Gut-Brain Interactions in Neurodegeneration: Microbiota's Role in Cognitive Aging

The gut-brain axis is an intricate communication network between the gastrointestinal tract and the central nervous system. Recent advancements have shed light on how the composition and activity of the gut microbiome can influence the development and course of neurodegenerative conditions frequently seen in aging, such as Alzheimer's disease, Parkinson’s disease, Mild Cognitive Impairment, and various forms of Dementia. Emerging evidence highlights mechanisms involving microbiota-derived metabolites, immune system modulation, and neural signaling pathways as principal routes through which the gut influences brain health and function. Despite accelerating progress, there remain substantial gaps in our understanding of the exact causal mechanisms and their translation into viable prevention or treatment approaches for neurodegenerative diseases. Notably, questions persist regarding individual variation in microbiome profiles, the temporal dynamics of gut-brain communication throughout aging, and the potential to harness these insights for therapeutic interventions aimed at cognitive preservation.

This Research Topic aims to provide a comprehensive exploration into the multifaceted roles of the gut microbiome in the initiation and progression of neurodegenerative diseases among older adults. Through targeted investigation of microbial contributions to neurodegeneration, the objective is to identify novel molecular pathways, risk factors, and innovative intervention strategies that leverage the gut-brain axis. By advancing our understanding of these interconnected systems, this effort seeks to inform the development of preventive, diagnostic, and therapeutic strategies addressing cognitive decline linked to neurodegeneration in aging populations.

This Research Topic is focused on elucidating the boundaries between gut microbial dynamics and neurodegenerative pathophysiology by interrogating both mechanistic and translational questions. We welcome original research, reviews, minireview and perspectives articles addressing, but not limited to, the following thematic areas:

o Mechanisms of microbial influence on neural pathways
o Role of gut-derived metabolites in cognitive decline
o Impact of gastrointestinal inflammation on neurodegeneration
o In vitro digestion studies on gut microbiota modulation
o Preclinical studies of gut microbiota interventions
o Clinical applications and therapeutic strategies targeting the microbiota

Article types and fees

This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

• Brief Research Report
• Case Report
• Clinical Trial
• Community Case Study
• Conceptual Analysis
• Curriculum, Instruction, and Pedagogy
• Data Report
• Editorial
• FAIR² Data
• ... View all formats

Articles that are accepted for publication by our external editors following rigorous peer review incur a publishing fee charged to Authors, institutions, or funders.

Article types

This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

• Brief Research Report
• Case Report
• Clinical Trial
• Community Case Study
• Conceptual Analysis
• Curriculum, Instruction, and Pedagogy
• Data Report
• Editorial
• FAIR² Data
• General Commentary
• Hypothesis and Theory
• Methods
• Mini Review
• Opinion
• Original Research
• Perspective
• Registered Report
• Review
• Study Protocol
• Systematic Review
• Technology and Code

Keywords: gut-brain axis, In vitro digestion models, Microbiota-gut-brain communication, Neurodegeneration, Age-related diseases, Alzheimer's disease, Parkinson's disease, Gut microbiota modulation, Aging

Important note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.