Chemotherapy-induced cognitive changes remain poorly understood, but several candidate mechanisms have been proposed. These include shared genetic risk factors for cancer and cognitive problems, such as low-efficiency efflux pumps, DNA repair deficits, and deregulated immune responses, which may interact with chemotherapy effects. Genetic factors modulate neural repair capacity and neurotransmitter activity, as well as antioxidant capacity, which may influence cognitive function. Studies show that chemotherapy affects cognitive functioning, particularly in domains like working memory and executive function, but not remote memory retrieval. Long-term cognitive changes are observed in a subgroup of cancer survivors, and these may be linked to structural and functional brain changes, as well as reduced P-300 event-related brain potential. Chemotherapy can cross the blood-brain barrier, leading to CNS disorders, and genetic variability in drug transporters like MDR1 may affect drug levels in the brain. DNA damage and oxidative stress are also implicated, with chemotherapy causing DNA damage that may contribute to cognitive decline. DNA repair deficits and telomere shortening may increase cancer risk and cognitive dysfunction. Cytokine deregulation may also play a role, with chemotherapy-induced cytokine changes linked to cognitive impairment. Genetic polymorphisms in genes like APOE and BDNF may influence cognitive outcomes. Neurotransmitter polymorphisms, such as COMT, affect dopamine metabolism and cognitive function. Hormonal changes, including reduced estrogen and testosterone, may also impact cognitive function. These mechanisms suggest that chemotherapy-induced cognitive changes may result from multiple interacting factors, including DNA damage, oxidative stress, cytokine activity, and genetic predispositions. Further research is needed to clarify these mechanisms and develop targeted interventions.Chemotherapy-induced cognitive changes remain poorly understood, but several candidate mechanisms have been proposed. These include shared genetic risk factors for cancer and cognitive problems, such as low-efficiency efflux pumps, DNA repair deficits, and deregulated immune responses, which may interact with chemotherapy effects. Genetic factors modulate neural repair capacity and neurotransmitter activity, as well as antioxidant capacity, which may influence cognitive function. Studies show that chemotherapy affects cognitive functioning, particularly in domains like working memory and executive function, but not remote memory retrieval. Long-term cognitive changes are observed in a subgroup of cancer survivors, and these may be linked to structural and functional brain changes, as well as reduced P-300 event-related brain potential. Chemotherapy can cross the blood-brain barrier, leading to CNS disorders, and genetic variability in drug transporters like MDR1 may affect drug levels in the brain. DNA damage and oxidative stress are also implicated, with chemotherapy causing DNA damage that may contribute to cognitive decline. DNA repair deficits and telomere shortening may increase cancer risk and cognitive dysfunction. Cytokine deregulation may also play a role, with chemotherapy-induced cytokine changes linked to cognitive impairment. Genetic polymorphisms in genes like APOE and BDNF may influence cognitive outcomes. Neurotransmitter polymorphisms, such as COMT, affect dopamine metabolism and cognitive function. Hormonal changes, including reduced estrogen and testosterone, may also impact cognitive function. These mechanisms suggest that chemotherapy-induced cognitive changes may result from multiple interacting factors, including DNA damage, oxidative stress, cytokine activity, and genetic predispositions. Further research is needed to clarify these mechanisms and develop targeted interventions.