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Journal of Biomedicine and Biotechnology
Volume 2006, Article ID 82323, 6 pages
Review Article

Oxidative Damage to RNA in Neurodegenerative Diseases

1Department of Psychiatry and Neurology, Asahikawa Medical College, Asahikawa 078-8510, Japan
2Department of Neurology, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan
3Department of Neurology, School of Medicine, Tohoku University, Sendai 980-8574, Japan
4Pharmaceutical Research Laboratories I, Pharmaceutical Research Division, Takeda Chemical Industries Limited, Osaka 532-8686, Japan
5Institute of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA

Received 5 January 2006; Accepted 21 April 2006

Copyright © 2006 Akihiko Nunomura et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Since 1999, oxidative damage to RNA molecules has been described in several neurological diseases including Alzheimer's disease, Parkinson's disease, Down syndrome, dementia with Lewy bodies, prion disease, subacute sclerosing panencephalitis, and xeroderma pigmentosum. An early involvement of RNA oxidation of vulnerable neuronal population in the neurodegenerative diseases has been demonstrated, which is strongly supported by a recent observation of increased RNA oxidation in brains of subjects with mild cognitive impairment. Until recently, little is known about consequences and cellular handling of the RNA damage. However, increasing body of evidence suggests detrimental effects of the RNA damage in protein synthesis and the existence of several coping mechanisms including direct repair and avoiding the incorporation of the damaged ribonucleotides into translational machinery. Further investigations toward understanding of the consequences and cellular handling mechanisms of the oxidative RNA damage may provide significant insights into the pathogenesis and therapeutic strategies of the neurodegenerative diseases.