
Publication title -
american journal of medical genetics part b: neuropsychiatric genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.393
H-Index - 126
eISSN - 1552-485X
pISSN - 1552-4841
DOI - 10.1002/ajmg.b.10067
Subject(s) - amyloid precursor protein , peripheral blood mononuclear cell , pathogenesis , reverse transcription polymerase chain reaction , gene expression , gene , messenger rna , alzheimer's disease , biology , microbiology and biotechnology , exon , real time polymerase chain reaction , disease , medicine , immunology , biochemistry , in vitro
Abstract Previous studies have suggested the involvement of amyloid precursor protein (APP) in Alzheimer's disease (AD), as exons 16 and 17 of the APP gene mutations have been found in some familial AD patients. Furthermore, overexpression and deposition of the beta amyloid peptide, a proteolytic product of APP, have been considered as a pathological hallmark of Alzheimer's disease. Therefore, it is of particular interest to determine the expression of APP gene at the transcription level for better understanding of the roles of APP gene in AD pathogenesis. In this work, we employed the quantitative reverse transcriptase‐polymerase chain reaction (RT‐PCR) to quantify APP mRNA transcripts in the peripheral mononuclear blood cells (PMBC) of 52 Alzheimer's patients, 28 vascular dementia (VD) patients, and 60 healthy elderly controls. The results showed that the amount (mean ± SEM) of APP transcripts per microgram of total cDNA was 4.05 ± 0.27, 2.73 ± 0.33, and 2.59 ± 0.27 amole in AD, VD, and healthy controls, respectively. There was a significant increase ( P < 0.05) in the expression of APP mRNA transcripts in AD compared with that in VD or in healthy controls. Thus, our data indicated that variation of APP gene expression in PMBC might be a pathogenic source of Alzheimer's disease. © 2003 Wiley‐Liss, Inc.