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Genetic Variants and Oxidative Stress in Alzheimer's Disease

Journal

CURRENT ALZHEIMER RESEARCH
Volume 17, Issue 3, Pages 208-223

Publisher

BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1567205017666200224121447

Keywords

Genetic variants; mitochondrial dysfunction; ROS; biomarkers; Alzheimer's disease; neurodegenerative disorder

Funding

  1. Poznan University of Medical Sciences [502-14-01111677-10813]

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In an aging society, the number of people suffering from Alzheimer's Disease (AD) is still growing. Currently, intensive research is being carried out on the pathogenesis of AD. The results of these studies indicated that oxidative stress plays an important role in the onset and development of this disease. Moreover, in AD oxidative stress is generated by both genetic and biochemical factors as well as the functioning of the systems responsible for their formation and removal. The genetic factors associated with the regulation of the redox system include TOMM40, APOE, LPR, MAPT, APP, PSEN1 and PSEN2 genes. The most important biochemical parameters related to the formation of oxidative species in AD are p53, Homocysteine (Hey) and a number of others. The formation of Reactive Oxygen Species (ROS) is also related to the efficiency of the DNA repair system, the effectiveness of the apoptosis, autophagy and mitophagy processes as well as the antioxidant potential. However, these factors are responsible for the development of many disorders, often with similar clinical symptoms, especially in the early stages of the disease. The discovery of markers of the early diagnosis of AD may contribute to the introduction of pharmacotherapy and slow down the progression of this disease.

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