DNA-repair in mild cognitive impairment and Alzheimer's disease

• Published in: DNA repair Vol. 12; no. 10; pp. 811 - 816
• Main Authors: Bucholtz, Nina, Demuth, Ilja
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.10.2013
• Subjects: Aged; Aged, 80 and over; Alzheimer Disease - etiology; Alzheimer Disease - genetics; Alzheimer Disease - metabolism; Case-Control Studies; Cognitive Dysfunction - etiology; Cognitive Dysfunction - genetics; Cognitive Dysfunction - metabolism; DNA Glycosylases - genetics; DNA Glycosylases - metabolism; DNA Polymerase beta - genetics; DNA Polymerase beta - metabolism; DNA Repair; DNA-(Apurinic or Apyrimidinic Site) Lyase - genetics; DNA-(Apurinic or Apyrimidinic Site) Lyase - metabolism; Humans; Oxidative Stress - genetics; Polymorphism, Single Nucleotide
• ISSN: 1568-7864; 1568-7856; 1568-7856
• DOI: 10.1016/j.dnarep.2013.07.005

While the pathogenesis of the sporadic form of Alzheimer disease (late onset Alzheimer disease, LOAD) is not fully understood, it seems to be clear that a combination of genetic and environmental factors are involved and influence the course of the disease. Among these factors, elevated levels of oxidative stress have been recognized and individual differences in the capacity to deal with DNA damage caused by its effects have been the subject of numerous studies. This review summarizes the research on DNA repair proteins and genes in the context of LOAD pathogenesis and its possible prodromal stage, mild cognitive impairment (MCI). The current status of the research in this field is discussed with respect to methodological issues which might have compromised the outcome of some studies and future directions of investigation on this subject are depicted.