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Quantitative Analysis of Presenilin‐1 mRNA Expression in Sporadic Alzheimer's Disease Brain
Author(s) -
Baba Hajime,
Ohnuma Tohru,
Shibata Nobuto,
Takahashi Tadashi,
Arai Heii
Publication year - 2001
Publication title -
psychogeriatrics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.647
H-Index - 32
eISSN - 1479-8301
pISSN - 1346-3500
DOI - 10.1111/j.1479-8301.2001.tb00051.x
Subject(s) - presenilin , real time polymerase chain reaction , messenger rna , biology , pathological , disease , alzheimer's disease , temporal cortex , pathology , microbiology and biotechnology , gene , medicine , genetics , neuroscience
Background : The majority of familial Alzheimer's disease (FAD) is caused by mutations in the presenilin‐1 (PS‐1) or presenilin‐2 (PS‐2) genes. The neuropathological changes in both FAD and sporadic late‐onset Alzheimer's disease (AD) are similar, suggesting that they share a common etiological pathway. Despite many attempts to investigate the function of PS in sporadic AD, no consensus has been reached as to the levels of expression in sporadic AD. Methods : PS‐1 mRNA content was measured in the frontal cortex of post‐mortem human brains from four sporadic AD cases and five controls. Real‐time quantitative polymerase chain reaction (PCR) was performed using a LightCycler rapid thermal cycler (Roche) with SYBR Green I fluorescence. Results : The results showed that the content of PS‐1 mRNA in the frontal cortex of sporadic AD cases was higher than those in controls (p<0.05). Conclusion : We quantified PS‐1 mRNA in the frontal cortex from sporadic AD and controls with a quantitative real‐time reverse transcriptase‐PCR (RT‐PCR) method. We found that the PS‐1 mRNA content in sporadic AD was higher than in controls suggesting that up‐regulated PS‐1 expression may be associated with some of the pathological changes found in sporadic AD.