CRISPR/Cas Mediated Intelligent Devices to Quantify Neuroinflammation in Parkinson's Disease

Neuroinflammation is increasingly recognized as a critical driver in the onset and progression of Parkinson’s disease (PD), Modern analytical science faces the challenge to continuously quantify inflammatory processes. Bridging these significant gaps in knowledge requires innovative tools and techniques that push the boundaries of scientific exploration. While advances in CRISPR/Cas-based biosensors have unlocked transformative possibilities, their practical application is hindered by challenges such as multiplex detection, real-time monitoring, and integration into efficient, sample-to-answer systems. This talk will present our current research in developing CRISPR/Cas-mediated intelligent devices aiming to create tools capable of real-time, highly sensitive detection of neurochemical signals.

Cytokines participate in the immune response and act as important mediators associated with the communication network of the neuroinflammation in PD. Cytokine levels orchestrate the time course of PD progression in a host. Thus, tracking the level of multiple cytokines in the brain continuously would advance our understanding of the relationship between PD development and inflammation, enhancing our ability to preciously treat the PD. We developed a CRISPR-based point-of-care diagnostic platform on glass fiber that provided visual fluorescent signal output with simplified user operation of an adjunctive integrated fluorescence device. It enables sample input to answer out of multiple cytokine’s concentration in one sample simultaneously within 75 mins with highly sensitive (<1 pg/mL), specific performance and low sample volume requirement. The CRISPR/Cas based analytical system was successfully applied for detection of more than five cytokines in clinical serum samples from PD and atypical parkinsonian disorders. With the aid of machine learning, it was observed that elevated levels of pro-inflammatory cytokines such as TNF-α, IL-10, and IFN-ϒ contributed to PD.