Curcumin alleviates cisplatin-induced learning and memory impairments

Öz, Mehmet C.; Atalık, Kısmet Esra Nurullahoğlu; Yerlikaya, Fatma Hümeyra; Demir, Enver Ahmet

doi:10.1016/j.nlm.2015.05.001

Cited by 60 publications

(43 citation statements)

References 51 publications

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“…Oxidative stress and mitochondrial dysfunction in the brain have been associated with other chemotherapeutic agents that induce cognitive impairments, such as adriamycin and cyclophosphamide [53–55], and antioxidant intervention has shown to be a promising therapy in preventing CRCI [56,57]. NAC is a precursor of glutathione, the most important intracellular antioxidant [58].…”

Section: Discussionmentioning

confidence: 99%

Cisplatin-induced mitochondrial dysfunction is associated with impaired cognitive function in rats

Lomeli

Czerniawski

et al. 2017

Free Radical Biology and Medicine

115

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Purpose Chemotherapy-related cognitive impairment (CRCI) is commonly reported following the administration of chemotherapeutic agents and comprises a wide variety of neurological problems. No effective treatments for CRCI are currently available. Here we examined the mechanisms involving cisplatin-induced hippocampal damage following cisplatin administration in a rat model and in cultured rat hippocampal neurons and neural stem/progenitor cells (NSCs). We also assessed the protective effects of the antioxidant, N-acetylcysteine in mitigating these damages. Experimental design Adult male rats received 6 mg/kg cisplatin in the acute studies. In chronic studies, rats received 5 mg/kg cisplatin or saline injections once per week for 4 weeks. N-acetylcysteine (250 mg/kg/day) or saline was administered for five consecutive days during cisplatin treatment. Cognitive testing was performed 5 weeks after treatment cessation. Cisplatin-treated cultured hippocampal neurons and NSCs were examined for changes in mitochondrial function, oxidative stress production, caspase-9 activation, and neuronal dendritic spine density. Results Acute cisplatin treatment reduced dendritic branching and spine density, and induced mitochondrial degradation. Rats receiving the chronic cisplatin regimen showed impaired performance in contextual fear conditioning, context object discrimination, and novel object recognition tasks compared to controls. Cisplatin induced mitochondrial DNA damage, impaired respiratory activity, increased oxidative stress, and activated caspase-9 in cultured hippocampal neurons and NSCs. N-acetylcysteine treatment prevented free radical production, ameliorated apoptotic cellular death and dendritic spine loss, and partially reversed the cisplatin-induced cognitive impairments. Conclusions Our results suggest that mitochondrial dysfunction and increased oxidative stress are involved in cisplatin-induced cognitive impairments. Therapeutic agents, such as N-acetylcysteine, may be effective in mitigating the deleterious effects of cisplatin.

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Section: Discussionmentioning

confidence: 99%

Cisplatin-induced mitochondrial dysfunction is associated with impaired cognitive function in rats

Lomeli

Czerniawski

et al. 2017

Free Radical Biology and Medicine

115

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“…An accumulation of cis-platinum in dorsal root ganglion neurons in the form of platinum-DNA adducts is thought to be a key mechanism driving such neurotoxicity (Zhu et al, 2016). In addition, as a known neurotoxic agent, cisplatin is suitable for use in NDD models, because it is known to cause memory and learning impairment through oxidative stress and neuroinflammation (Moneim, 2014; Oz et al, 2015; Zhou et al, 2016; Chen C. et al, 2017). Cisplatin modulates glutamate receptors and induces neural activation through the central upregulation of AMPARs and NMDARs (Holland et al, 2014).…”

Section: Glutamate Receptors As Potential Targets In Neurotoxic Agentmentioning

confidence: 99%

Neurotoxic Agent-Induced Injury in Neurodegenerative Disease Model: Focus on Involvement of Glutamate Receptors

Jakaria

Park

Haque

et al. 2018

Front. Mol. Neurosci.

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Glutamate receptors play a crucial role in the central nervous system and are implicated in different brain disorders. They play a significant role in the pathogenesis of neurodegenerative diseases (NDDs) such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. Although many studies on NDDs have been conducted, their exact pathophysiological characteristics are still not fully understood. In in vivo and in vitro models of neurotoxic-induced NDDs, neurotoxic agents are used to induce several neuronal injuries for the purpose of correlating them with the pathological characteristics of NDDs. Moreover, therapeutic drugs might be discovered based on the studies employing these models. In NDD models, different neurotoxic agents, namely, kainic acid, domoic acid, glutamate, β-N-Methylamino-L-alanine, amyloid beta, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, 1-methyl-4-phenylpyridinium, rotenone, 3-Nitropropionic acid and methamphetamine can potently impair both ionotropic and metabotropic glutamate receptors, leading to the progression of toxicity. Many other neurotoxic agents mainly affect the functions of ionotropic glutamate receptors. We discuss particular neurotoxic agents that can act upon glutamate receptors so as to effectively mimic NDDs. The correlation of neurotoxic agent-induced disease characteristics with glutamate receptors would aid the discovery and development of therapeutic drugs for NDDs.

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“…Although the neuropathological mechanisms underlying chemobrain is yet to be understood clearly, there have been evidences suggesting that hippocampus may be an important area that is vulnerable to chemotherapy-induced neurotoxicity in recent studies (13). In various previous rodent researches, evidences proving that chemobrain is related to impaired neurogenesis of hippocampus (14,15), neuroin ammation (16,17), oxidative stress, mitochondrial dysfunction (18,19), and structural damage to neurons have been cumulating. Several recent neuroimaging studies have reported reduced total volume and inward deformities in hippocampal sub elds in breast cancer patients (20,21).…”

Section: Introductionmentioning

confidence: 99%

Structural and Functional Brain Alterations in Post-Chemotherapy Cognitive Impairment in Gastric Cancer: A Longitudinal Multimodal Neuroimaging Study

Ahn

Lee

Jung

et al. 2020

Preprint

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Backgrounds: Despite clinical significance of chemobrain, no longitudinal study has been made on change in cognitive function related to chemotherapy in gastric cancer. The aim of this study is to define structural and functional changes in brains of gastric cancer patients caused by chemotherapy-induced cognitive impairment after adjuvant chemotherapy. Methods: 13 gastric cancer patients with adjuvant chemotherapy (CTx+ group), 9 gastric patients without adjuvant chemotherapy (CTx- group), and 10 healthy controls (HC) were enrolled for this study. We performed self-report questionnaires, neurocognitive tests, voxel-based morphometry (VBM), hippocampus-seeded resting-state functional magnetic resonance imaging (rsfMRI) and diffusion tensor imaging (DTI) analysis twice at before and 3 months after chemotherapy. Results: Compared to CTx- group, CTx+ group exhibited statistically significant decrease in attention and executive function over time, and also exhibited dysfunction in delayed recognition performance. Results in resting state functional connectivity analysis show significant group-by-time interaction in left hippocampus-anterior thalamus. In addition, DTI analysis had interesting results that showed reduced fractional anisotropy (FA), and increased mean diffusivity (MD) in left hippocampus. However, results from VBM analysis confirms that chemotherapy does not cause structural changes in brain. Conclusion: To the best of our knowledge, this is the first longitudinal neuroimaging study on the effect of chemotherapy in gastric cancer patients. Based on the results of this study, we suggest that neuropathological processes and clinical presentation of chemobrain is ultimately similar disease as age-related neurodegenerative disorder. Results of this study help in viewing underlying basis of chemobrain at a new angle and puts emphasis in importance of continuous assessment and intervention.

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Curcumin alleviates cisplatin-induced learning and memory impairments

Cited by 60 publications

References 51 publications

Cisplatin-induced mitochondrial dysfunction is associated with impaired cognitive function in rats

Cisplatin-induced mitochondrial dysfunction is associated with impaired cognitive function in rats

Neurotoxic Agent-Induced Injury in Neurodegenerative Disease Model: Focus on Involvement of Glutamate Receptors

Structural and Functional Brain Alterations in Post-Chemotherapy Cognitive Impairment in Gastric Cancer: A Longitudinal Multimodal Neuroimaging Study

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