Neurochemistry international最新文献

筛选
英文 中文
In Vitro Effects of Recombinant Human Neuritin on Hair Cell Recovery Post-Gentamicin Injury in SC Lineage-Tracing Models: Involvement of Notch and FGFR Signaling. 重组人神经素对SC谱系追踪模型中庆大霉素损伤后毛细胞恢复的体外影响:Notch和FGFR信号通路的参与
IF 4.4 3区 医学
Neurochemistry international Pub Date : 2025-01-17 DOI: 10.1016/j.neuint.2025.105935
Haiyan Wang, Xue Zhang, Fei Gui, Xiaopin Sun, Rong Chen, Guanwu Yin, Yu Hong, Jin Huang, Lei Yang
{"title":"In Vitro Effects of Recombinant Human Neuritin on Hair Cell Recovery Post-Gentamicin Injury in SC Lineage-Tracing Models: Involvement of Notch and FGFR Signaling.","authors":"Haiyan Wang, Xue Zhang, Fei Gui, Xiaopin Sun, Rong Chen, Guanwu Yin, Yu Hong, Jin Huang, Lei Yang","doi":"10.1016/j.neuint.2025.105935","DOIUrl":"https://doi.org/10.1016/j.neuint.2025.105935","url":null,"abstract":"<p><p>Hair cell (HC) loss, frequently induced by ototoxic agents such as gentamicin, leads to irreversible hearing loss. Because of the restricted regenerative capabilities of the mammalian inner ear, the exploration of therapeutic strategies to restore damaged HCs is critically needed. Recombinant human Neuritin (rhNeuritin), a neurotrophic factor with established roles in promoting cell survival and regeneration across various systems, presents itself as a promising therapeutic candidate for HC repair. In this study, we elucidate the protective effects of rhNeuritin on injured HCs and its capacity to facilitate HC regeneration post-damage. Through the use of cochlear Supporting Cell (SC) lineage-tracing models in neonatal mice, we demonstrate that SC trans-differentiation serves as the origin of HC regeneration following damage. Simultaneously, we uncover that rhNeuritin potentiates the proliferation of SC precursor cells. Mechanistic insights reveal that rhNeuritin-induced cochleae exhibit downregulation of the critical Notch pathway mediator, Hes1, and upregulation of the essential FGFR pathway component Erm, which together may underpin HC regeneration and the proliferation of SC precursors. Notably, rhNeuritin demonstrates significant preservation of HC structural integrity. These findings collectively highlight the therapeutic potential of rhNeuritin in addressing hearing loss resulting from HC damage, thereby opening a new avenue for the restoration of auditory function.</p>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":" ","pages":"105935"},"PeriodicalIF":4.4,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142997942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
TDP-43 transports ferritin heavy chain mRNA to regulate oxidative stress in neuronal axons. TDP-43转运铁蛋白重链mRNA调控神经元轴突氧化应激。
IF 4.4 3区 医学
Neurochemistry international Pub Date : 2025-01-17 DOI: 10.1016/j.neuint.2025.105934
Jyunki Jinno, Rehab F Abdelhamid, Junko Morita, Ryoko Saga, Yusuke Yamasaki, Atsushi Kadowaki, Kotaro Ogawa, Yasuyoshi Kimura, Kensuke Ikenaka, Goichi Beck, Kousuke Baba, Yoshitaka Nagai, Emiko Kasahara, Atsuo Sekiyama, Tasuku Hirayama, Isao Hozumi, Tatsuya Hasegawa, Toshiyuki Araki, Hideki Mochizuki, Seiichi Nagano
{"title":"TDP-43 transports ferritin heavy chain mRNA to regulate oxidative stress in neuronal axons.","authors":"Jyunki Jinno, Rehab F Abdelhamid, Junko Morita, Ryoko Saga, Yusuke Yamasaki, Atsushi Kadowaki, Kotaro Ogawa, Yasuyoshi Kimura, Kensuke Ikenaka, Goichi Beck, Kousuke Baba, Yoshitaka Nagai, Emiko Kasahara, Atsuo Sekiyama, Tasuku Hirayama, Isao Hozumi, Tatsuya Hasegawa, Toshiyuki Araki, Hideki Mochizuki, Seiichi Nagano","doi":"10.1016/j.neuint.2025.105934","DOIUrl":"https://doi.org/10.1016/j.neuint.2025.105934","url":null,"abstract":"<p><p>Amyotrophic lateral sclerosis (ALS) is characterized by the mislocalization and abnormal deposition of TAR DNA-binding protein 43 (TDP-43). This protein plays important roles in RNA metabolism and transport in motor neurons and glial cells. In addition, abnormal iron accumulation and oxidative stress are observed in the brain and spinal cord of patients with ALS exhibiting TDP-43 pathology and in animal models of ALS. We have previously demonstrated that TDP-43 downregulation significantly affects the expression of ferritin heavy chain (Fth1) mRNA in the axonal regions of neurons. Nevertheless, the mechanisms by which TDP-43 contributes to oxidative stress and iron accumulation in the central nervous system remain elusive. In this study, we aimed to investigate whether Fth1 mRNA is a target transported to the axon by TDP-43 using biophysical and biochemical analyses. Our results revealed Fth1 mRNA as a target mRNA transported to axons by TDP-43. Moreover, we demonstrated that TDP-43 regulates iron homeostasis and oxidative stress in neurons via Fth1 mRNA transport to the axons, possibly followed by a local translation of the ferritin heavy chain in the axons. This study suggests that TDP-43 plays an important role in preventing iron-mediated oxidative stress in neurons, with its loss contributing to ALS pathogenesis.</p>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":" ","pages":"105934"},"PeriodicalIF":4.4,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142997946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Inhibition of Kv1.1 channels ameliorates Cu(II)-induced microglial activation and cognitive impairment in mice. 抑制Kv1.1通道可改善Cu(II)诱导的小鼠小胶质细胞激活和认知障碍。
IF 4.4 3区 医学
Neurochemistry international Pub Date : 2025-01-14 DOI: 10.1016/j.neuint.2025.105936
Wenwen Ni, Jiani Ding, Ping Gong, Xiaofang Tan, Juan Li
{"title":"Inhibition of Kv1.1 channels ameliorates Cu(II)-induced microglial activation and cognitive impairment in mice.","authors":"Wenwen Ni, Jiani Ding, Ping Gong, Xiaofang Tan, Juan Li","doi":"10.1016/j.neuint.2025.105936","DOIUrl":"10.1016/j.neuint.2025.105936","url":null,"abstract":"<p><p>Microglia-mediated neuroinflammation plays a critical role in neuronal damage in neurodegenerative disorders such as Alzheimer's disease. Evidence shows that voltage-gated potassium (Kv) channels regulate microglial activation. We previously reported that copper dyshomeostasis causes neuronal injury via activating microglia. This study was designed to explore the role of Kv1.1 channels in copper-evoked microglial neuroinflammation. BV-2 microglial cells were treated with Cu(II). DiBAC4(3) was used to measure membrane potential. Microglial activation and neuronal loss were detected by enzyme-linked immunosorbent assay, Western blotting, and immunostaining. Learning and memory function was assessed with Morris water maze task. Cu(II) caused a hyperpolarized membrane potential in microglial cells, an effect abolished by functional Kv1.1 blockade. Blockade of Kv1.1 and knock-down of Kv1.1 with small interfering RNA repressed Cu(II)-induced microglial production of pro-inflammatory mediators. Also, Kv1.1 inhibition attenuated activation of PI3K/Akt-ERK1/2 signaling pathway and production of mitochondrial reactive oxidative species as well as nuclear factor-κB activation in Cu(II)-stimulated microglia. Moreover, the Cu(II)-caused, microglia-mediated neurotoxicity (indicated by reduced neuronal survival and increased dendritic loss) was attenuated by Kv1.1 knock-down. In an in vivo mouse model, hippocampal injection of Cu(II) caused elevated Kv1.1 mRNA (but not other Kv1 channels) expression and enhanced microglial Kv1.1 immunoreactivity in the hippocampus. Furthermore, blockade of Kv1.1 attenuated Cu(II)-induced microglial activation and neuronal dendritic loss in the hippocampus and learning and memory dysfunction. These findings suggest that inhibition of Kv1.1 ameliorates Cu(II)-induced microglial activation and cognitive impairment. Thus, it might represent a potential molecular target for anti-inflammatory therapy of neurodegenerative disorders.</p>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":" ","pages":"105936"},"PeriodicalIF":4.4,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142997944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The role of mitochondrial remodeling in neurodegenerative diseases. 线粒体重塑在神经退行性疾病中的作用。
IF 4.4 3区 医学
Neurochemistry international Pub Date : 2025-01-09 DOI: 10.1016/j.neuint.2024.105927
Duanqin Guan, Congmin Liang, Dongyan Zheng, Shizhen Liu, Jiankun Luo, Ziwei Cai, He Zhang, Jialong Chen
{"title":"The role of mitochondrial remodeling in neurodegenerative diseases.","authors":"Duanqin Guan, Congmin Liang, Dongyan Zheng, Shizhen Liu, Jiankun Luo, Ziwei Cai, He Zhang, Jialong Chen","doi":"10.1016/j.neuint.2024.105927","DOIUrl":"10.1016/j.neuint.2024.105927","url":null,"abstract":"<p><p>Neurodegenerative diseases are a group of diseases that pose a serious threat to human health, such as Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD) and Amyotrophic Lateral Sclerosis (ALS). In recent years, it has been found that mitochondrial remodeling plays an important role in the onset and progression of neurodegenerative diseases. Mitochondrial remodeling refers to the dynamic regulatory process of mitochondrial morphology, number and function, which can affect neuronal cell function and survival by regulating mechanisms such as mitochondrial fusion, division, clearance and biosynthesis. Mitochondrial dysfunction is an important intrinsic cause of the pathogenesis of neurodegenerative diseases. Mitochondrial remodeling abnormalities are involved in energy metabolism in neurodegenerative diseases. Pathological changes in mitochondrial function and morphology, as well as interactions with other organelles, can affect the energy metabolism of dopaminergic neurons and participate in the development of neurodegenerative diseases. Since the number of patients with PD and AD has been increasing year by year in recent years, it is extremely important to take effective interventions to significantly reduce the number of morbidities and to improve people's quality of life. More and more researchers have suggested that mitochondrial remodeling and related dynamics may positively affect neurodegenerative diseases in terms of neuronal and self-adaptation to the surrounding environment. Mitochondrial remodeling mainly involves its own fission and fusion, energy metabolism, changes in channels, mitophagy, and interactions with other cellular organelles. This review will provide a systematic summary of the role of mitochondrial remodeling in neurodegenerative diseases, with the aim of providing new ideas and strategies for further research on the treatment of neurodegenerative diseases.</p>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":" ","pages":"105927"},"PeriodicalIF":4.4,"publicationDate":"2025-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142969080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Understanding the intricacies of cellular mechanisms in remyelination: The role of circadian rhythm. 理解髓鞘再生中细胞机制的复杂性:昼夜节律的作用。
IF 4.4 3区 医学
Neurochemistry international Pub Date : 2025-01-03 DOI: 10.1016/j.neuint.2025.105929
Yufen Tang, Lu Zhang, Peng Huang, Zhou She, Senlin Luo, Hong Peng, Yuqiong Chen, Jinwen Luo, Wangxin Duan, Yangyang Xiao, Lingjuan Liu, Liqun Liu
{"title":"Understanding the intricacies of cellular mechanisms in remyelination: The role of circadian rhythm.","authors":"Yufen Tang, Lu Zhang, Peng Huang, Zhou She, Senlin Luo, Hong Peng, Yuqiong Chen, Jinwen Luo, Wangxin Duan, Yangyang Xiao, Lingjuan Liu, Liqun Liu","doi":"10.1016/j.neuint.2025.105929","DOIUrl":"10.1016/j.neuint.2025.105929","url":null,"abstract":"<p><p>The term \"circadian rhythm\" refers to the 24-h oscillations found in various physiological processes in organisms, responsible for maintaining bodily homeostasis. Many neurological diseases mainly involve the process of demyelination, and remyelination is crucial for the treatment of neurological diseases. Current research mainly focuses on the key role of circadian clocks in the pathophysiological mechanisms of multiple sclerosis. Various studies have shown that the circadian rhythm regulates various cellular molecular mechanisms and signaling pathways involved in remyelination. The process of remyelination is primarily mediated by oligodendrocyte precursor cells (OPCs), oligodendrocytes, microglia, and astrocytes. OPCs are activated, proliferate, migrate, and ultimately differentiate into oligodendrocytes after demyelination, involving many key signaling pathway and regulatory factors. Activated microglia secretes important cytokines and chemokines, promoting OPC proliferation and differentiation, and phagocytoses myelin debris that inhibits remyelination. Astrocytes play a crucial role in supporting remyelination by secreting signals that promote remyelination or facilitate the phagocytosis of myelin debris by microglia. Additionally, cell-to-cell communication via gap junctions allows for intimate contact between astrocytes and oligodendrocytes, providing metabolic support for oligodendrocytes. Therefore, gaining a deeper understanding of the mechanisms and molecular pathways of the circadian rhythm at various stages of remyelination can help elucidate the fundamental characteristics of remyelination and provide insights into treating demyelinating disorders.</p>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":" ","pages":"105929"},"PeriodicalIF":4.4,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142930426","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Discovery of the therapeutic potential of naltriben against glutamate-induced neurotoxicity. 发现硝三苯治疗谷氨酸引起的神经毒性的潜力。
IF 4.4 3区 医学
Neurochemistry international Pub Date : 2025-01-03 DOI: 10.1016/j.neuint.2025.105928
Hyomin Ahn, Hyomin Lee, Wonseok Choi, Hyebin Lee, Kang-Gon Lee, Inchan Youn, Wooyoung Hur, Sungmin Han, Chiman Song
{"title":"Discovery of the therapeutic potential of naltriben against glutamate-induced neurotoxicity.","authors":"Hyomin Ahn, Hyomin Lee, Wonseok Choi, Hyebin Lee, Kang-Gon Lee, Inchan Youn, Wooyoung Hur, Sungmin Han, Chiman Song","doi":"10.1016/j.neuint.2025.105928","DOIUrl":"10.1016/j.neuint.2025.105928","url":null,"abstract":"<p><p>Glutamate-induced neuronal death is associated with neurodegeneration including cerebral ischemia. Several μ-opioid receptor antagonists exhibit a neuroprotective activity and have been considered as a potential therapeutic option for neurodegenerative disorders. For the first time, our current study unveiled the neuroprotective activity of selective δ-opioid receptor antagonists. A potent, selective δ-opioid receptor antagonist naltriben, also known as a potent TRPM7 agonist, displayed the prominent protective effect against glutamate-induced toxicity through opioid receptor-independent, TRPM7-independent mechanisms in HT22 cells. Naltriben activated Nrf2 pathway, and alleviated glutamate-induced Ca<sup>2+</sup> influx, ROS production, and apoptosis. Moreover, intraperitoneal administration of naltriben at 20 mg/kg greatly reduced the infarct volume in the subcortical photothrombotic ischemia mouse model in vivo. The neuroprotective activity of naltriben was enhanced by a longer pretreatment, indicating that like Nrf2 activators, naltriben also requires the cellular priming for its full protective effects. Together, these results suggested naltriben as a potential therapeutic agent in conditions related with glutamate-induced neurotoxicity.</p>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":" ","pages":"105928"},"PeriodicalIF":4.4,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142930418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Neurosteroids and Translocator Protein (TSPO) in neuroinflammation. 神经炎症中的神经类固醇和转运蛋白(TSPO)。
IF 4.4 3区 医学
Neurochemistry international Pub Date : 2025-01-01 Epub Date: 2024-12-15 DOI: 10.1016/j.neuint.2024.105916
Elisa Angeloni, Lorenzo Germelli, Barbara Costa, Claudia Martini, Eleonora Da Pozzo
{"title":"Neurosteroids and Translocator Protein (TSPO) in neuroinflammation.","authors":"Elisa Angeloni, Lorenzo Germelli, Barbara Costa, Claudia Martini, Eleonora Da Pozzo","doi":"10.1016/j.neuint.2024.105916","DOIUrl":"10.1016/j.neuint.2024.105916","url":null,"abstract":"<p><p>Neurosteroids have a crucial role in physiological intrinsic regulations of the Central Nervous System functions. They are derived from peripheral steroidogenic sources and from the de novo neurosteroidogenic capacity of brain cells. Significant alterations of neurosteroid levels have been frequently observed in neuroinflammation and neurodegenerative diseases. Such level fluctuations may be useful for both diagnosis and treatment of these pathological conditions. Beyond steroid administration, enhancing the endogenous production by Translocator Protein (TSPO) targeting has been proposed to restore these altered pathological levels. However, the neurosteroid quantification and the prediction of their final effects are often troublesome, sometimes controversial and context dependent, due to the complexity of neurosteroid biosynthetic pathway and to the low produced amounts. The aim of this review is to report recent advances, and technical limitations, in neurosteroid-related strategies against neuroinflammation.</p>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":" ","pages":"105916"},"PeriodicalIF":4.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142833576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
PDE4D inhibitors: Opening a new era of PET diagnostics for Alzheimer's disease. PDE4D抑制剂:开启阿尔茨海默病PET诊断新时代
IF 4.4 3区 医学
Neurochemistry international Pub Date : 2025-01-01 Epub Date: 2024-12-06 DOI: 10.1016/j.neuint.2024.105903
Luyang Shi, Xue Wang, Hongzong Si, Wangdi Song
{"title":"PDE4D inhibitors: Opening a new era of PET diagnostics for Alzheimer's disease.","authors":"Luyang Shi, Xue Wang, Hongzong Si, Wangdi Song","doi":"10.1016/j.neuint.2024.105903","DOIUrl":"10.1016/j.neuint.2024.105903","url":null,"abstract":"<p><p>As the incidence of Alzheimer's disease (AD) continues to rise, the need for an effective PET radiotracer to facilitate early diagnosis has become more pressing than ever before in modern medicine. Phosphodiesterase (PDE) is closely related to cognitive impairment and neuroinflammatory processes in AD. Current research progress shows that specific PDE4D inhibitors radioligands can bind specifically to the PDE4D enzyme in the brain, thereby showing pathology-related signal enhancement in AD animal models, indicating the potential of these ligands as effective radiotracers. At the same time, we need to pay attention to the important role computer aided drug design (CADD) plays in advancing AD drug design and PET imaging. Future research will verify the potential of these ligands in clinical applications through computer simulation techniques, providing patients with timely intervention and treatment, which is of great significance.</p>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":" ","pages":"105903"},"PeriodicalIF":4.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794043","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Neurometabolite and cognitive changes in hypothyroid patients in response to treatment: In-vivo 1H MRS study. 甲状腺功能减退症患者的神经代谢物和认知变化对治疗的反应:体内 1H MRS 研究。
IF 4.4 3区 医学
Neurochemistry international Pub Date : 2025-01-01 Epub Date: 2024-12-09 DOI: 10.1016/j.neuint.2024.105915
Mukesh Kumar, Sadhana Singh, Poonam Rana, Maria D'souza, S Senthil Kumaran, Tarun Sekhri, Subash Khushu
{"title":"Neurometabolite and cognitive changes in hypothyroid patients in response to treatment: In-vivo <sup>1</sup>H MRS study.","authors":"Mukesh Kumar, Sadhana Singh, Poonam Rana, Maria D'souza, S Senthil Kumaran, Tarun Sekhri, Subash Khushu","doi":"10.1016/j.neuint.2024.105915","DOIUrl":"10.1016/j.neuint.2024.105915","url":null,"abstract":"<p><p>The disturbances in thyroid hormones lead to altered brain metabolism, function, and cognition. Neuroimaging studies have shown structural and functional changes in hypothyroidism. Present study investigates the neuro-metabolite changes in dorsolateral prefrontal cortex (DLPFC) and posterior parietal cortex (PPC) and associated decline cognitive function in hypothyroid patients before and after thyroxine treatment. We performed neuropsychological test and <sup>1</sup>H MRS in hypothyroid patients (n = 25) and controls (n = 30). In addition, follow-up data was also collected from 19 patients treated with levo-thyroxine for 32 weeks. The concentration of the neurometabolites were calculated using LCModel. MRS data were analyzed using analysis of covariance (ANCOVA), with age and gender as covariates. A paired t-test was conducted to compare the baseline hypothyroid with the follow-up. Partial correlations were utilised to assess possible associations between neuropsychological scores and neurometabolites with age and gender as covariates. Spearman correlation was performed between thyroid hormone levels and neurometabolites. Hypothyroid patients showed an impairment in delayed recall, immediate recall of semantic, visual retention, recognition of objects memory, attention, and motor function at baseline, which improved significantly after thyroxine therapy. At baseline, patients with hypothyroidism exhibited significantly higher levels of choline compounds (GPC + PCh) [Cho]. No significant normalization of Cho levels was observed, despite achieving euthyroidism with thyroxine treatment. Cho levels showed a positive correlation with TSH in PPC and a negative correlation with T4 in DLPFC and PCC. Cho levels also showed negative correlations with delayed recall, immediate recall of semantic, visual retention memory and MMSE scores. The MRS findings show increased levels of Cho in hypothyroid patients compared to healthy controls. These Cho levels are not reversible within 32 weeks of treatment, suggesting that a longer follow-up may be needed to see if levels can be normalized.</p>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":" ","pages":"105915"},"PeriodicalIF":4.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142799036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Role of PI3Kγ in the polarization, migration, and phagocytosis of microglia. PI3Kγ在小胶质细胞极化、迁移和吞噬中的作用。
IF 4.4 3区 医学
Neurochemistry international Pub Date : 2025-01-01 Epub Date: 2024-12-13 DOI: 10.1016/j.neuint.2024.105917
Xinghua Liang, Yuan Hu, Xinyue Li, Xi Xu, Zhonglan Chen, Yalin Han, Yingying Han, Guangping Lang
{"title":"Role of PI3Kγ in the polarization, migration, and phagocytosis of microglia.","authors":"Xinghua Liang, Yuan Hu, Xinyue Li, Xi Xu, Zhonglan Chen, Yalin Han, Yingying Han, Guangping Lang","doi":"10.1016/j.neuint.2024.105917","DOIUrl":"10.1016/j.neuint.2024.105917","url":null,"abstract":"<p><p>Phosphoinositide 3-kinase γ (PI3Kγ) is a signaling protein that is constitutively expressed in immune competent cells and plays a crucial role in cell proliferation, apoptosis, migration, deformation, and immunology. Several studies have shown that high expression of PI3Kγ can inhibit the occurrence of inflammation in microglia while also regulating the polarization of microglia to inhibit inflammation and enhance microglial migration and phagocytosis. It is well known that the regulation of microglial polarization, migration, and phagocytosis is key to the treatment of most neurodegenerative diseases. Therefore, in this article, we review the important regulatory role of PI3Kγ in microglia to provide a basis for the treatment of neurodegenerative diseases.</p>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":" ","pages":"105917"},"PeriodicalIF":4.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142826549","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信