come as a result of this process including several cancers and Xeroderma pigmentosum. The effect of oxidatively damaged RNA has resulted in a number of human diseases and is especially associated with chronic degeneration. This type of damage has been observed in many neurodegenerative diseases such as Amyotrophic lateral sclerosis, Alzheimer’s, Parkinson’s, dementia with Lewy bodies, and several prion diseases. It is important to note that this list is rapidly growing and data suggests that RNA oxidation occurs early in the development of these diseases, rather than as an effect of cellular decay. RNA and DNA lesions are both associated with the development of diabetes mellitus type 2. Repair Mechanisms DNA Damage Response When DNA is damaged such as due to a lesion, a complex signal transduction pathway is activated which is responsible for recognizing the damage and instigating the cell’s response for repair. Compared to the other lesion repair mechanisms, DDR is the highest level of repair and is employed for the most complex lesions. DDR consists of various pathways, the most common of which are the DDR kinase signaling cascades. These are controlled by phosphatidylinositol 3-kinase-related kinases (PIKK), and range from DNA-dependent protein kinase (DNA-PKcs) and ataxia telangiectasia-mutated (ATM) most involved in repairing DSBs to the more versatile Rad3-related (ATR). ATR is crucial to human cell viability, while ATM mutations cause the severe disorder ataxia-telangiectasia leading to neurodegeneration, cancer, and immunodeficiency. These three DDR kinases all recognize damage via protein-protein interactions which localize the kinases to the areas of damage. Next, further protein-protein interactions and posttranslational modifications (PTMs) complete the kinase activation, and a series of phosphorylation events takes place. DDR kinases perform repair regulation at three levels - via PTMs, at the level of chromatin, and at the level of the nucleus. Base Excision Repair Base excision repair (BER) is responsible for removing damaged bases in DNA. This mechanism specifically works on excising small base lesions which do not distort the DNA double helix, in contrast to the nucleotide excision repair pathway which is employed in correcting more prominent distorting lesions. DNA glycosylases initiate BER by both recognizing the faulty or incorrect bases and then removing them, forming AP sites lacking any purine or pyrimidine. AP endonuclease then cleaves the AP site, and the single-strand break is either processed by short-patch BER to replace a single nucleotide long-patch BER to create 2-10 replacement nucleotides. Single Stranded Break