Impact of gut microbiota dysbiosis on cancer-related cognitive impairment

Abstract

Advances in cancer treatment have significantly improved survival rates among patients. However, many also experience cognitive changes as an adverse effect of both the disease and its therapies. This phenomenon is observed not only in patients with central nervous system (CNS) tumors but also in those with tumors located outside the CNS, and across all age groups.

Studies of patients with non-CNS malignancies have shown that cancer-related cognitive impairment (CRCI)—including deficits in memory, attention, executive function, and processing speed—affects up to 75% of patients during treatment and up to 30% prior to treatment. The gut–brain axis (GBA) is a complex, bidirectional communication system that has been identified as a potential link between neurodegeneration and alterations in the gut microbiota, influencing various brain functions. Gut microbes can produce a range of molecules, such as neurotransmitters, that enable neurochemical interactions with the host’s enteric, central, and autonomic nervous systems. While the specific changes may vary, cancer treatment-induced disruptions in the gut microbiota can compromise its protective and immunomodulatory roles, leading to increased production of harmful metabolites by pathogenic microbes. The role of the gut–brain axis and gut microbiota in CRCI remains largely unknown among many cancer care specialists. CRCI is often overlooked by healthcare professionals. The primary objective of this review is to highlight this underrecognized issue. Research into the cancer microbiota is an emerging field gaining importance in clinical oncology. Several studies have documented significant changes in gut microbial composition following cancer treatments, with reduced microbial diversity being the most reported alteration. This review synthesizes current clinical and preclinical evidence linking gut microbiota to CRCI, with a particular focus on future research directions—especially concerning disruptions in the gut–brain axis.