Forced running exercise attenuates hippocampal neurogenesis impairment and the neurocognitive deficits induced by whole-brain irradiation via the BDNF-mediated pathway

Ji, Jian-feng; Ji, Shengjun; Sun, Rui; Li, Kun; Zhang, Yuan; Zhang, Liyuan; Tian, Ye

doi:10.1016/j.bbrc.2013.12.031

Cited by 97 publications

(64 citation statements)

References 20 publications

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“…Impairment of hippocampal neurogenesis is proposed to be one of the important factors for CRT-induced cognitive decline, prominently memory loss [72,73] . Our previous results have shown that forced running after cranial irradiation can ameliorate the impairment of hippocampal neurogenesis and significantly prevent radiation-induced cognitive decline in rats [74] . And it is believed that radiation-induced cell killing in neural progenitor populations makes major contribution to the neurogenesis impairment [75] .…”

Section: Neurogenesismentioning

confidence: 92%

Radiation-induced cognitive impairment

2015

Ther Targets Neurol Dis

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Radiation-induced cognitive impairment is one of the late adverse effects of cranial radiation therapy (CRT) for cancer patients with primary and metastatic brain tumors, head and neck cancers etc. It affects approximately 40-50% patients who survive for >6 months and severely reduces the quality of survivors' life. With the advancement of radiation therapy technology, the survival of brain tumor patients is significantly improved, thus understanding the etiology of CRT-induced cognitive impairment and developing the potential strategies of the management of this side-effect have become more important than ever. Some valuable insights have been obtained through extensive preclinical studies. It is suggested that radiation-induced cognitive impairment is due to the dysfunctions of hippocampus-dependent learning, memory and spatial information processing after radiation exposure. Until now, research results have shown that radiation-induced cognitive impairment and neurodegenerative disorders such as Alzheimer disease (AD), Parkinson's disease (PD), Huntington's disease (HD) and aging-related cognitive decline, share some similar pathogenic factors, including chronic oxidative stress and inflammation, impairment in neurogenesis and angiogenesis. Blockade of these factors by antioxidants, anti-inflammatory drugs, transplant of neural stem cells, systemic hypoxia etc. can significantly ameliorate cognitive decline in cranially irradiated experimental animals. These studies shed the light on the pathogenesis of radiation-induced cognitive impairment and may have important implication in developing novel therapeutic interventions for surviving cancer patients who suffer from cognitive decline after CRT.

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Section: Neurogenesismentioning

confidence: 92%

Radiation-induced cognitive impairment

2015

Ther Targets Neurol Dis

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“…Impairment of hippocampal neurogenesis contributes to IR-induced cognitive deficits. studies (Ji et al 2014) have found both voluntary and forced running exercise could ameliorate the IR-induced impairment of hippocampal neurogenesis via BDnF.…”

Section: Bdnfmentioning

confidence: 98%

Cytokines: shifting the balance between glioma cells and tumor microenvironment after irradiation

Zhou

Jiang

et al. 2014

J Cancer Res Clin Oncol

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Malignant gliomas invariably recur after irradiation, showing radioresistance. Meanwhile, cranial irradiation can bring some risk for developing cognitive dysfunction. There is increasing evidence that cytokines play their peculiar roles in these processes. On the one hand, cytokines directly influence the progression of malignant glioma, promoting or suppressing tumor progression. On the other hand, cytokines indirectly contribute to the immunologic response against gliomas, exhibiting pro-inflammatory or immunosuppressive activities. We propose that cytokines are not simply unregulated products from tumor cells or immune cells, but mediators finely adjust the balance between glioma cells and tumor microenvironment after irradiation. The paper, therefore, focuses on the changes of cytokines after irradiation, analyzing how these mediate the response of tumor cells and normal cells to irradiation. In addition, cytokine-based immunotherapeutic strategies, accompanied with irradiation, for the treatment of gliomas are also discussed.

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“…Another study found that 3 weeks forced running increased hippocampal proliferation and BDNF protein in one-month old rats [7]. The hippocampal proliferation and BDNF protein were also enhanced in middle age mice by 5 weeks treadmill exercise [8].…”

Section: Voluntary Running Enhanced Proliferation Bymentioning

confidence: 99%

“…For instance, treadmill exercise increased hippocampal BDNF expression, and promoted hippocampal proliferation [7][8][9]. However, another study reported that treadmill exercise increased hippocampal proliferation but did not increased BDNF protein [10].…”

Section: Introductionmentioning

confidence: 99%

Voluntary Running Enhances Hippocampal Proliferation by Increasing Hippocampal NGF, BDNF, and IGF-1

Xu¹,

Zhang²,

Song

et al. 2017

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Neurotrophic factors and growth factors are known to have positive effects on hippocampal proliferation.However, previous findings on the effects of these factors on exercise-induced hippocampal proliferation are inconsistent. In this study, we investigated the effects of voluntary running on hippocampal proliferation and the expression levels of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and insulin-like growth factor 1 (IGF-1) in hippocampus. Twenty-four male C57BL/6 mice were randomly divided into four groups: control groups 1 and 2 (C1, n = 6; C2, n = 6) and running groups 1 and 2 (R1, n = 6; R2, n = 6). Mice from C1 and C2 were placed individually in standard cages for eight weeks; mice from R1 and R2 were housed individually in cages with a running wheel for eight weeks. At the fifth week, C1 and R1 mice were injected with BrdU for 7 consecutive days. On the first day of the ninth week, the C1 and R1 mice were anaesthetized and hippocampal neuronal proliferation was assessed using immunohistochemistry; the mice in C2 and R2 were sacrificed to test the expression levels of NGF, BDNF, and IGF-1 mRNA in hippocampus using RT-PCR. The results indicated that voluntary running significantly increased the number of BrdU-positive cells in the dentate gyrus (DG), and significantly upregulated the levels of NGF, BDNF, and IGF-1 mRNA in the hippocampus. In conclusion, our findings indicated that hippocampal proliferation was enhanced by voluntary running, which was associated with increased NGF, BDNF, and IGF-1 mRNA levels in the hippocampus.

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Forced running exercise attenuates hippocampal neurogenesis impairment and the neurocognitive deficits induced by whole-brain irradiation via the BDNF-mediated pathway

Cited by 97 publications

References 20 publications

Radiation-induced cognitive impairment

Radiation-induced cognitive impairment

Cytokines: shifting the balance between glioma cells and tumor microenvironment after irradiation

Voluntary Running Enhances Hippocampal Proliferation by Increasing Hippocampal NGF, BDNF, and IGF-1

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