6th Edition of World Nursing Science Conference 2026

Abstract

Purpose: This theory-based analysis presents the gut-brain axis (GBA) as a systems-level biological framework for understanding age-related cognitive decline and proposes a nursing-relevant logic model to guide the development of future interventions and clinical research. By linking age-related gut microbiome disruption (dysbiosis) to cognitive outcomes through inflammation, neuroendocrine, and metabolic pathways, the goal is to integrate biological theory with nursing science to promote holistic, non-pharmacologic strategies that help maintain cognitive function in older adults. 
Background: The gut-brain axis describes a bidirectional communication system linking the gastrointestinal and central nervous systems through neural (e.g., vagus nerve), immune (e.g., cytokine signaling), endocrine (e.g., cortisol, gut peptides), and microbial (e.g., short-chain fatty acids, tryptophan metabolites) pathways. Current evidence shows that aging is associated with a decline in gut microbial diversity and compromised gut barrier integrity, increasing vulnerability to chronic low-grade inflammation and systemic oxidative stress. These changes weaken the blood-brain barrier and impair cognitive functions such as episodic memory, processing speed, and executive function, which are early signs of neurodegenerative decline. Factors like chronic inflammation, infections, antibiotic use, and polypharmacy further disrupt the microbiome, adding to the risks of accelerated cognitive decline. 
Logic Linking Theory to Nursing Research: Framing the gut-brain axis as a biological theory of cognitive aging aligns with the nursing sciences’ systems-thinking perspective. Within this framework, dysbiosis becomes a modifiable risk factor embedded in a nursing logic model that targets diet, stress, inflammation, and autonomic regulation. Dietary supplementation emerges as a testable pathway for intervention: a nutrient-based, non-invasive, and non-pharmacological strategy to improve vagal tone, mitigate inflammation, and restore microbial balance. This model encourages nurse scientists to empirically test whether targeted supplementation can influence neurocognitive health, offering measurable endpoints such as memory performance, perceived energy, attention, and mood. The theoretical integration of the GBA into nursing research fosters the development of holistic, preventative interventions grounded in person-centered care, functional maintenance, and cognitive resilience. 
Conclusion: The gut-brain axis framework offers a straightforward and adaptable foundation for nurse-led research into the biological and behavioral determinants of cognitive aging. By creating a logic model that links dysbiosis to cognitive decline and highlights intervention points, this proposed framework bridges complex biological science with practical nursing strategies relevant to diverse older adult populations and care settings. Future research should explore interventions that evaluate the impact of dietary supplements as practical and scalable methods to enhance cognitive health by strengthening the gut-brain axis. 

Learning Outcomes:
•  Identify key gut–brain axis mechanisms and their role in age-related cognitive decline.
•  Translate gut–brain science into a nursing logic model for modifiable interventions.
•  Evaluate supplementation as a nursing-led intervention for cognitive resilience.