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Beta-Amyloid Aggregation Inhibitors as Therapeutic Agents for Alzheimer’s Disease

등록일
2008년 8월 12일 14시 06분 54초
접수번호
1469
발표코드
목18G3심 이곳을 클릭하시면 발표코드에 대한 설명을 보실 수 있습니다.
발표시간
목 15시 : 40분
발표형식
심포지엄
발표분야
의약화학 - Recent Drug Development of Neurodegenerative Disease
저자 및
공동저자
김영호, 이지우1
디지탈바이오텍 중앙연구소, Korea
1서울대학교 약학대학 약학과, Korea
Alzheimer's disease (AD) is a neurodegenerative disease characterized by dementia, cognitive impairment, and memory loss. AD is characterized by the accumulation of senile amyloid plaques composed of beta amyloid (Abeta) peptide and numerous neurofibrillary tangles formed from filaments of highly phosphorylated tau proteins in the brain. The insoluble amyloid plaques is formed by a process called amyloidosis whereby Abeta peptide aggregates into toxic and insoluble oligomer and/or fibers. Thus, an attractive therapeutic strategy in principle is to inhibit and preferably reverse Abeta peptide aggregation itself, because this appears to be the first step in the pathogenic process of amyloidosis that is not associated with some natural biological function. We discovered that a series of benzofuran inhibited the Abeta peptide aggregation in vitro and displayed promising activities in in vivo models. Efficacy and safety profiles of the drug candidate named DBTAI-1339 will be presented.

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