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ISSN 2063-5346
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Biochemical metabolism of brain and Neuregulin-1/ErbB signaling in the hippocampus after doxorubicin administration

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Noura Yousef Abd Elsalam Ali, Amal Saeed El Shal , Wesam Mostafa Soliman El bakly, Shimaa Ali Abd Elrahman , Doaa Mahmoud Abdel Hameed Salah
» doi: 10.48047/ecb/2023.12.1.610

Abstract

The metabolic fate of glucose in the brain depends upon the cell type and the selective expression of metabolic enzymes. Neurons are predominantly oxidative, while astrocytes are mostly glycolytic. In addition to the production of adenosine‐5′‐triphosphate (ATP), glucose is also used to generate metabolic intermediates for the synthesis of fatty acids and other lipids required for membrane and myelin synthesis ; amino acids for protein synthesis and neurotransmitter production; and 5‐carbon sugars for the synthesis of nucleotides); and to produce glycogen in astrocytes. Doxorubicin (Dox) is an effective anthracycline chemotherapeutic developed for the treatment of solid tumors and hematologic malignancies. NRG1 is suggested as a susceptibility gene for several psychiatric disorders, including schizophrenia, bipolar disorder, and depression. NRG1 is well known to play an essential role in neuronal development as well as in maintaining normal function in the mature nervous system. Recent biochemical studies have shown that NRG1 can be neuroprotective for cortical neurons, motor neurons, dopaminergic neurons, cochlear sensory neurons, and PC12 cells. Previous research showed that aberrant changes in these NRG1-related pathways are tightly linked to the pathogenesis of depression. It is tempting to hypothesize that Dox may inhibit neural NRG1/ErbB signaling, thereby triggering the neurotoxicity and behavioral changes

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