Abstract
Multi-target intervention and synergistic treatment are critical for the drug development of Alzheimer’s disease (AD) due to its complex and multifactional nature. Oxidative stress and amyloid β peptides (Aβ) accumulation have been recognized as therapeutic targets for AD. Herein, with ability to inhibit Aβ aggregation and the broad-spectrum antioxidant properties, the large amino acid mimicking selenium-doped carbon quantum dots (SeCQDs) are presented as novel nanoagents for multi-target therapy of AD. Compared with the precursor, selenocystine, SeCQDs which maintain the intrinsic properties of both selenium and carbon quantum dots (CQDs) possess good biocompatibility and a remarkable ROS-scavenging activity. Moreover, the functionalized α-carboxyl and amino groups on edge of SeCQDs can trigger multivalent interactions with Aβ, leading to the ability of SeCQDs to inhibit Aβ aggregation. In vivo study demonstrated that SeCQDs can significantly ameliorate the Aβ induced memory deficits, reduce Aβ accumulation and inhibit neuron degeneration in AD model rats. The versatility of functionalization and potential ability to cross the blood-brain barrier (BBB) make SeCQDs as prospective nanodrugs for treating AD.
Highlights
Alzheimer’s disease (AD) as one of the most prevalent types of dementia has been reported to affect approximately 10% of people aged 65 years or more (Palop and Mucke, 2010; Zhang et al, 2019; Kim et al, 2020)
A typical lattice spacing of 0.32 nm was clearly observed in the high-resolution transmission electron microscopy (TEM) (HRTEM) images (Figure 2B), which was similar to the bulk graphite (002 facet) (Li et al, 2017; Rosenkrans et al, 2020)
The composition of selenium-doped carbon quantum dots (SeCQDs) was analyzed using X-ray photoelectron spectroscopy (XPS), which revealed that SeCQDs were primarily composed of carbon, oxygen, nitrogen, and selenium (Figure 2E, Supplementary Figure S3)
Summary
Alzheimer’s disease (AD) as one of the most prevalent types of dementia has been reported to affect approximately 10% of people aged 65 years or more (Palop and Mucke, 2010; Zhang et al, 2019; Kim et al, 2020). The exact pathological mechanism of AD remains to be elucidated, a significant body of evidence has demonstrated the existence of cross-talk between Aβ deposition and neurodegeneration in AD (Palop and Mucke, 2010; Zhang et al, 2019; Kim et al, 2020). Of Aβ into soluble oligomers and subsequent aggregates plays a critical role in the pathogenesis of AD (Zhang et al, 2019). The aggregates-induced dysfunction has been known to be a possible cause of AD through various molecular signaling pathways including abnormal production of reactive oxygen species (ROS), which will trigger a series of damages of cellular components and lead to the oxidative stress in AD (Lei et al, 2021).
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