Carbon Quantum Dots in Alzheimer’s Disease

Abstract: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder primarily affecting the elderly, characterized by cognitive decline and memory impairment. The accumulation of amyloid- β (Aβ) peptides, particularly Aβ42, into neurotoxic plaques is a key pathological hallmark, leading to neuronal damage and cognitive dysfunction. Given the limited efficacy of existing treatments, targeting Aβ aggregation presents a promising therapeutic approach. This review explores the potential of carbon quantum dots (CQDs) synthesized via pulsed laser ablation (PLA) and functionalized with targeting agents for disrupting Aβ aggregation and mitigating AD pathology. Selenium-doped CQDs (SeCQDs) and aptamer-functionalized CQDs (Apta@CQDs) demonstrate specific interactions with Aβ42, reducing cytotoxicity and enhancing biocompatibility. CQDs exert neuroprotective effects by minimizing oxidative stress and modulating Aβ aggregation through red-light-responsive phototherapy. In vitro studies confirm their ability to inhibit β-sheet formation and prevent Aβ- induced toxicity, while in vivo models, including Caenorhabditis elegans and 5xFAD mice, show reduced Aβ deposition, improved cognitive function, and enhanced neuronal survival. CQDs offer a multimodal therapeutic strategy for AD by disrupting Aβ aggregation, reducing oxidative stress, and enhancing neuroprotection. Their unique physicochemical properties highlight their potential as innovative, non-invasive nanodrugs for AD treatment, warranting further exploration in clinical applications.