Irreversible destruction of amyloid fibril plaques by conjugated polymer based fluorogenic nanogrenades

Dou, Wei; Lv, Ying; Tan, Chunyan; Chen, Guorong; He, Xiao‐Peng

doi:10.1039/c6tb01351a

Cited by 14 publications

(12 citation statements)

References 31 publications

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“…To examine whether Aβ‐induced cytotoxicity could be alleviated by a BiVO 4 ‐based photoelectrode, we performed a 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5 diphenyltetrazolium bromide (MTT) reduction assay, a widely used tool for assessing Aβ‐mediated cell death. [11c,36] Rat pheochromocytoma (PC12) cells were used as a model cell line because of their sensitivity to the toxicity of Aβ aggregates . Aβ aggregates decreased cell viability drastically to 51% ( Figure A), indicating high toxicity of Aβ aggregates to PC12 cells.…”

Section: Resultsmentioning

confidence: 99%

“…Excessively produced Aβ monomers have a high propensity to self‐assemble into oligomers and insoluble β‐sheet‐rich aggregates . Because Aβ peptides start to aggregate long before the onset of AD symptoms, many efforts have been made to reverse AD pathology by clearing amyloid deposits . However, the extremely high stability of amyloid structures makes it challenging to dissociate Aβ aggregates.…”

Section: Introductionmentioning

confidence: 99%

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Photoactive Bismuth Vanadate Structure for Light‐Triggered Dissociation of Alzheimer's β‐Amyloid Aggregates

Kim

Lee

Choi

et al. 2018

Adv Funct Materials

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Bismuth vanadate (BiVO 4 ) is an attractive, low-cost n-type semiconductor that exhibits excellent photoelectrocatalytic properties, chemical stability, and biocompatibility. This study reports a newly discovered function of BiVO 4 dissociating highly stable, self-assembled amyloid aggregates associated with Alzheimer's disease. A visible light-active, nanoporous BiVO 4 platform is developed to break β-amyloid (Aβ) assemblies and alleviate Aβ aggregateinduced toxicity. Multiple photochemical and microscopic analyses reveal that β-sheet-rich, long Aβ fibrils are effectively destabilized and broken into small-sized, soluble species by BiVO 4 photoelectrode under illumination of a white light-emitting diode and an anodic bias. The photoactivated BiVO 4 under anodic bias generates oxidative stress, such as superoxide ions and hole-derived hydrogen peroxide, which causes photooxidation of Aβ residues and irreversible disassembly of Aβ aggregates. The efficacy of photoelectrocatalytic dissociation of Aβ aggregates is enhanced by Mo-doped BiVO 4 , which facilitates the separation of electron-hole pairs by improving electrontransport properties of BiVO 4 . Furthermore, it is verified that both pristine and Mo-doped BiVO 4 photoelectrodes are nontoxic and effective in reducing Aβ-associated cytotoxicity. The work shows the potential of BiVO 4 -based photoelectrode platforms for the dissociation of neurotoxic, highly stable Aβ assemblies using light energy.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Photoactive Bismuth Vanadate Structure for Light‐Triggered Dissociation of Alzheimer's β‐Amyloid Aggregates

Kim

Lee

Choi

et al. 2018

Adv Funct Materials

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“…A photosensitive polymer nanodot was designed by modifying it with a photosensitizer for efficient suppression of Aβ aggregation [ 189 ]. Dou et al produced fluorogenic “nanogrenades” based on super-molecular assembly between organic dyes and conjugated polymers [ 190 ]. The quenched fluorescence of dyes in the nanogrenades was recovered after binding with hydrophobic Aβ fibril plaques.…”

Section: Nanomaterialsmentioning

confidence: 99%

Nanomaterials for Modulating the Aggregation of β-Amyloid Peptides

et al. 2021

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The aberrant aggregation of amyloid-β (Aβ) peptides in the brain has been recognized as the major hallmark of Alzheimer’s disease (AD). Thus, the inhibition and dissociation of Aβ aggregation are believed to be effective therapeutic strategiesforthe prevention and treatment of AD. When integrated with traditional agents and biomolecules, nanomaterials can overcome their intrinsic shortcomings and boost their efficiency via synergistic effects. This article provides an overview of recent efforts to utilize nanomaterials with superior properties to propose effective platforms for AD treatment. The underlying mechanismsthat are involved in modulating Aβ aggregation are discussed. The summary of nanomaterials-based modulation of Aβ aggregation may help researchers to understand the critical roles in therapeutic agents and provide new insight into the exploration of more promising anti-amyloid agents and tactics in AD theranostics.

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“…The disruption or remodeling of existing Aβ fibrils is an important therapeutic strategy for AD treatment, [53,54] so the ability of CPDs to disaggregate mature Aβ 40 fibrils was evaluated. CPDs led to a dramatic decrease of ThT fluorescence intensity within 4 h in a dose-dependent manner, as shown in Figure 3a, implying the disassembly of Aβ 40 fibrils by CPDs.…”

Section: Disaggregation Of Aβ 40 Fibrilsmentioning

confidence: 99%

Nitrogen‐Doped Carbonized Polymer Dots: A Potent Scavenger and Detector Targeting Alzheimer's β‐Amyloid Plaques

Gao

Wang

Dong

et al. 2020

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The fibrillization and deposition of β‐amyloid protein (Aβ) are recognized to be the pathological hallmarks of Alzheimer's disease (AD), which signify the need for the effective detection and inhibition of Aβ accumulation. Development of multifunctional agents that can inhibit Aβ aggregation, rapidly disaggregate fibrils, and image aggregates is one of the effective strategies to treat and diagnose AD. Herein, the multifunctionality of nitrogen‐doped carbonized polymer dots (CPDs) targeting Aβ aggregation is reported. CPDs inhibit the fibrillization of Aβ monomers and rapidly disintegrate Aβ fibrils by electrostatic interactions, hydrogen‐bonding and hydrophobic interactions with Aβ in a time scale of seconds to minutes. Moreover, the interactions make CPDs label Aβ fibrils and emit enhanced red fluorescence by the binding, so CPDs can be used for in vivo imaging of the amyloids in transgenic Caenorhabditis elegans CL2006 as an AD model. Importantly, CPDs are demonstrated to scavenge the in vivo amyloid plaques and to promote the lifespan extension of CL2006 strain by alleviating the Aβ‐triggered toxicity. Taken together, the multifunctional CPDs show an exciting prospect for further investigations in Aβ‐targeted AD treatment and diagnosis, and this study provides new insight into the development of carbon materials in AD theranostics.

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Irreversible destruction of amyloid fibril plaques by conjugated polymer based fluorogenic nanogrenades

Abstract: Supramolecular assembly between conjugated polymers and fluorescent dyes produces a unique class of fluorogenic “nanogrenades” with the ability to image as well as irreversibly destruct amyloid β fibril plaques by simple white-light irradiation.

Cited by 14 publications

References 31 publications

Photoactive Bismuth Vanadate Structure for Light‐Triggered Dissociation of Alzheimer's β‐Amyloid Aggregates

Photoactive Bismuth Vanadate Structure for Light‐Triggered Dissociation of Alzheimer's β‐Amyloid Aggregates

Nanomaterials for Modulating the Aggregation of β-Amyloid Peptides

Nitrogen‐Doped Carbonized Polymer Dots: A Potent Scavenger and Detector Targeting Alzheimer's β‐Amyloid Plaques

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