Abstract
Radiation therapy is the most effective non-surgical treatment of primary brain tumors and metastases. Preclinical studies have provided valuable insights into pathogenesis of radiation-induced injury to the central nervous system. Radiation-induced brain injury can damage neuronal, glial and vascular compartments of the brain and may lead to molecular, cellular and functional changes. Given its central role in memory and adult neurogenesis, the majority of studies have focused on the hippocampus. These findings suggested that hippocampal avoidance in cranial radiotherapy prevents radiation-induced cognitive impairment of patients. However, multiple rodent studies have shown that this problem is more complex. As the radiation-induced cognitive impairment reflects hippocampal and non-hippocampal compartments, it is of critical importance to investigate molecular, cellular and functional modifications in various brain regions as well as their integration at clinically relevant doses and schedules. We here provide a literature overview, including our previously published results, in order to support the translation of preclinical findings to clinical practice, and improve the physical and mental status of patients with brain tumors.
Highlights
Preclinical studies have provided valuable knowledge about the pathogenic mechanisms involved in radiation-induced injury
Cognitive impairment occur in 50%–90% of adult patients with brain tumors who survive more than six months after fractionated irradiation, frequently in the absence of corresponding anatomical abnormalities [1]
Single irradiation with a dose of 40 Gy led to less obvious decrease of oligodendrocyte type-2 astrocytes (O-2A) cells (30%–35%) and their numbers remained constant with time
Summary
Preclinical studies have provided valuable knowledge about the pathogenic mechanisms involved in radiation-induced injury. During the past 10 years, several preclinical studies have demonstrated that interventional therapies that modulate neuroinflammation can prevent or ameliorate radiation-induced functional deficits. Translating these novel preclinical findings to clinical practice has the potential to improve the physical and mental status in patients with brain primary tumors and metastases. Late radiation-induced changes are often progressive and irreversible They are characterized by leukoencephalopathy syndrome, vascular abnormalities (i.e., teleangiectasias, endothelial thickening, hyalinization, fibrinoid deposition, thrombosis and occlusion of vessels), true radionecrosis, brain parenchyma calcifications and increasing white matter abnormalities. In this review we characterize the previous and recent outcomes of preclinical studies dealing with mechanisms or consequences of the radiation-induced brain injury and potential neuroprotective interventions
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