The most common form of dementia in the U.S. is Alzheimer��s disease, which is consistently in the top 10 causes of death in the elderly. While the mechanism behind the progression of this disease remains unclear, the importance of amyloid-b as a causative factor in AD is well known. This small peptide is accepted as triggering the initial event that drives the disease. The Ab peptide is a product of sequential cleavage of the amyloid-b precursor protein, and it has a tendency to aggregate. The 40 amino acid peptide is the most abundant form of Ab, and is not as aggregate-prone as the less common 42 amino acid peptide. The 42:40 peptide ratio increases in early onset, familial AD, indicating that Ab42 may play a greater role in initial pathology than Ab40. The peptide aggregates become more insoluble as they continue to accumulate a characteristic that can be discerned by sequential extraction under progressively more denaturing conditions. This allows for categorization of Ab by solubility, which can help provide insights into the pathophysiology of the disease process. The aggregation process ultimately leads to mature amyloidfibrils which form deposits known as amyloid plaques. Amyloid plaques are found in two different forms: diffuse plaques and neuritic plaques. DPs lack a dense core and are associated with normal aging. NPs possess an amyloid core, associate with dystrophic neurites, and increase in AD. NPs, coupled with tangles of hyperphosphorylated tau, are the basis of an AD diagnosis in postmortem tissue. Apart from Ab accumulation, many other factors may contribute to the disease process. An increase in oxidative stress found in the form of oxidized DNA, RNA, and protein adducts may also contribute to the progression of the disease. The occurrence of nucleotide oxidation has the greatest potential for long-term, pathophysiologic consequences, as nucleotide mutations may result in Publications Using Abomle AZ960 incorrect synthesis of numerous proteins repeated over the life of the cell. For example, 8-hydroxyguanine can incorrectly base pair with adenine and introduce mutations during DNA synthesis. The effects of oxidative stress on DNA has been focused on more than RNA, even though RNA may be more vulnerable to oxidative insults than DNA given its generally single-stranded state and accessibility to the oxidantproducing mitochondria. RNA oxidation is increased in AD and certain adducts are more abundant than others. Although current practice includes incorporating chemotherapy or radiation into surgical resection treatment protocols, gastric cancer survival rates remain poor. Gastric cancer is a heterogeneous disease in both histology and genetics; hence, patient outcome is difficult to predict using classic histological classifications. Gastric carcinogenesis is considered to be a multifactorial and multistep process that involves the activation of oncogenes and the inactivation of tumor suppressor genes at different stages of gastric cancer progression. Recently, several new oncogenes and tumor suppressor genes associated with gastric cancer have been identified, which may be helpful for early diagnosis and for the development of targeted therapies. To improve patient prognosis, further understanding of the molecular mechanisms of cancer progression and the development of new therapeutic tools based on these mechanisms is required. In addition, loss of AP-2 expression seems to be associated with malignant transformation and tumor progression and is independently associated with an elevated risk of subsequent metastatic behavior of stage I cutaneous malignant melanoma.