Pathogenesis of Cognitive Decline Following Therapeutic Irradiation for Head and Neck Tumors

Impaired human hippocampal neurogenesis after treatment for central nervous system malignancies

“…These findings, limited as they are to a single case, are consistent with the preclinical data from rodent models of cranial radiation therapy 14,15 and support the idea that radiation exposure accounts for a significant portion of the observed hippocampal pathology. Radiation exposure to the medial temporal lobes consistently emerges as a critical risk factor for cognitive decline after treatment, 20 and our findings provide a potential cellular basis for that observation.…”

Impaired human hippocampal neurogenesis after treatment for central nervous system malignancies

“…These findings, limited as they are to a single case, are consistent with the preclinical data from rodent models of cranial radiation therapy 14,15 and support the idea that radiation exposure accounts for a significant portion of the observed hippocampal pathology. Radiation exposure to the medial temporal lobes consistently emerges as a critical risk factor for cognitive decline after treatment, 20 and our findings provide a potential cellular basis for that observation.…”

Cognitive Function Before and After Intensity-Modulated Radiation Therapy in Patients With Nasopharyngeal Carcinoma: A Prospective Study

“…However, a large portion of patients complaining of poor memory have no radiologic evidence of brain necrosis. Although the cognitive deficits may be subtle, many domains of cognition are likely to be affected (4,12,32). In this study no patient had the finding of temporal lobe necrosis on follow-up images.…”

Emerging Roles of Glycogen Synthase Kinase 3 in the Treatment of Brain Tumors

“…This cognitive decline observed may be due to IR-induced damage to the hippocampus, a critical area of the brain responsible for learning and memory (Yazlovitskaya et al, 2006). Consistent with these findings, radiation to the hippocampus is associated with more pronounced cognitive deficits compared with radiation to other areas of the brain (Abayomi, 2002). As GSK3 inhibition has been shown to protect neurocognitive function following cranial irradiation, the therapeutic value of GSK3 in cancer may also be related, in part, to its effects on DNA repair and its emerging role in neuroprotection of normal neuronal tissues from radiation induced apoptosis (Thotala et al, 2008; Yang et al, 2009, 2011).…”

Impaired human hippocampal neurogenesis after treatment for central nervous system malignancies

“…These findings, limited as they are to a single case, are consistent with the preclinical data from rodent models of cranial radiation therapy 14,15 and support the idea that radiation exposure accounts for a significant portion of the observed hippocampal pathology. Radiation exposure to the medial temporal lobes consistently emerges as a critical risk factor for cognitive decline after treatment, 20 and our findings provide a potential cellular basis for that observation.…”

Cognitive Function Before and After Intensity-Modulated Radiation Therapy in Patients With Nasopharyngeal Carcinoma: A Prospective Study

“…However, a large portion of patients complaining of poor memory have no radiologic evidence of brain necrosis. Although the cognitive deficits may be subtle, many domains of cognition are likely to be affected (4,12,32). In this study no patient had the finding of temporal lobe necrosis on follow-up images.…”

Emerging Roles of Glycogen Synthase Kinase 3 in the Treatment of Brain Tumors

“…This cognitive decline observed may be due to IR-induced damage to the hippocampus, a critical area of the brain responsible for learning and memory (Yazlovitskaya et al, 2006). Consistent with these findings, radiation to the hippocampus is associated with more pronounced cognitive deficits compared with radiation to other areas of the brain (Abayomi, 2002). As GSK3 inhibition has been shown to protect neurocognitive function following cranial irradiation, the therapeutic value of GSK3 in cancer may also be related, in part, to its effects on DNA repair and its emerging role in neuroprotection of normal neuronal tissues from radiation induced apoptosis (Thotala et al, 2008; Yang et al, 2009, 2011).…”

Impaired human hippocampal neurogenesis after treatment for central nervous system malignancies

“…These findings, limited as they are to a single case, are consistent with the preclinical data from rodent models of cranial radiation therapy 14,15 and support the idea that radiation exposure accounts for a significant portion of the observed hippocampal pathology. Radiation exposure to the medial temporal lobes consistently emerges as a critical risk factor for cognitive decline after treatment, 20 and our findings provide a potential cellular basis for that observation.…”

Cognitive Function Before and After Intensity-Modulated Radiation Therapy in Patients With Nasopharyngeal Carcinoma: A Prospective Study

“…However, a large portion of patients complaining of poor memory have no radiologic evidence of brain necrosis. Although the cognitive deficits may be subtle, many domains of cognition are likely to be affected (4,12,32). In this study no patient had the finding of temporal lobe necrosis on follow-up images.…”

Emerging Roles of Glycogen Synthase Kinase 3 in the Treatment of Brain Tumors

“…This cognitive decline observed may be due to IR-induced damage to the hippocampus, a critical area of the brain responsible for learning and memory (Yazlovitskaya et al, 2006). Consistent with these findings, radiation to the hippocampus is associated with more pronounced cognitive deficits compared with radiation to other areas of the brain (Abayomi, 2002). As GSK3 inhibition has been shown to protect neurocognitive function following cranial irradiation, the therapeutic value of GSK3 in cancer may also be related, in part, to its effects on DNA repair and its emerging role in neuroprotection of normal neuronal tissues from radiation induced apoptosis (Thotala et al, 2008; Yang et al, 2009, 2011).…”