논문 (학술지)
Regulatory Activities of Dopamine and Its Derivatives toward Metal-Free and Metal-Induced Amyloid-beta Aggregation, Oxidative Stress, and Inflammation in Alzheimer's Disease
| 등록번호 | RPMS-2019-0290759585 | SCI 구분
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※구분 : SCI(SCIE포함), 비SCI |
SCI |
|---|---|---|---|
| 저자명 (주·공동저자) | Nam Eunju; Derrick Jeffrey S.; Lee Seunghee; Kang Juhye; Han Jiyeon; Lee Shin Jung C.; Chung Su Wol; Lim Mi Hee | ||
| 논문구분 | 국외전문학술지 | 학술지명 | ACS CHEMICAL NEUROSCIENCE |
| ISSN | 1948-7193 | 학술지 출판일자 | 2018-11-21 |
| 학술지 볼륨번호 | 9 | 논문페이지 | 2655 ~ 2666 |
| 학술지 임팩트팩터 | 4.211 | 기여율 | 25 % |
| DOI | 10.1021/acschemneuro.8b00122 | ||
| 초록 | A catecholamine neurotransmitter, dopamine (DA), is suggested to be linked to the pathology of dementia; however, the involvement of DA and its structural analogues in the pathogenesis of Alzheimer’s disease (AD), the most common form of dementia, composed of multiple pathogenic factors has not been clear. Herein, we report that DA and its rationally designed structural derivatives (1−6) based on DA’s oxidative transformation are able to modulate multiple pathological elements found in AD [i.e., metal ions, metalfree amyloid-β (Aβ), metal-bound Aβ (metal−Aβ), and reactive oxygen species (ROS)], with demonstration of detailed molecular-level mechanisms. Our multidisciplinary studies validate that the protective effects of DA and its derivatives on Aβ aggregation and Aβ-mediated toxicity are induced by their oxidative transformation with concomitant ROS generation under aerobic conditions. In particular, DA and the derivatives (i.e., 3 and 4) show their noticeable anti-amyloidogenic ability toward metal-free Aβ and/or metal−Aβ, verified to occur via their oxidative transformation that facilitates Aβ oxidation. Moreover, in primary pan-microglial marker (CD11b)-positive cells, the major producers of inflammatory mediators in the brain, DA and its derivatives significantly diminish inflammation and oxidative stress triggered by lipopolysaccharides and Aβ through the reduced induction of inflammatory mediators as well as upregulated expression of heme oxygenase-1, the enzyme responsible for production of antioxidants. Collectively, we illuminate how DA and its derivatives could prevent multiple pathological features found in AD. The overall studies could advance our understanding regarding distinct roles of neurotransmitters in AD and identify key interactions for alleviation of AD pathology. | ||
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