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Angew. Chem.-Int. Edit., 14 JUL 2015 | DOI: 10.1002/anie.201504310
Photoexcited Porphyrins as a Strong Suppressor of β-Amyloid Aggregation and Synaptic Toxicity
Abstract
Byung Il Lee1,‡, Dr. Seongsoo Lee2,3,‡, Yoon Seok Suh2, Joon Seok Lee1, Ae-kyeong Kim2, Dr. O-Yu Kwon4, Dr. Kweon Yu2,* and Prof. Dr. Chan Beum Park1,*
1 Department of Materials Science and Engineering, Korea Advanced Institute of Science and Technology, 335 Science Road, Daejeon 305-701 (Republic of Korea)
2 Neurophysiology Research Group, Bionano Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Department of Functional Genomics, Korea University of Science and Technology (UST), Daejeon 305-333 (Korea)
3 Gwangju Center, Korea Basic Science Institute (KBSI), Gwangju 500-757 (Korea)
4 Department of Anatomy, College of Medicine, Chungnam National University, Daejeon 301-747 (Korea)
‡These authors contributed equally to this work.
* Corresponding authors
Abstract
The abnormal assembly of β-amyloid (Aβ) peptides into neurotoxic, β-sheet-rich amyloid aggregates is a major pathological hallmark of Alzheimer’s disease (AD). Light-induced photosensitizing molecules can regulate Aβ amyloidogenesis. Multiple photochemical analyses using circular dichroism, atomic force microscopy, dot blot, and native gel electrophoresis verified that photoactivated meso-tetra(4-sulfonatophenyl)porphyrin (TPPS with M=2H+, Zn2+, Cu2+, Mn2+) successfully inhibits Aβ aggregation in vitro. Furthermore, Aβ toxicity was relieved in the photoexcited-TPPS-treated Drosophila AD model. TPPS suppresses neural cell death, synaptic toxicity, and behavioral defects in the Drosophila AD model under blue light illumination. Behavioral phenotypes, including larval locomotion defect and short lifespan caused by Aβ overexpression, were also rescued by blue light-excited TPPS.
Keywords : Alzheimer’s disease; Drosophila model; photosensitizers; porphyrins; β-amyloids
논문정보
- Research article
- 2015년 07월 (BRIC 등록일 2015-07-20)
- 국내 연구진
- 바이오·의료융합 > 바이오센싱 및 나노바이오물질
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