AChE mRNA expression as a possible novel biomarker for the diagnosis of coronary artery disease and Alzheimer's disease, and its association with oxidative stress


ARCHIVES OF PHYSIOLOGY AND BIOCHEMISTRY, vol.128, no.2, pp.352-359, 2022 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 128 Issue: 2
  • Publication Date: 2022
  • Doi Number: 10.1080/13813455.2019.1683584
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, BIOSIS, CAB Abstracts, Chemical Abstracts Core, EMBASE, Food Science & Technology Abstracts, MEDLINE, Veterinary Science Database
  • Page Numbers: pp.352-359
  • Keywords: Alzheimer's disease, acetylcholinesterase, gene expression, oxidative stress, neurodegenerative disorder, TOTAL ANTIOXIDANT STATUS, AMYLOID-BETA, PROTEIN OXIDATION, SULFHYDRYL-GROUPS, ACETYLCHOLINESTERASE, GLUTATHIONE, SERUM, BRAIN, MALONDIALDEHYDE, AGGREGATION
  • Anadolu University Affiliated: Yes


Oxidative metabolic reactions and their by products have played a role in coronary artery disease (CAD) and Alzheimer's disease (AD) pathogenesis. This study was carried out on 28 patients with AD, 21 patients with CAD, and 28 healthy as control. Oxidative stress biomarkers and acetylcholinesterase (AChE) activity were assayed in plasma. mRNA expression of AChE was investigated in leukocytes of patients with CAD and AD. Thus, Alzheimer's and coronary artery patients were observed that the protein carbonyl levels and mRNA expression of AChE were increased (p<.05, p<.01, respectively). The plasma total thiol levels were decreased compared to the control group (p<.05). There was a significant relationship between amyloid beta (A beta) accumulation and oxidative stress, cholinergic gene expression. AChE gene expression and protein oxidation were increased in patients with AD and CAD. These results suggest that increased release of AChE from cells produces neurotoxic beta-amyloid plaques and may cause neurodegenerative diseases.