Journal of Gastrointestinal & Digestive System
Open Access

Colorectal cancer (CRC) and Alzheimer's disease (AD) are two distinct yet interconnected medical conditions that have garnered significant attention in the realm of biomedical research. While CRC primarily affects the gastrointestinal tract, AD is characterized by progressive neurodegeneration. Interestingly, recent studies have highlighted potential links between these diseases, particularly in understanding the risk factors associated with colorectal cancer liver metastasis in a mouse model of Alzheimer's disease. One of the primary risk factors contributing to CRC liver metastasis in Alzheimer's disease is chronic inflammation. In both conditions, inflammatory processes play a pivotal role in disease progression. In AD, neuroinflammation driven by the accumulation of beta-amyloid plaques and tau protein tangles leads to neuronal damage and cognitive decline. Similarly, in CRC, chronic inflammation within the gastrointestinal tract promotes tumor initiation, progression, and metastasis. The interplay between these inflammatory pathways may create a conducive environment for CRC cells to metastasize to the liver in the context of Alzheimer's disease. Moreover, dysregulation of the gutbrain axis has emerged as a potential risk factor linking AD and CRC liver metastasis. The gut microbiota, comprising a complex ecosystem of microorganisms, influences both neurological and gastrointestinal health. In Alzheimer's disease, alterations in the gut microbiome have been observed, contributing to systemic inflammation and neuroinflammation. Concurrently, disruptions in the gut microbiota composition have been implicated in CRC development and metastasis. Thus, the dysbiotic state of the gut microbiome in AD may exacerbate the risk of CRC liver metastasis by modulating immune responses and promoting pro-tumorigenic microenvironments. Furthermore, genetic predispositions and molecular pathways shared between AD and CRC could underlie the increased susceptibility to liver metastasis. For instance, the apolipoprotein E (APOE) gene, commonly associated with AD risk, has also been implicated in CRC progression and metastasis. Additionally, signaling pathways such as Wnt/β-catenin, which are dysregulated in both diseases, play crucial roles in promoting tumor cell migration and invasion, including metastatic spread to distant organs like the liver. The convergence of genetic and molecular factors in AD and CRC pathways may synergistically enhance the metastatic potential of colorectal cancer cells. In the context of therapeutic interventions, addressing these interconnected risk factors holds promise for mitigating CRC liver metastasis in Alzheimer's disease. Targeting chronic inflammation through anti-inflammatory agents or immunomodulatory therapies could dampen the pro-metastatic microenvironment and inhibit tumor progression. Modulating the gut microbiome via prebiotics, probiotics, or fecal microbiota transplantation may restore microbial homeostasis, thereby reducing inflammation and CRC metastatic risk. The understanding the risk factors for colorectal cancer liver metastasis in a mouse model of Alzheimer's disease unveils intricate connections between these seemingly disparate diseases. Chronic inflammation, dysregulated gut-brain axis, shared genetic predispositions, and molecular pathways collectively contribute to heightened susceptibility to CRC metastasis in the context of AD. By elucidating these interrelated mechanisms, novel therapeutic strategies can be devised to intervene early and mitigate the impact of CRC liver metastasis in individuals with Alzheimer's disease. Unveiling risk factors for colorectal cancer liver metastasis in Alzheimer's disease involves understanding the interplay between neurodegenerative and oncological processes. Patients with Alzheimer's disease may have altered immune responses, reduced cellular repair mechanisms, and lifestyle factors that contribute to increased cancer risks. Cognitive impairments could delay cancer diagnosis and treatment, exacerbating metastatic potential.

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The author has no potential conflicts of interest.