The Mystery of Chemotherapy Brain: Kynurenines, Tubulin and Biophoton Release

Sordillo, Peter P.; Sordillo, Laura A.

doi:10.21873/anticanres.14061

Cited by 12 publications

(7 citation statements)

References 126 publications

(141 reference statements)

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“…Indeed, earlier studies have linked cognition to tubulin and tubulin inhibiting chemotherapy with dysfunctional memory ( Craddock et al., 2012 ; Tuszynski et al., 2020 ; Kalra et al., 2020 ). With the same token, treatment with colchicine, a microtubule-disassembling drug, disrupts cognition, further connecting tubulin to information processing ( Dent, 2017 ; Chaldakov, 2018 ; Sordillo and Sordillo, 2020 ). Interestingly, tubulin interacts directly with Cx43, the gap junction molecule involved in astrocytic syncytia, suggesting a role in the homeostasis of these cells ( Giepmans et al., 2001 ).…”

Section: Cell-cell Fusion and Information Processingmentioning

confidence: 99%

Virus-Induced Membrane Fusion in Neurodegenerative Disorders

Osorio

Sfera

Anton

et al. 2022

Front. Cell. Infect. Microbiol.

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A growing body of epidemiological and research data has associated neurotropic viruses with accelerated brain aging and increased risk of neurodegenerative disorders. Many viruses replicate optimally in senescent cells, as they offer a hospitable microenvironment with persistently elevated cytosolic calcium, abundant intracellular iron, and low interferon type I. As cell-cell fusion is a major driver of cellular senescence, many viruses have developed the ability to promote this phenotype by forming syncytia. Cell-cell fusion is associated with immunosuppression mediated by phosphatidylserine externalization that enable viruses to evade host defenses. In hosts, virus-induced immune dysfunction and premature cellular senescence may predispose to neurodegenerative disorders. This concept is supported by novel studies that found postinfectious cognitive dysfunction in several viral illnesses, including human immunodeficiency virus-1, herpes simplex virus-1, and SARS-CoV-2. Virus-induced pathological syncytia may provide a unified framework for conceptualizing neuronal cell cycle reentry, aneuploidy, somatic mosaicism, viral spreading of pathological Tau and elimination of viable synapses and neurons by neurotoxic astrocytes and microglia. In this narrative review, we take a closer look at cell-cell fusion and vesicular merger in the pathogenesis of neurodegenerative disorders. We present a “decentralized” information processing model that conceptualizes neurodegeneration as a systemic illness, triggered by cytoskeletal pathology. We also discuss strategies for reversing cell-cell fusion, including, TMEM16F inhibitors, calcium channel blockers, senolytics, and tubulin stabilizing agents. Finally, going beyond neurodegeneration, we examine the potential benefit of harnessing fusion as a therapeutic strategy in regenerative medicine.

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Section: Cell-cell Fusion and Information Processingmentioning

confidence: 99%

Virus-Induced Membrane Fusion in Neurodegenerative Disorders

Osorio

Sfera

Anton

et al. 2022

Front. Cell. Infect. Microbiol.

View full text Add to dashboard Cite

show abstract

“…Drugs that target the microtubule network directly through hyperstabilizing (PCTX, DCTX, and ixabepilone) or destabilizing (vincristine and vinblastine) it, may lead to chemobrain as well ( Mihlon et al, 2010 ). Abnormalities in microtubules were reported to cause cognition and memory problems, and damage to microtubules correlated with numerous neurological diseases ( Sordillo and Sordillo, 2020 ). Accordingly, PCTX, the microtubule-stabilizing agent, was demonstrated to cause impaired memory acquisition in rodent models.…”

Section: Central Neurotoxicity: Chemobrainmentioning

confidence: 99%

Mechanisms of Chemotherapy-Induced Neurotoxicity

et al. 2022

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Since the first clinical trials conducted after World War II, chemotherapeutic drugs have been extensively used in the clinic as the main cancer treatment either alone or as an adjuvant therapy before and after surgery. Although the use of chemotherapeutic drugs improved the survival of cancer patients, these drugs are notorious for causing many severe side effects that significantly reduce the efficacy of anti-cancer treatment and patients’ quality of life. Many widely used chemotherapy drugs including platinum-based agents, taxanes, vinca alkaloids, proteasome inhibitors, and thalidomide analogs may cause direct and indirect neurotoxicity. In this review we discuss the main effects of chemotherapy on the peripheral and central nervous systems, including neuropathic pain, chemobrain, enteric neuropathy, as well as nausea and emesis. Understanding mechanisms involved in chemotherapy-induced neurotoxicity is crucial for the development of drugs that can protect the nervous system, reduce symptoms experienced by millions of patients, and improve the outcome of the treatment and patients’ quality of life.

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“…Recent studies have also provided more evidence for biochemical reactions, ion-transmembrane, and energy level transition of biomolecular activities in neuronal tissues that can produce biophotons in mediating intra-extracellular communication, which may affect the photonic signal transmission in the myelinated axons [29,30]. In this article, photonic communication based on the nerve's thin-film model is investigated.…”

Section: Figure 1 a Schematic Diagram Of Myelinated Axon In The Nerve...mentioning

confidence: 99%

Optical Modeling and Characterization of Demyelinated Nerve Using Graphene-Based Photonic Structure

et al. 2022

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The myelin sheath, as an insulation layer in nerve cells, plays an essential role in neural communication and signal conduction. Loss of myelin, referred to as demyelination, is associated with many mental disorders. Detecting the tiny demyelinated parts in nerve fibers can provide early diagnosis of some mental disorders and create effective treatment plans. This paper establishes a new engineering approach for differentiation between demyelinated and myelinated axons by analyzing spectral responses resulting from the optical simulation framework. We propose computational modeling on the photonic communication of nerve fibers and develop a graphene-based neurophotonic device that can be used to detect the regions demyelinated on the nerve fiber. We first model a nanoscale thin-film configuration of the multilayered myelinated axon to evaluate photons transmission in the nerve fibers under geometric defects as demyelination. Then, the nerve's optical characteristics are achieved by focusing on the reflectance of light incidence on the nerve model with the change of the demyelination size to distinguish demyelinated-from myelinated nerves by the spectral contrast. Undertaking the different levels of demyelination progression, we theoretically explore the variations of effective refractive index using an analytical solution technique. Ultimately, we design a nanostructure configured with silicon dioxide, graphene, and gold nanoparticles to function as a biochip recognizing myelinated axon damage under the surface plasmon effect. This device can promote a practical procedure to distinguish nanoscale demyelinated and myelinated axons, which can be utilized for neural sensing of tiny brain tissues as a neurophotonic needle.

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The Mystery of Chemotherapy Brain: Kynurenines, Tubulin and Biophoton Release

Cited by 12 publications

References 126 publications

Virus-Induced Membrane Fusion in Neurodegenerative Disorders

Virus-Induced Membrane Fusion in Neurodegenerative Disorders

Mechanisms of Chemotherapy-Induced Neurotoxicity

Optical Modeling and Characterization of Demyelinated Nerve Using Graphene-Based Photonic Structure

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