Carbon Nanodot-Sensitized Modulation of Alzheimer's [beta]-Amyloid Self-Assembly, Disassembly, and Toxicity

The self-assembly of amyloidogenic peptides into [beta]-sheet-rich aggregates is a general feature of many neurodegenerative diseases, including Alzheimer's disease, which signifies the need for the effective attenuation of amyloid aggregation toward alleviating amyloid-associated neurotoxicity...

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Veröffentlicht in:Small (Weinheim an der Bergstrasse, Germany) Germany), 2017-09, Vol.13 (34)
Hauptverfasser: Chung, You Jung, Kim, Kayoung, Lee, Byung Il, Park, Chan Beum
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Sprache:eng
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Zusammenfassung:The self-assembly of amyloidogenic peptides into [beta]-sheet-rich aggregates is a general feature of many neurodegenerative diseases, including Alzheimer's disease, which signifies the need for the effective attenuation of amyloid aggregation toward alleviating amyloid-associated neurotoxicity. This study reports that photoluminescent carbon nanodots (CDs) can effectively suppress Alzheimer's [beta]-amyloid (A[beta]) self-assembly and function as a [beta]-sheet breaker disintegrating preformed A[beta] aggregates. This study synthesizes CDs using ammonium citrate through one-pot hydrothermal treatment and passivates their surface with branched polyethylenimine (bPEI). The bPEI-coated CDs (bPEI@CDs) exhibit hydrophilic and cationic surface characteristics, which interact with the negatively charged residues of A[beta] peptides, suppressing the aggregation of A[beta] peptides. Under light illumination, bPEI@CDs display a more pronounced effect on A[beta] aggregation and on the dissociation of [beta]-sheet-rich assemblies through the generation of reactive oxygen species from photoactivated bPEI@CDs. The light-triggered attenuation effect of A[beta] aggregation using a series of experiments, including photochemical and microscopic analysis, is verified. Furthermore, the cell viability test confirms the ability of photoactivated bPEI@CDs for the suppression of A[beta]-mediated cytotoxicity, indicating bPEI@CDs' potency as an effective anti-A[beta] neurotoxin agent.
ISSN:1613-6810
1613-6829
DOI:10.1002/smll.201700983