[Base excision repair in Alzheimer's disease]

Alzheimer's disease (AD) is the most common neurodegenerative disease in people over 65 years of age. Estimates indicate that about 200 thousand Pole suffer from AD while in the world about 30 million people. Forecasts show that in developed countries the number of people with neurodegenerative diseases by 2025 will increase by several hundred percent compared to 1980. Results of carried out tests suggest several causes of this disease, in which an important role is played by age, genetic and environmental factors. An important role is played by oxidizing agents. They damage the genetic material and reduce activity of enzymes responsible for the repair of this damage contributing to the development of neurodegenerative diseases including AD. In this paper we discuss the relationship between the activity level of the main system removing oxidative DNA damage, named base excision repair (BER), which recognizes and repairs damaged DNA bases, as well as the key proteins involved in this type of DNA repair and AD. We also describe the important role of genetic polymorphism in genes encoding BER proteins, modulating the activity of this type of repair. This indicates the possibility to increase the knowledge of the AD mechanism based on the BER system, which may contribute to the identification of molecular markers of this disease in the future.