bims-glymed Biomed News
on Glycogen metabolism in disease
Issue of 2024–12–08
fifteen papers selected by
Tash Khan, Harvard University
  1. Identification of structural stability and fragility of mouse liver glycogen via label-free Raman spectroscopy coupled with convolutional neural network algorithm.
  2. Dysregulation of energy metabolism in Alzheimer's disease.
  3. When a negative (charge) is not a positive: sialylation and its role in cancer mechanics and progression.
  4. miRNAs in HCC, pathogenesis, and targets.
  5. PI3K Signaling at the Crossroads of Lipid Metabolism and Cancer.
  6. Regulation of ROS signaling by TIGAR induces cancer-modulating responses in the tumor microenvironment.
  7. MTSS1: beyond the integration of actin and membrane dynamics.
  8. Altered hypoxia- and redox-related transcriptional signatures in mitochondrial-DNA-depleted PC-3 cells.
  9. Glucose-induced LINC01419 reprograms the glycolytic pathway by recruiting YBX1 to enhance PDK1 mRNA stability in hepatocellular carcinoma.
  10. Co-evolution of glioma and immune microenvironment.
  11. Current advances on the role of ferroptosis in tumor immune evasion.
  12. Getting the right combination to break the epigenetic code.
  13. O-GlcNAcylation in ovarian tumorigenesis and its therapeutic implications.
  14. FAHD1 and mitochondrial metabolism: a decade of pioneering discoveries.
  15. The effect of Mozart's K.448 on epilepsy: A systematic literature review and supplementary research on music mechanism.
  1. Int J Biol Macromol. 2024 Dec 03. pii: S0141-8130(24)09151-7. [Epub ahead of print] 138340
    Identification of structural stability and fragility of mouse liver glycogen via label-free Raman spectroscopy coupled with convolutional neural network algorithm.
    Liang Wang, Zhang-Wen Ma, Jia-Wei Tang, Jing-Yi Mou, Qing-Hua Liu, Zi-Yi Wang, Xin Liu, Meng-Ying Zhang, Dao-Quan Tang.
      Glycogen structure is closely associated with its physiological functions. Previous studies confirmed that liver glycogen structure had two dominant states: mainly stable during the day and largely fragile at night. However, the diurnal change of glycogen structure is impaired, with dominant fragility in diseased conditions such as diabetes mellitus and liver fibrosis. Therefore, the persistent structural fragility of glycogen particles could be a potential molecular-level pathological biomarker for early screening of certain liver diseases. However, the current method for identifying glycogen structural stability and fragility suffers from sophisticated procedures and reliance on expensive instruments, which demands developing novel methods for rapidly discriminating the two types of glycogen particles. This study applied surface-enhanced Raman spectroscopy (SERS) to generate SERS spectra of glycogen samples, revealing distinct structural differences between fragile and stable glycogen particles. Machine learning models were then constructed to predict the structural states of unknown glycogen samples via SERS spectra, according to which the convolutional neural network (CNN) model achieved the best discrimination capacity. Taken together, the SERS technique coupled with the CNN model can identify stable and fragile liver glycogen samples, facilitating the application of glycogen structural fragility as a biomarker in diagnosing liver diseases.
    Keywords:  Deep learning; Diurnal change; Glycogen; Raman spectrometry; Raman spectroscopy; Structural fragility
    DOI:  https://doi.org/10.1016/j.ijbiomac.2024.138340
  2. J Neurol. 2024 Dec 02. 272(1): 2
    Dysregulation of energy metabolism in Alzheimer's disease.
    Yue Yuan, Gang Zhao, Yang Zhao.
      Alzheimer's disease (AD) is one of the most common neurodegenerative diseases. Its etiology and associated mechanisms are still unclear, which largely hinders the development of AD treatment strategies. Many studies have shown that dysregulation of energy metabolism in the brain of AD is closely related to disease development. Dysregulation of brain energy metabolism in AD brain is associated with reduced glucose uptake and utilization, altered insulin signaling pathways, and mitochondrial dysfunction. In this study, we summarized the relevant pathways and mechanisms regarding the dysregulation of energy metabolism in AD. In addition, we highlight the possible role of mitochondrial dysfunction as a central role in the AD process. A deeper understanding of the relationship between energy metabolism dysregulation and AD may provide new insights for understanding learning memory impairment in AD patients and in improving AD prevention and treatment.
    Keywords:  Alzheimer’s disease; Glucose metabolism; Glucose transporters; Mitochondrial autophagy; Mitochondrial dysfunction; Mitochondrial genetics; O-GlcNAc; Tau protein; β-Amyloid
    DOI:  https://doi.org/10.1007/s00415-024-12800-8
  3. Front Oncol. 2024 ;14 1487306
    When a negative (charge) is not a positive: sialylation and its role in cancer mechanics and progression.
    Issa Funsho Habeeb, Toheeb Eniola Alao, Daniella Delgado, Alexander Buffone.
      Sialic acids and sialoglycans are critical actors in cancer progression and metastasis. These terminal sugar residues on glycoproteins and glycolipids modulate key cellular processes such as immune evasion, cell adhesion, and migration. Aberrant sialylation is driven by overexpression of sialyltransferases, resulting in hypersialylation on cancer cell surfaces as well as enhancing tumor aggressiveness. Sialylated glycans alter the structure of the glycocalyx, a protective barrier that fosters cancer cell detachment, migration, and invasion. This bulky glycocalyx also increases membrane tension, promoting integrin clustering and downstream signaling pathways that drive cell proliferation and metastasis. They play a critical role in immune evasion by binding to Siglecs, inhibitory receptors on immune cells, which transmit signals that protect cancer cells from immune-mediated destruction. Targeting sialylation pathways presents a promising therapeutic opportunity to understand the complex roles of sialic acids and sialoglycans in cancer mechanics and progression, which is crucial for developing novel diagnostic and therapeutic strategies that can disrupt these processes and improve cancer treatment outcomes.
    Keywords:  cancer; glycocalyx; mechanobiology; metastasis; migration; sialylation
    DOI:  https://doi.org/10.3389/fonc.2024.1487306
  4. Hepatology. 2024 Nov 29.
    miRNAs in HCC, pathogenesis, and targets.
    Guisheng Song, Xiaofan Yu, Hongtao Shi, Bo Sun, Stuart Amateau.
      Liver cancer is the third leading cause of cancer-related mortality worldwide. Hepatocellular carcinoma (HCC), the most common type of primary liver cancer is driven by complex genetic, epigenetic, and environmental factors. MicroRNAs, a class of naturally-occurring small non-coding RNAs play crucial roles in HCC by simultaneously modulating expression of multiple genes in a fine-tuning manner. Significant progress has been made in understanding how miRNAs influence key oncogenic pathways, including cell proliferation, apoptosis, angiogenesis, and epithelial-mesenchymal transition (EMT), as well as their role in modulating the immune microenvironment in HCC. Due to the unexpected stability of miRNAs in the blood and fixed HCC tumors, recent advancements also highlight their potential as non-invasive diagnostic tools. Restoring or inhibiting specific miRNAs have offered promising strategies for targeted HCC treatment by suppressing malignant hepatocyte growth and enhancing antitumor immunity. In this comprehensive review, we consolidate previous research and provide the latest insights into how miRNAs regulate HCC and their therapeutic and diagnostic potential. We delve into dysregulation of miRNA biogenesis in HCC, the roles of miRNAs in proliferation and apoptosis of malignant hepatocytes, angiogenesis and metastasis of HCC, immune microenvironment in HCC and drug resistance. We also discuss the therapeutic and diagnostic potential of miRNAs and delivery approaches of miRNA drugs to overcome the limitations of current HCC treatment options. By thoroughly summarizing the roles of miRNAs in HCC, our goal is to advance the development of effective therapeutic drugs with minimal adverse effects and to establish precise tools for early diagnosis of HCC.
    DOI:  https://doi.org/10.1097/HEP.0000000000001177
  5. Adv Exp Med Biol. 2024 Dec 01.
    PI3K Signaling at the Crossroads of Lipid Metabolism and Cancer.
    Sevval Yilmaz, Onur Cizmecioglu.
      The proto-oncogenic PI3K pathway is crucial for the integration of growth factor signaling and metabolic pathways to facilitate the coordination for cell growth. Since transformed cells have the ability to upregulate their anabolic pathways and selectively modulate a subset of metabolites functioning as anti- or pro-tumorigenic signal mediators, the question of how the levels of these metabolites are regulated has also become the center of attention for cancer researchers. Apart from its well-defined roles in glucose metabolism and peptide anabolism, the PI3K pathway appears to be a significant regulator of lipid metabolism and a potentiator of proto-oncogenic bioactive lipid metabolite signaling. In this review, we aim to describe the crosstalk between the PI3K pathway and bioactive lipid species of the three main lipid classes.
    Keywords:  Akt; Lipid metabolism; PI3K pathway; Signal transduction; Sphingolipids
    DOI:  https://doi.org/10.1007/5584_2024_832
  6. Proc Natl Acad Sci U S A. 2024 Dec 10. 121(50): e2416076121
    Regulation of ROS signaling by TIGAR induces cancer-modulating responses in the tumor microenvironment.
    Eric C Cheung, Douglas Strathdee, David Stevenson, Jack Coomes, Karen Blyth, Karen H Vousden.
      The consequences of reactive oxygen species (ROS) in cancer cells are complex and have been shown to both promote and retard tumorigenesis in different models. In mouse models of pancreatic ductal adenocarcinoma (PDAC), loss of the antioxidant defense gene Tigar results in both a reduction in the development of early pancreatic intraepithelial neoplasia and an increase in invasive and metastatic capacity, accompanied by decreased survival of mice lacking pancreatic TIGAR. We previously demonstrated that increased ROS following loss of TIGAR promotes various cancer cell-intrinsic changes that contribute to metastatic capacity, including epithelial to mesenchymal transition, enhanced migration and invasion, and an increase in ERK signaling. In this study, we show that pancreatic overexpression of TIGAR decreases metastatic capacity and migratory phenotypes in an aggressive model of PDAC, consistent with the concept that dynamic modulation of TIGAR in PDAC contributes to the development and progression of these tumors. Using TIGAR deficient and overexpressing mouse models, we find that the impact of modulation of TIGAR and ROS in PDAC cells also has a profound effect on the normal stromal cells surrounding the tumor. Loss of TIGAR promotes the production of cytokines by cancer cells that induce changes in the surrounding fibroblasts to adopt a tumor-supportive phenotype. Furthermore, these cytokines also attract macrophages that support PDAC dissemination and metastasis. Taken together our work shows that TIGAR-modulated ROS in PDAC can control cell intrinsic and extrinsic changes to impact tumor aggression.
    Keywords:  oxidative stress; pancreatic cancer; tumor microenvironment
    DOI:  https://doi.org/10.1073/pnas.2416076121
  7. Cell Mol Life Sci. 2024 Dec 03. 81(1): 472
    MTSS1: beyond the integration of actin and membrane dynamics.
    Liudmila Matskova, Shixing Zheng, Elena Kashuba, Ingemar Ernberg, Pontus Aspenström.
      MTSS1 is a ubiquitously expressed intracellular protein known mainly for its involvement in basic cellular processes, such as the regulation of actin organization and membrane architecture. MTSS1 has attracted much attention for its role as a tumor suppressor, being absent or expressed at reduced levels in advanced and metastasizing cancers. Occasionally, MTSS1 is, instead, upregulated in metastasis and, in some cases, even in primary tumors. In addition to these well-established functions of MTSS1 linked to its I-BAR- and WH2-domains, the protein is involved in modulating cell-cell contacts, cell differentiation, lipid metabolism, and vesicle formation and acts as a scaffolding protein for several E3 ubiquitin ligases. MTSS1 is classified as a housekeeping protein and is never mutated despite the several pathologic phenotypes linked to its dysregulation. Despite MTSS1's involvement in fundamental signaling pathways, MTSS1 gene ablation is not ubiquitously lethal, although it affects embryonic development. Due to MTSS1´s involvement in many seemingly disparate processes, with many cases lacking mechanistic explanations, we found it timely to review the recent data on MTSS1's role at the cellular level, as well as in health and disease, to direct further studies on this interesting multifunctional protein.
    Keywords:  I-BAR; Invasion; Lipid metabolism; Membrane architecture; Metastasis; Tumor suppressor
    DOI:  https://doi.org/10.1007/s00018-024-05511-w
  8. Biochem Biophys Res Commun. 2024 Dec 02. pii: S0006-291X(24)01644-9. [Epub ahead of print]742 151108
    Altered hypoxia- and redox-related transcriptional signatures in mitochondrial-DNA-depleted PC-3 cells.
    Ricardo Alva, Jacob E Wiebe, Jeffrey A Stuart.
      Rho 0 (ρ0) cells are widely used as a tool to investigate how the absence of respiring mitochondria affects a variety of physiological and pathological processes. Prominently, ρ0 cells have been used to study the role of mitochondrial reactive oxygen species (ROS) production and/or mitochondrial respiration in the stabilization of the hypoxia-inducible factor (HIF) in hypoxia. In this study, we cultured ρ0 and WT PC-3 cells in 5% O2 (physioxia) and Plasmax medium for 2 weeks prior to transcriptomic and functional analyses. RNA-seq showed that ρ0 PC-3 cells exhibit impaired induction of HIF-regulated genes when exposed to hypoxia, compared to wild-type (WT) cells. Surprisingly, when comparing the transcriptomes of ρ0 and WT cells in physioxia (5% O2), we found a strong presence of HIF-related gene signatures in ρ0 cells compared to WT. Among the HIF targets found to be upregulated in ρ0 cells are CA9, EGLN3, EPAS1, HK2, ENO2, and SLC2A1. Moreover, several Nrf2 targets were upregulated in ρ0 cells, including NQO1, HMOX1, GPX2, and SLC7A11, which is in line with ρ0 cells showing a significantly higher H2O2 efflux rate than WT cells. Given the alterations in HIF-dependent and Nrf2-dependent gene expression and basal ROS production observed in ρ0 PC-3 cells, we conclude that caution should be taken when interpreting the results from experiments that focus on ROS production and HIF signaling using ρ0 cells as a model.
    Keywords:  HIF; Hypoxia; Mitochondrial DNA; Nrf2; ROS; rho(0) cells
    DOI:  https://doi.org/10.1016/j.bbrc.2024.151108
  9. Clin Transl Med. 2024 Dec;14(12): e70122
    Glucose-induced LINC01419 reprograms the glycolytic pathway by recruiting YBX1 to enhance PDK1 mRNA stability in hepatocellular carcinoma.
    Yanfang Liu, Junjiao Song, Qili Shi, Bing Chen, Wenying Qiu, Yizhe Liu, Shenglin Huang, Xianghuo He.
      Metabolic reprogramming provides the necessary energy for the development of malignant tumours and is emerging as a novel tumour treatment strategy. However, the widespread expression of metabolic enzymes in diverse cell types makes the development of specific drugs that target cancer cells without affecting normal cellular functions challenging. Accumulating evidence has demonstrated the essential roles of long non-coding RNAs (lncRNAs) in the regulatory network associated with glucose metabolism in tumour cells. The mechanism and therapeutic potential of cancer-specific lncRNAs in modulating tumour glucose metabolism warrant in-depth exploration. Here we revealed that glucose-induced LINC01419 promoted the growth and metastasis of HCC cells by driving metabolic reprogramming. Mechanistically, LINC01419 directly interacted with Y-box binding protein 1 (YBX1) in the cytoplasm and facilitated its binding to PDK1 mRNA, thus enhancing PDK1 mRNA stability and increasing lactate production. Furthermore, YY1 contributed to the transcriptional activation of LINC01419 in HCC under high-glucose conditions. Notably, administration of an N-acetylgalactosamine (GalNAc)-conjugated siRNA specifically targeting LINC01419 markedly retarded the growth of orthotopic xenograft tumours. These findings provide evidence for an unprecedented regulatory mechanism of LINC01419 involving metabolic reprogramming in human cancer. The newly identified LINC01419/YBX1-PDK1 axis may represent a promising therapeutic target for HCC. Moreover, GalNAc-siLINC01419 holds significant potential for clinical application. KEY POINTS: This study highlights the considerable regulatory role of LINC01419 in the metabolism of HCC. The newly identified LINC01419/YBX1-PDK1 axis constitutes a valuable target. Hepatic-specific delivery of GalNAc-siLINC01419 presents a promising therapeutic strategy for HCC.
    Keywords:  LINC01419; PDK1; glycolytic pathway; hepatocellular carcinoma; mRNA stability
    DOI:  https://doi.org/10.1002/ctm2.70122
  10. J Immunother Cancer. 2024 Dec 03. pii: e009175. [Epub ahead of print]12(12):
    Co-evolution of glioma and immune microenvironment.
    Mahmoud M Elguindy, Jacob S Young, Winson S Ho, Rongze O Lu.
      Glioma evolution is governed by a multitude of dynamic interactions between tumor cells and heterogenous neighboring, non-cancerous cells. This complex ecosystem, termed the tumor microenvironment (TME), includes diverse immune cell types that have gained increasing attention for their critical and paradoxical roles in tumor control and tumorigenesis. Recent work has revealed that the cellular composition and functional state of immune cells in the TME can evolve extensively depending on the tumor stage and intrinsic features of surrounding glioma cells. Concurrently, adaptations to the glioma cellular phenotype, including activation of various cellular states, occur in the context of these immune cell alterations. In this review, we summarize important features of the immune TME that play key roles during each stage of glioma progression, from initiation to immune escape, invasion and recurrence. Understanding the complex interplay between tumor and immune cells is critical for the development of effective immunotherapies for glioma treatment.
    Keywords:  Immune modulatory; Immunosuppression; Immunotherapy; Tumor microenvironment - TME
    DOI:  https://doi.org/10.1136/jitc-2024-009175
  11. Discov Oncol. 2024 Dec 02. 15(1): 736
    Current advances on the role of ferroptosis in tumor immune evasion.
    Changlin Gao, Haoran Zhang, Xianwei Wang.
      Ferroptosis is a non-apoptotic form of regulated cell death characterized by iron accumulation and uncontrolled lipid peroxidation, leading to plasma membrane rupture and intracellular content release. Cancer immunotherapy, especially immune checkpoint inhibitors (ICIs) targeting PD-1 and PD-L1, has been considered a breakthrough in cancer treatment, achieving encouraging clinical anti-tumor effects in a variety of cancers. However, tumor immune evasion is indispensable to immunotherapy failure. The mechanisms of tumor immune evasion are quite complex, and its occurrence is inseparable from the ferroptosis in tumor microenvironment (TME). Thus, a comprehensive understanding of the role of ferroptosis in tumor immune evasion is crucial to enhance the efficacy of immunotherapy. In this review, we provide an overview of the recent advancements in understanding ferroptosis in cancer, covering molecular mechanisms and interactions with the TME. We also summarize the potential applications of ferroptosis induction in immunotherapy, as well as ferroptosis inhibition for cancer treatment in various conditions. We finally discuss ferroptosis as a double-edged sword, including the current challenges and future directions regarding its potential for cancer treatment.
    Keywords:  Cancer immunotherapy; Ferroptosis; Tumor immune evasion; Tumor microenvironment
    DOI:  https://doi.org/10.1007/s12672-024-01573-1
  12. Nat Rev Clin Oncol. 2024 Dec 02.
    Getting the right combination to break the epigenetic code.
    Seda S Tolu, Aaron D Viny, Jennifer E Amengual, Barbara Pro, Susan E Bates.
      Rapid advances in the field of epigenetics have facilitated the development of novel therapeutics targeting epigenetic mechanisms that are hijacked by cancer cells to support tumour growth and progression. Several epigenetic agents have been approved by the FDA for the treatment of cancer; however, the efficacy of these drugs is dependent on the underlying biology and drivers of the disease, with inherent differences between solid tumours and haematological malignancies. The efficacy of epigenetic drugs as single agents remains limited across most cancer types, which has spurred the clinical development of combination therapies, with the hope of attaining synergistic activity and/or overcoming treatment resistance. In this Review we discuss clinical advances that have been achieved with the use of epigenetic agents in combination with chemotherapies, immunotherapies or other targeted agents, including epigenetic-epigenetic combinations, as well as limitations and challenges associated with these combinatorial strategies. So far, the success of combination therapies targeting epigenetic mechanisms has generally been confined to haematological malignancies, with limited efficacy observed in patients with solid tumours. Nevertheless, this Review captures the field of epigenetic combination therapies across the spectra of haematology and oncology, highlighting opportunities for precision therapy to effectively harness the potential of epigenetic agents and produce meaningful improvements in clinical outcomes.
    DOI:  https://doi.org/10.1038/s41571-024-00972-1
  13. Transl Oncol. 2024 Nov 30. pii: S1936-5233(24)00344-9. [Epub ahead of print]51 102220
    O-GlcNAcylation in ovarian tumorigenesis and its therapeutic implications.
    Lu Xia, Jie Mei, Min Huang, Dandan Bao, Zhiwei Wang, Yizhe Chen.
      Ovarian cancer is a prevalent malignancy among women, often associated with a poor prognosis. Post-translational modifications (PTMs), particularly O-GlcNAcylation, have been implicated in the progression of ovarian cancer. Emerging evidence indicates that dysregulation of O-GlcNAcylation contributes to the initiation and malignant progression of ovarian cancer. This review discusses the potential role of O-GlcNAcylation in ovarian tumorigenesis, with a focus on its regulation of various cellular signaling pathways, including p53, RhoA/ROCK/MLC, Ezrin/Radixin/Moesin (ERM), and β-catenin. This review also emphasizes the O-GlcNAcylation of critical proteins in ovarian cancer, such as SNAP-23, SNAP-29, E-cadherin, and calreticulin. Additionally, the potential of O-GlcNAcylation to enhance immunotherapy for ovarian cancer patients is explored. Several compounds targeting OGT and OGA in ovarian cancer are also highlighted. Targeting the dynamic and versatile nature of O-GlcNAcylation could undoubtedly contribute to more effective treatments and improved outcomes for ovarian cancer patients.
    Keywords:  Immunotherapy; O-GlcNAcylation; OGA; OGT; Ovarian cancer; PTM
    DOI:  https://doi.org/10.1016/j.tranon.2024.102220
  14. FEBS J. 2024 Dec 06.
    FAHD1 and mitochondrial metabolism: a decade of pioneering discoveries.
    Elia Cappuccio, Max Holzknecht, Michèle Petit, Anne Heberle, Yana Rytchenko, Athanasios Seretis, Ciro L Pierri, Hubert Gstach, Pidder Jansen-Dürr, Alexander K H Weiss.
      This review consolidates a decade of research on fumarylacetoacetate hydrolase domain containing protein 1 (FAHD1), a mitochondrial oxaloacetate tautomerase and decarboxylase with profound implications in cellular metabolism. Despite its critical role as a regulator in mitochondrial metabolism, FAHD1 has remained an often-overlooked enzyme in broader discussions of mitochondrial function. After more than 12 years of research, it is increasingly clear that FAHD1's contributions to cellular metabolism, oxidative stress regulation, and disease processes such as cancer and aging warrant recognition in both textbooks and comprehensive reviews. The review delves into the broader implications of FAHD1 in mitochondrial function, emphasizing its roles in mitigating reactive oxygen species (ROS) levels and regulating complex II activity, particularly in cancer cells. This enzyme's significance is further highlighted in the context of aging, where FAHD1's activity has been shown to influence cellular senescence, mitochondrial quality control, and the aging process. Moreover, FAHD1's involvement in glutamine metabolism and its impact on cancer cell proliferation, particularly in aggressive breast cancer subtypes, underscores its potential as a therapeutic target. In addition to providing a comprehensive account of FAHD1's biochemical properties and structural insights, the review integrates emerging hypotheses regarding its role in metabolic reprogramming, immune regulation, and mitochondrial dynamics. By establishing a detailed understanding of FAHD1's physiological roles and therapeutic potential, this work advocates for FAHD1's recognition in foundational texts and resources, marking a pivotal step in its integration into mainstream metabolic research and clinical applications in treating metabolic disorders, cancer, and age-related diseases.
    Keywords:  FAHD1; ODx; ROS; TCA cycle; aging and cellular senescence; cancer metabolism; glutamine metabolism; mitochondrial dysfunction; mitochondrial metabolism
    DOI:  https://doi.org/10.1111/febs.17345
  15. Epilepsy Behav. 2024 Dec 04. pii: S1525-5050(24)00490-6. [Epub ahead of print]163 110108
    The effect of Mozart's K.448 on epilepsy: A systematic literature review and supplementary research on music mechanism.
    Cheng Yen Wang, Jiayang Guo, Xiaoping Guo.
      The "Mozart effect" in epilepsy was first identified by Hughes et al. in 1998. In their treatment of 29 (ages 3-47) patients with epilepsy, including children, the patients showed a significant reduction in epileptic activity on the EEG while listening to "Mozart's Sonata for Two Pianos K.448" (Hereafter referred to as "Mozart's K.448"), a phenomenon that has come to be known as the "Mozart effect" of epilepsy. For more than 26 years now this unique and valuable finding has attracted increasing attention and research. This review aims to examine and discuss the relevant literature on the "Mozart effect" and to further explore the adjunctive therapeutic effects of the "Mozart effect" in patients with epilepsy. While reviewing the research, we were surprised to find that no one has ever analyzed the unique organization of Mozart's K.448 score based on music theory, and that research on the underlying musical mechanisms of Mozart's K.448 is still stuck on Hughe's "hypotheses" and "computer analyses" from 26 years ago, this is a regrettable research gap. Therefore, this paper attempts to fill this gap and analyze the unique organizational structure of Mozart's K448 music score from the perspective of music specialty for the first time. We selected three musical segments from the beginning of the piano performance to the 300-second and 30-second piano scores to analyze the internal structure of Mozart's K.448, our analysis results verify that Hughe's hypothesis that Mozart's k.448 has "periodic repetition" is reasonable, thus supplementing the research on the potential musical mechanism of Mozart effect.
    Keywords:  Epilepsy; Literature review; Mozart effect; Musical mechanisms
    DOI:  https://doi.org/10.1016/j.yebeh.2024.110108
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