Parvalbumin interneurons contribute to spontaneous hemodynamic fluctuations.

Colorectal cancer (CRC) ranks among the most prevalent tumours of the digestive system and stands as the second leading cause of cancer-related deaths worldwide (Refs , ). Emerging evidence underscores the contribution of diets deficient in dietary fibre, whole grains and other protective nutrients, along with adverse lifestyle patterns, to the rising incidence and mortality associated with CRC, which remains a major public health concern (Ref. ). The disease develops from benign or precancerous polyps in the majority of cases, which gradually transform over several years, eventually infiltrating the bowel wall, spreading to adjacent lymph nodes or metastasizing to distant organs. This prolonged progression frequently results in delayed diagnosis, whereas early detection and polypectomy of precancerous polyps can prevent CRC progression (Ref. ). Colon polyps can be classified into low-risk and high-risk categories based on their potential to progress to CRC. This classification is essential for determining appropriate screening intervals and prevention strategies (Ref. ). Based on their growth patterns, current histological practices categorize these lesions into two main types: serrated polyps and adenomatous polyps (APs). APs are further divided into three subtypes: villous polyps (VP), tubulovillous polyps (TVP) and tubular adenomas (TA). Similarly, serrated polyps are classified into hyperplastic polyps (HP), sessile serrated adenomas (SSA synonyms: sessile serrated lesions or polyps) and traditional serrated adenomas (TSA) (Refs –). Therefore, it is crucial to identify the risk factors associated with colorectal polyps (CPs) based on their histological characteristics to enhance prevention and management strategies. CRC risk factors can be classified into non-modifiable and modifiable risk factors. Among the non-modifiable factors are characteristics such as ethnicity, sex and age, alongside hereditary mutations and certain medical conditions like inflammatory bowel diseases (IBD), cystic fibrosis and acromegaly (Refs –). Research indicates that about 5–10% of CRC instances are linked to known genetic backgrounds, while the rest occur in individuals without any notable family history or genetic predisposition (Ref. ). In contrast, modifiable risk factors are related to lifestyle choices, such as physical inactivity, obesity and dietary habits. Additionally, smoking and alcohol use have been associated with an elevated risk of developing CRC (Refs –). Moreover, the gut microbiome’s vast array of bacteria has sparked interest in how infectious agents may contribute to cancer development. This growing body of research underscores the complex interplay between genetic factors, environmental exposures and microbial influences in the pathogenesis of CRC (Ref. ). Recent research has indicated a possible connection between infection and its role as a risk factor for adenomatous polyps and CRC (Refs , ). Although primarily inhabit the stomach, studies have revealed a notable correlation between infection and various non-gastric diseases, such as neurodegenerative disorders, IBD, celiac disease, hepatic disorders and CRC (Refs –). Epidemiological evidence underscores a significant association between infection and an increased risk and aggressiveness of CRC (Refs , ), with an odds ratio of 1.32 (95% CI: 1.07–1.61) for any colorectal adenoma and 1.90 (95% CI: 1.05–3.56) for advanced neoplasms and this association remains significant after adjusting for established risk factors such as smoking, alcohol consumption and body mass index (Ref. ). Nevertheless, the specific biological mechanisms that contribute to this heightened risk are still not fully understood.