Activation of cMet signaling as a novel treatment for cognitive deficits and neuroinflammation after traumatic brain injury

The Devilbiss Lab at Rowan University focuses on understanding and treating cognitive dysfunction following concussion and mild traumatic brain injury (mTBI). Building on the lab's expertise in neuromodulators such as norepinephrine and dopamine and on investigations of the locus coeruleus-norepinephrine system, this project examines activation of cMet signaling as a novel therapeutic strategy to address cognitive deficits and neuroinflammation after traumatic brain injury. The Devilbiss Lab studies how neuromodulatory systems regulate neuronal communication and information processing across large networks, recognizing that attention, memory and sensory processing depend on tightly regulated levels of neuromodulators; deviations impair these functions. Utilizing the lab's established combination of single neuron and multichannel electrophysiology, computational neuroscience, neuropharmacology, neurochemistry, anatomy, and behavioral techniques, researchers will interrogate how cMet pathway modulation interacts with neuromodulatory control to restore or enhance cognitive performance in awake, behaving rat models of concussion and mTBI.

This project situates cMet signaling within the broader context of neuromodulatory regulation of cognition. The lab's prior focus on the locus coeruleus-norepinephrine system and its role in post-injury cognitive sequelae provides a foundation for exploring how cMet activation might mitigate dysregulated neurotransmitter dynamics, reduce neuroinflammatory responses, and improve behavioral outcomes. Experimental approaches will leverage electrophysiological recordings to measure neuronal representation and network-level processing, while computational analyses will characterize changes in information coding associated with injury and with putative cMet-targeted interventions. Neuropharmacological manipulations will allow controlled activation of cMet signaling in vivo, and neurochemical assays will assess subsequent changes in neuromodulator levels and inflammatory markers. Anatomical studies will document structural and cellular changes, and behavioral paradigms will evaluate attention, memory, and sensory processing across recovery trajectories.

A key translational component of the lab's work is comparing animal-model findings to clinical data obtained through industry partnerships. By aligning preclinical measures of neural function and behavior with clinical observations, the project aims to develop objective biomarkers of brain injury and recovery that can guide therapeutic development. The exploration of cMet activation as a treatment modality is framed as a complementary strategy to existing neuromodulatory approaches: rather than replacing investigations into norepinephrine and dopamine systems, it seeks to integrate cMet pathway modulation into a multifaceted therapeutic framework for cognitive impairment after concussion and mTBI.

Ultimately, the project as conducted by Devilbiss and colleagues aims to move from mechanistic understanding toward actionable treatment strategies. Through rigorous, multi-level experimentation and translational alignment with clinical data, the research will investigate whether targeted activation of cMet signaling can meaningfully reduce neuroinflammation, normalize neuromodulatory function, and restore cognitive capacities compromised by traumatic brain injury. The work is grounded in the lab's methodological strengths and its overarching goal to produce objective measures of injury and recovery while developing viable interventions for post-concussion cognitive impairment.