Functionalized Carbon Quantum Dots: A Promising Nanomaterial For Investigating Their Potential In Neurodegenerative Disease Treatment

Neurodegenerative diseases such as Parkinson's Disease (PD), Alzheimer's Disease (AD), and Huntington's Disease (HD) remain incurable, despite extensive research into therapeutic development. In the United States of America, the annual cost of PD and AD in terms of patient care and lost productivity is approximately $200 billion. Consequently, there is a critical and unaddressed need for the development of innovative drugs and drug delivery systems that can decelerate, stop, or ideally reverse neurodegenerative diseases. The dissertation presented here focuses on devising strategies to target PD through multiple mechanisms, including the inhibition of protein aggregation and the reduction of oxidative stress. This approach is significant because prior studies have shown that protein aggregation and oxidative stress mutually enhance each other's detrimental effects in PD, leading to the death of neurons. In this study, we demonstrate that carbon nanodots CNDs disrupt the conversion of soluble amyloid proteins into toxic forms in a dose-responsive manner, achieving up to a 70% reduction in fibril formation at a concentration of 5 mg/mL. Additionally, CNDs did not affect mitochondrial membrane potential nor trigger apoptosis at concentrations up to 5 mg/mL. Notably, CNDs were effective in scavenging reactive oxygen species (ROS) even at low concentrations, with a 50% decrease in ROS at 100µg/mL when exposed to free radical generators. These findings suggest that CNDs have neuroprotective capabilities that could play a role in addressing complex neurodegenerative conditions like PD. The tolerance of SHSY-5Y cells to CNDs and their capacity to recover from induced apoptosis further corroborate this potential. Alongside biocompatibility data, CNDs present a promising single-step solution for the treatment of neurodegenerative diseases.