White and Gray Matter Abnormalities After Cranial Radiation in Children and Mice

Nieman, Brian J.; Guzman, A. Elizabeth de; Gazdzinski, Lisa M.; Lerch, Jason P.; Chakravarty, M. Mallar; Pipitone, Jon; Strother, Douglas; Fryer, Chris; Bouffet, Éric; Laughlin, Suzanne; Laperrière, Normand; Riggs, Lily; Skocic, Jovanka; Mabbott, Donald

doi:10.1016/j.ijrobp.2015.07.2293

Cited by 54 publications

(48 citation statements)

References 52 publications

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“…Using the mouse, we have been able to describe the extent and localization of brain changes in response to pediatric whole‐brain irradiation (Gazdzinski et al., ), and define the most vulnerable periods in brain development (de Guzman et al., ). Importantly, we directly showed that our findings in these tightly controlled mouse studies relate closely to human brain imaging results (Nieman et al., ).…”

Section: Commentarysupporting

confidence: 78%

MRI to Assess Neurological Function

et al. 2018

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Section: Commentarysupporting

confidence: 78%

MRI to Assess Neurological Function

et al. 2018

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“…Xiong et al (2013) detected lower FA in the temporal region in the post-RT-ED group than that of the pre-RT group. The possible explanation for this discrepancy may be that WM is more sensitive to RT in the early delayed period (Nieman, et al, 2015) and temporal injury may mainly occur in WM in this period. While GM become sensitive to RT and change gradually in the late delayed period.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, the decreased cortical thickness in the PreCG in the post-RT-ED group may indicate RT-induced motor dysfunction, but the increased cortical thickness in the bSTS, LOC, ICC, and bilateral IPC in the post-RT-LD group may reflect that these regions compensate the impaired functions in the early stage to a certain extent. Actually, the increase of cortical thickness measured with MRI is affected by several factors in the cellular level, such as inflammation and gliosis (Nieman, et al, 2015) or central compensation after particular brain nerve deficits over time (zu Eulenburg, et al, 2010). In addition, it is important to emphasize that the interpretations directly relating macroscopic differences in cortical thickness measured with MRI to differences on the cellular level should be taken with caution.…”

Section: Discussionmentioning

confidence: 99%

Radiation-induced abnormal cortical thickness in patients with nasopharyngeal carcinoma after radiotherapy

Lin

Niu

et al. 2017

NeuroImage: Clinical

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Conventional MRI studies showed that radiation-induced brain necrosis in patients with nasopharyngeal carcinoma (NPC) in years after radiotherapy (RT) could involve brain gray matter (GM) and impair brain function. However, it is still unclear the radiation-induced brain morphological changes in NPC patients with normal-appearing GM in the early period after RT. In this study, we acquired high-resolution brain structural MRI data from three groups of patients, 22 before radiotherapy (pre-RT) NPC patients with newly diagnosed but not yet medically treated, 22 NPC patients in the early-delayed stage after radiotherapy (post-RT-ED), and 20 NPC patients in the late-delayed stage after radiotherapy (post-RT-LD), and then analyzed the radiation-induced cortical thickness alteration in NPC patients after RT. Using a vertex-wise surface-based morphometry (SBM) approach, we detected significantly decreased cortical thickness in the precentral gyrus (PreCG) in the post-RT-ED group compared to the pre-RT group. And the post-RT-LD group showed significantly increased cortical thickness in widespread brain regions, including the bilateral inferior parietal, left isthmus of the cingulate, left bank of the superior temporal sulcus and left lateral occipital regions, compared to the pre-RT group, and in the bilateral PreCG compared to the post-RT-ED group. Similar analysis with ROI-wise SBM method also found the consistent results. These results indicated that radiation-induced brain injury mainly occurred in the post-RT-LD group and the cortical thickness alterations after RT were dynamic in different periods. Our findings may reflect the pathogenesis of radiation-induced brain injury in NPC patients with normal-appearing GM and an early intervention is necessary for protecting GM during RT.

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“…The inconsistence, on one aspect, could be related with diverse histological constitution in the brain between mice and humans. Specifically, the volume ratio of grey matter in the whole brain is notably higher in mice than in humans [30], and thus mice brains have more neurons to consume in the degenerative process. On another aspect, due to a long asymptomatic period, patients consenting to PET examination may be already at late-stage AD.…”

Section: Discussionmentioning

confidence: 99%

Age- and Brain Region-Specific Changes of Glucose Metabolic Disorder, Learning, and Memory Dysfunction in Early Alzheimer’s Disease Assessed in APP/PS1 Transgenic Mice Using 18F-FDG-PET

Men

Zhu

et al. 2016

IJMS

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Alzheimer’s disease (AD) is a leading cause of dementia worldwide, associated with cognitive deficits and brain glucose metabolic alteration. However, the associations of glucose metabolic changes with cognitive dysfunction are less detailed. Here, we examined the brains of APP/presenilin 1 (PS1) transgenic (Tg) mice aged 2, 3.5, 5 and 8 months using 18F-labed fluorodeoxyglucose (18F-FDG) microPET to assess age- and brain region-specific changes of glucose metabolism. FDG uptake was calculated as a relative standardized uptake value (SUVr). Morris water maze (MWM) was used to evaluate learning and memory dysfunction. We showed a glucose utilization increase in multiple brain regions of Tg mice at 2 and 3.5 months but not at 5 and 8 months. Comparisons of SUVrs within brains showed higher glucose utilization than controls in the entorhinal cortex, hippocampus, and frontal cortex of Tg mice at 2 and 3.5 months but in the thalamus and striatum at 3.5, 5 and 8 months. By comparing SUVrs in the entorhinal cortex and hippocampus, Tg mice were distinguished from controls at 2 and 3.5 months. In MWM, Tg mice aged 2 months shared a similar performance to the controls (prodromal-AD). By contrast, Tg mice failed training tests at 3.5 months but failed all MWM tests at 5 and 8 months, suggestive of partial or complete cognitive deficits (symptomatic-AD). Correlation analyses showed that hippocampal SUVrs were significantly correlated with MWM parameters in the symptomatic-AD stage. These data suggest that glucose metabolic disorder occurs before onset of AD signs in APP/PS1 mice with the entorhinal cortex and hippocampus affected first, and that regional FDG uptake increase can be an early biomarker for AD. Furthermore, hippocampal FDG uptake is a possible indicator for progression of Alzheimer’s cognition after cognitive decline, at least in animals.

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White and Gray Matter Abnormalities After Cranial Radiation in Children and Mice

Cited by 54 publications

References 52 publications

MRI to Assess Neurological Function

MRI to Assess Neurological Function

Radiation-induced abnormal cortical thickness in patients with nasopharyngeal carcinoma after radiotherapy

Age- and Brain Region-Specific Changes of Glucose Metabolic Disorder, Learning, and Memory Dysfunction in Early Alzheimer’s Disease Assessed in APP/PS1 Transgenic Mice Using 18F-FDG-PET

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