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The Institute for Eurasian Turkic Studies is a collaborative research center with the International Center for Central Asian Studies (IICAS) under UNESCO. Especially, The Eurasian Initiative and the New Silk Road Initiative are increasing the need for research on Eurasian Turks in the Eurasian region, specializing in Eurasian Turks. Therefore, our institute was established with the purpose of revitalizing the research of Turks who had played a key role in Eurasia and the Silk Road. The researchers have participated in the study of the Turkic Belt countries in the fields of politics, economics, society, history, language, literature, culture, and art of Eurasia, and our institute was established to carry out joint research in these respective fields. It is possible to do comparative studies with neighboring countries and neighboring ethnic groups as well as Korea. Through this research, we will play a central role in the study of Eurasian Turcology in Korea and will contribute to the improvement of relations with Turkbelt countries by working as a research institute in cooperation with Eurasia Turkic Research Centers abroad. Our institute was established in February of 2016. Since then, it has been designated a Dongduk Women's University Policy Research Institute in May, 2016, and is a partner research institute cooperating with the International Center for Central Asian Studies, a category 2 organization under UNESCO.
Alzheimer disease (AD) is marked by increases in oxidative damage to macromolecules such as sugars, lipids, proteins and nucleic acids. Notably, such damage is not limited to the lesions of the disease but instead involves all vulnerable neurons. These findings of oxidative abnormalities clearly predate gross described neuronal cytopathology and support the primacy of oxidative damage as an early and dynamic change of AD. Here, we review possible sources of oxidative damage as it applies to AD. Contrary to in vitro findings, correlations between cases with various extents of amyloid-β deposits or neurofibrillary tangles (NFT) show that oxidative damage is in fact reduced with increasing senile plaque and neurofibrillary tangle density (Nunomura et al., 1999a). for amyloid-β, there is a direct negative linear correlation with oxidative damage (Nunomura et al., 1999b). These findings indicate that the formation of the amyloid-β plaques and NFT, long thought of as a deleterious process leading to neuronal death, may in fact be a cytoprotective response (Morsch et al.,1999) to reduce oxidative damage.