The Role of TGF-β in Cognitive Decline Associated with Radiotherapy in Brain Tumor

Abstract

Cognitive decline is a late adverse event in brain tumor survivors. The patients receiving radiation treatment exhibit a wide range of damage and impairment in attention, memory, and executive function compared to the untreated group. After radiation treatment, various changes are observed in astrocytes, oligodendrocytes, white matter, and vasculature. The major affected areas are the hippocampus and prefrontal cortex. Neurogenesis impairment is one of the primary mechanisms responsible for cognitive dysfunction. Various cytokines and growth factors are responsible for inducing apoptosis of neural cells, which results in impaired neurogenesis in response to radiotherapy. Transforming growth factor (TGF-β) is one of the key cytokines released in response to radiation. TGF-β plays a major role in neuronal apoptosis through various pathways such as the MAP kinase pathway, JAK/STAT pathway, and protein kinase pathway. In contrast, activation of the ALK5 pathway via TGF-β improves neurogenesis. So, the current review article focuses on the detailed effects of TGF-β on neuronal cells concerning radiation exposure. This in-depth knowledge will help researchers focus more on the TGF-β pathway and come up with new treatment schedules which will help reduce cognitive dysfunctions in brain tumor patients produced as a result of radiation therapy.