Dysregulation in myelination mediated by persistent neuroinflammation: Possible mechanisms in chemotherapy-related cognitive impairment

Briones, Teresita L.; Woods, Julie

doi:10.1016/j.bbi.2013.07.175

Cited by 87 publications

(68 citation statements)

References 47 publications

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“…Rats in the control group received normal saline of equal volume to control for the effects of stress induced by the injection. The dosages selected were based on our previous work [15, 26], which showed that animals tolerated these doses with minimal weight loss, fatigue, or death. Both CMF and normal saline injections were given intraperitoneally once a week for a total of 4 weeks and rats were weighed every other day during the chemotherapeutic regimen.…”

Section: Methodsmentioning

confidence: 99%

RETRACTED: Involvement of insulin-like growth factor-1 in chemotherapy-related cognitive impairment

Briones

Woods

Wadowska

2015

Behavioural Brain Research

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Here we examined the involvement of insulin-like growth factor 1 (IGF-1) on chemotherapy-induced cognitive impairment. Sixty-four ovariectomized female Sprague-Dawley rats were included in the study and given cyclophosphamide, methothrexate, and 5-Fluorouracil (CMF) drug combination or saline (control). CMF was given once a week for 4 weeks. In one experiment, behavioral testing using the cued learning and spontaneous object recognition tasks were performed either: at the end of treatment or 4 weeks after treatment. In another experiment, rats from the chemotherapy and saline groups received either: continuous insulin-like growth factor 1 (IGF-1) or vehicle delivered subcutaneously via osmotic pump for 21 days (started the week after completion of therapy). Bromodeoxyuridine injections were given for 3 consecutive days starting at 2 weeks after completion of chemotherapy to assess the survival of proliferating cells. Increased levels of IGF-1 and activation of its receptor as well as increased activation of Akt and Erk1/2, its downstream signaling pathways was seen immediately after completion of chemotherapy but decreased 4 weeks after treatment. Behavioral testing showed CMF-induced cognitive impairment after completion of therapy and persisted for 4 weeks. We also found that giving IGF-1 significantly increased activation of its receptor, and the Akt and Erk1/2 pathways, and most importantly attenuated chemotherapy-induced cognitive impairment. CMF-induced neuronal apoptosis was also seen and the ratio of surviving cells that proliferate was higher compared to the number of apoptotic cells in the CMF rats given IGF-1. These results suggest that IGF-1 is involved in CMF-induced cognitive impairment by modulating cell death and cell proliferation.

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Section: Methodsmentioning

confidence: 99%

RETRACTED: Involvement of insulin-like growth factor-1 in chemotherapy-related cognitive impairment

Briones

Woods

Wadowska

2015

Behavioural Brain Research

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“…3). A priori, the genotype effect might be explained by a difference in motor response speed from differential neuromuscular transmission due to a TNFα-mediated effect on myelination (Briones and Woods, 2014). However, this explanation is inconsistent with the lack of an effect of genotype on the fastest 10% of reaction times, and would also not be a plausible reason for the amplified genotype effect seen during sleep deprivation as compared to baseline.…”

Section: Discussionmentioning

confidence: 99%

TNFα G308A polymorphism is associated with resilience to sleep deprivation-induced psychomotor vigilance performance impairment in healthy young adults

Satterfield

Wisor

Field

et al. 2015

Brain, Behavior, and Immunity

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Cytokines such as TNFα play an integral role in sleep/wake regulation and have recently been hypothesized to be involved in cognitive impairment due to sleep deprivation. We examined the effect of a guanine to adenine substitution at position 308 in the TNFα gene (TNFα G308A) on psychomotor vigilance performance impairment during total sleep deprivation. A total of 88 healthy women and men (ages 22–40) participated in one of five laboratory total sleep deprivation experiments. Performance on a psychomotor vigilance test (PVT) was measured every 2 to 3 h. The TNFα 308A allele, which is less common than the 308G allele, was associated with greater resilience to psychomotor vigilance performance impairment during total sleep deprivation (regardless of time of day), and also provided a small performance benefit at baseline. The effect of genotype on resilience persisted when controlling for between-subjects differences in age, gender, race/ethnicity, and baseline sleep duration. The TNFα G308A polymorphism predicted less than 10% of the overall between-subjects variance in performance impairment during sleep deprivation. Nonetheless, the differential effect of the polymorphism at the peak of performance impairment was more than 50% of median performance impairment at that time, which is sizeable compared to the effects of other genotypes reported in the literature. Our findings provided evidence for a role of TNFα in the effects of sleep deprivation on psychomotor vigilance performance. Furthermore, the TNFα G308A polymorphism may have predictive potential in a biomarker panel for the assessment of resilience to psychomotor vigilance performance impairment due to sleep deprivation.

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“…However, neurotoxicity is a frequent accompaniment of cancer chemotherapy 5 . Chemobrain, also known as “chemofog,” is a cognitive impairment consisting of deficits in attention, executive and motor function, memory, and speed of information processing, following chemotherapy for a multitude of cancers 6,7 . These deficits, while usually temporary, can persist for several years after completion of drug treatment in a subgroup (17-34%) of patients and can dramatically affect many aspects of daily living, such as employment, social functioning, and community integration 8 .…”

Section: Introductionmentioning

confidence: 99%

5-Fluorouracil chemotherapy upregulates cytokines and alters hippocampal dendritic complexity in aged mice

Groves

Farris

Anderson

et al. 2017

Behavioural Brain Research

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5-fluorouracil (5-Fu) is commonly used chemotherapy drug, but it can lead to the impairment of cognitive function. The pathogenesis of this injury is unknown but may involve modifications to dendritic structure and/or alterations in dendritic spine density and morphology. Dendritic spines are sites of excitatory synaptic transmission and changes in spine structure and dendrite morphology are thought to represent a morphological correlate of altered brain functions associated with hippocampal dependent learning and memory. A total of 28 one-year-old C57BL6/J male mice were used in this study; 14 mice received 5-Fu treatment and 14 were given saline injections. One month post treatment, 14 cytokines were measured at the same time Golgi samples were taken. 8 analytes were significantly elevated in mice treated with 5-Fu. 5-Fu significantly compromised the dendritic architecture and reduced spine density throughout the hippocampal tri-synaptic network. The present data provide the evidence that 5-Fu has deleterious effects on mature neurons associated with hippocampal learning and memory.

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Dysregulation in myelination mediated by persistent neuroinflammation: Possible mechanisms in chemotherapy-related cognitive impairment

Cited by 87 publications

References 47 publications

RETRACTED: Involvement of insulin-like growth factor-1 in chemotherapy-related cognitive impairment

RETRACTED: Involvement of insulin-like growth factor-1 in chemotherapy-related cognitive impairment

TNFα G308A polymorphism is associated with resilience to sleep deprivation-induced psychomotor vigilance performance impairment in healthy young adults

5-Fluorouracil chemotherapy upregulates cytokines and alters hippocampal dendritic complexity in aged mice

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