Faculty mentor/PI email address
aitawf@rowan.edu, lecomte@rowan.edu, iannuzzelli@rowan.edu
Gut Microbiota Dysbiosis in Down Syndrome: Implications for Gastrointestinal and Neurological Health
Keywords
microbiome, down syndrome, bacteria, inflammation
Date of Presentation
5-6-2026 12:00 AM
Poster Abstract
Down syndrome (DS) is the most common autosomal aneuploidy and has strong associations with increased gastrointestinal, neurological, and immune disorders. Emerging evidence suggests that gut microbiota dysbiosis may play a prominent role in disorders of gut-brain interaction, including constipation and irritable bowel syndrome affecting over half of individuals with DS. This review examines how gut microbiota alterations can contribute to chronic systemic inflammation and neurological manifestations in DS. Included articles were published between 2014 and 2025 and evaluated microbiota composition, inflammatory markers, and gastrointestinal or neurological outcomes in human or animal models of DS.
Across seven studies, characteristic microbiome shifts included increases in Prevotella and Sutterella with decreases in Firmicutes and Roseburia, alongside other short-chain fatty acid-producing species. Additionally, a sustained increase in pro-inflammatory cytokines (ie, interleukin-6, tumor necrosis factor-alpha, etc.) supported the presence of sustained systemic inflammation. The combination of these findings revealed reduced butyrate (a major energy source for colonic cells) availability, impaired antioxidant defense mechanisms, and accumulation of neurotoxic metabolites including lipopolysaccharide and amyloid-beta. Together, these alterations compromise intestinal and blood-brain barrier integrity, promote neuroinflammation, and may contribute to early Alzheimer-like pathology in DS.
Gut dysbiosis also appears to exacerbate gastrointestinal dysfunction, suggesting a link between microbial imbalance and clinical symptoms. Given these findings, microbiome-targeted therapies such as probiotics, dietary interventions, and fecal microbiota transplantation represent promising avenues for improving both gastrointestinal and neurological health in DS. Future investigations are needed to clarify causal pathways to guide therapeutic development.
Disciplines
Congenital, Hereditary, and Neonatal Diseases and Abnormalities | Digestive System Diseases | Medicine and Health Sciences | Nervous System Diseases
Included in
Congenital, Hereditary, and Neonatal Diseases and Abnormalities Commons, Digestive System Diseases Commons, Nervous System Diseases Commons
Gut Microbiota Dysbiosis in Down Syndrome: Implications for Gastrointestinal and Neurological Health
Down syndrome (DS) is the most common autosomal aneuploidy and has strong associations with increased gastrointestinal, neurological, and immune disorders. Emerging evidence suggests that gut microbiota dysbiosis may play a prominent role in disorders of gut-brain interaction, including constipation and irritable bowel syndrome affecting over half of individuals with DS. This review examines how gut microbiota alterations can contribute to chronic systemic inflammation and neurological manifestations in DS. Included articles were published between 2014 and 2025 and evaluated microbiota composition, inflammatory markers, and gastrointestinal or neurological outcomes in human or animal models of DS.
Across seven studies, characteristic microbiome shifts included increases in Prevotella and Sutterella with decreases in Firmicutes and Roseburia, alongside other short-chain fatty acid-producing species. Additionally, a sustained increase in pro-inflammatory cytokines (ie, interleukin-6, tumor necrosis factor-alpha, etc.) supported the presence of sustained systemic inflammation. The combination of these findings revealed reduced butyrate (a major energy source for colonic cells) availability, impaired antioxidant defense mechanisms, and accumulation of neurotoxic metabolites including lipopolysaccharide and amyloid-beta. Together, these alterations compromise intestinal and blood-brain barrier integrity, promote neuroinflammation, and may contribute to early Alzheimer-like pathology in DS.
Gut dysbiosis also appears to exacerbate gastrointestinal dysfunction, suggesting a link between microbial imbalance and clinical symptoms. Given these findings, microbiome-targeted therapies such as probiotics, dietary interventions, and fecal microbiota transplantation represent promising avenues for improving both gastrointestinal and neurological health in DS. Future investigations are needed to clarify causal pathways to guide therapeutic development.