摘要
Accumulation and aggregation of beta-amyloid (A beta) peptides result in neuronal death, leading to cognitive dysfunction in Alzheimer's disease. The self-assembled A beta molecules form various intermediate aggregates including oligomers that are more toxic to neurons than the mature aggregates, including fibrils. Thus, one strategy to alleviate A beta toxicity is to facilitate the conversion of A beta intermediates to larger aggregates such as fibrils. In this study, we designed a peptide named A3 that significantly enhanced the formation of amorphous aggregates of A beta by accelerating the aggregation kinetics. Thioflavin T fluorescence experiments revealed an accelerated aggregation of A beta monomers, accompanying reduced A beta cytotoxicity. Transgenic Caenorhabditis elegans over-expressing amyloid precursor protein exhibited paralysis due to the accumulation of A beta oligomers, and this phenotype was attenuated by feeding the animals with A3 peptide. These findings suggest that the A beta aggregation-promotion effect can potentially be useful for developing strategies to reduce A beta toxicity.
- 出版日期2017-8
- 单位国家纳米科学中心