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Advanced Neurology Graphene quantum dots approach in AD

presenilins (e.g., presenilin 1 and presenilin 2). These injury and maintaining cellular homeostasis. Moreover,
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mutations compromise neuronal cells that are crucial for their high biocompatibility and low toxicity properties
memory, cognition, and behavior. The expression of make them an ideal treatment option to be used in in vivo
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APP is tightly regulated by microRNA (miRNA), notably and in vitro studies. Various studies have shown that
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miRNA-193b. Reduced expression of miRNA-193b GQDs exhibit very low cytotoxicity in vitro due to their
correlates with increased APP levels in the cerebrospinal small size and high oxygen content. 72,73 On the other
fluid and blood-derived exosomes of AD patients. This hand, in vivo studies using GQDs have reported no
suggests that miRNA-193b can be used as a biomarker for significant material accumulation in major organs, with
AD diagnosis and for monitoring disease progression. 63,64 rapid clearance observed even in scenarios with multiple
dosing. GQDs have also been applied in various therapies,
8.1. Significance of QDs in the treatment of AD such as photodynamic therapy, highlighting their ability
In an in vivo experiment, Xiao et al. administered the in biomedical applications. However, further research is
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combination of GQDs and peptides, including glycine- needed to understand their long-term safety and develop
proline-glutamate, to transgenic mice with APP and standardized measures for assessing toxicity in clinical
presenilin 1. They observed a reduction in platelets and applications.
the potential of this combination to prevent Aβ1-42 fibril Another significant area is the application of GQDs in
formation. A decrease in inflammatory cytokines, such ApoE diagnosis and the investigation of their mechanistic
as tumor necrosis factor α and interleukin 6, was linked processes as treatment therapies. Due to their high
to the improvement of memory in the mice. One of the sensitivity, GQDs can be utilized as effective biomarkers
main characteristics of AD is the accumulation of tau in AD diagnosis to examine ApoE isoforms associated with
protein into NFTs, and GQDs represent a major type of AD risk. The detection of ApoEε4 – a genetic risk factor
nanomaterial that addresses difficulties associated with for AD – in the brain or in bodily fluids using GQDs
small-molecule therapy for AD. The small size of GQDs holds potential for risk prediction and early diagnosis.
provides them a special ability to penetrate biological The fluorescence optical properties of GQDS have the
barriers, such as the blood–brain barrier, for targeted capability to develop highly sensitive assays to analyze
delivery of drugs or imaging agents to the brain. Studies specific ApoE isoforms. In a recent study, a QD-based
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have shown the potential of GQDs in obstructing the probe conjugated with an anti-Aβ protein antibody was
membrane interactions of Aβ in their various forms – injected into the cerebrum and ventricles of mutated
monomers, oligomers, and fibrils – thereby preventing human APP695swe and App717 V-F transgenic mice, as
peptide–peptide aggregation involved in the formation of well as healthy mice. Immunohistochemical visualization
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toxic amyloid plaques. GQDs restore membrane fluidity in revealed that Aβ protein was distributed within the
neuroblastoma SH-SY5Y cells disrupted by Aβ oligomers, hippocampus area of APP transgenic mice. In these mice,
the most neurotoxic form of Aβ. This was demonstrated fluorescence was majorly observed in the hippocampus,
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using confocal fluorescence microscopy and discrete sagittal septum, cerebral cortex, and striatum. In addition,
molecular dynamics simulations, which showed favorable the fluorescence intensity was higher compared to that
interactions between GQDs and Aβ species. These in healthy mice. 76-78 This finding suggests that a QD-Aβ-
findings highlight the role of GQDs as effective agents in antibody conjugated probe can be utilized to visualize
breaking down Aβ aggregation pathways and mitigating intracerebral Aβ accumulation in vivo. According to
downstream neurodegenerative cascade of events. Walton-Raaby et al., there are two types of GQDs—
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In addition to targeting Aβ, GQDs also interact with tau GQD7 and GQD28—found to bind to different forms
protein aggregates, another hallmark of AD. Studies have of tau protein, such as monomers, PHFs, and straight
shown that GQD variants, such as GQD7 and GQD28, filaments. GQD28 exhibits a considerable affinity for the
bind to specific pathological regions of tau protein, protofibril interface—a major site for the disaggregation
including PHFs and straight filaments. For instance, the activity of epigallocatechin-3-gallate. On the other hand,
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GQD28 shows a high affinity for the protofibril interface, GQD7 exhibits a stronger interaction with the PHF6.
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which is an important site for tau disaggregation and Studies have also reported that GQD binding sites could
filament disassembly, thereby inhibiting the progression of be used for the detection, disassembly, and prevention of
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AD via a dual mechanism (Aβ and tau). 68,69 Furthermore, tau protein aggregation in AD. Furthermore, in imaging
GQDs exhibit oxidative stress-reducing properties by techniques, GQDs can be utilized as a contrast agent, such
scavenging the stimulators of neuronal damage—reactive as in fluorescence microscopy, for visualization of neurons
oxygen species. These redox-active properties play a and visible pathological changes associated with AD.
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fundamental role in protecting neurons from oxidative They can be functionalized with specific ligands to target

Volume 4 Issue 4 (2025) 23 doi: 10.36922/an.7087