Molecular links between inflammatory bowel disease and Alzheimer’s disease through immune signaling and inflammatory pathways

🎖️ Top 10% JournalJan 2, 2026World journal of gastroenterology

Molecular connections between inflammatory bowel disease and Alzheimer's disease through immune and inflammation pathways

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Alzheimers & Treatments on OpenScience ↗PubMed ↗DOI ↗

Abstract

Chronic colitis, a hallmark of inflammatory bowel disease, accelerates amyloid-β pathology and cognitive impairment in transgenic mouse models.

Inflammatory bowel disease, which includes ulcerative colitis and Crohn's disease, is associated with an increased risk of Alzheimer's disease.
Systemic inflammation linked to inflammatory bowel disease may disrupt the gut-brain axis, contributing to the development of amyloid-β plaques.
Evidence suggests that chronic inflammation can enhance cognitive decline and neurodegeneration.
Current understanding of the molecular mechanisms connecting inflammatory bowel disease and Alzheimer's disease remains limited.
Age-related gut inflammation and dysbiosis may worsen Alzheimer's disease pathology, indicating a need for targeted treatments.
Therapies that address inflammation in inflammatory bowel disease could potentially mitigate the progression of Alzheimer's disease.

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Inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD), has been increasingly associated with the progression of neurodegenerative disorders, particularly Alzheimer's disease (AD). Emerging data from population-based meta-analyses andexperimental models demonstrate that systemic inflammation associated with IBD exacerbates disruption of the gut-brain axis (GBA). This disruption promotes the deposition of amyloid-β (Aβ) plaques, and cognitive decline. Together, these effects contribute to the progression of AD. Chronic colitis, a hallmark of IBD, accelerates Aβ pathology and induces cognitive impairment in transgenic mouse models, providing direct evidence of the detrimental effects of gut inflammation on neurodegeneration. Although numerous clinical and meta-analytical studies have examined the prevalence of AD in IBD patients, the molecular mechanisms underlying this association remain inadequately understood. In particular, the roles of immune regulation and GBA interactions require further investigation. This review aims to critically compile current evidence that elucidates the shared pathophysiological mechanisms underlying this association, such as chronic systemic inflammation, gut dysbiosis, and dysregulated immune responses. Although anti-inflammatory therapies, probiotics, and modulation of the gut microbiota have the potential to reduce the risk of AD and slow its progression, age-related gut inflammation and dysbiosis can aggravate AD pathology. This underscores the necessity for treatments that specifically target IBD-associated inflammation to limit AD progression. In addition, this review also meticulously examines how immune signaling and regulatory pathways in IBD, such as triggering receptor expressionmyeloid cell receptor activation; NLRP3 inflammasome-driven inflammation; disrupted interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha (TNF-α) signaling; and elevated C-reactive protein levels, contribute to increased amyloidogenesis. This paper proposes a comprehensive framework for therapeutic strategies targeting IBD-related inflammation and elucidates their potential to attenuate the progression of AD. in vivo via

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