Neurochemistry international最新文献

{"title":"Neuroprotective effects of nutraceuticals and natural products in Traumatic Brain Injury.","authors":"K M Bhargavi, Niya Gowthami, G K Chetan, M M Srinivas Bharath","doi":"10.1016/j.neuint.2024.105904","DOIUrl":"https://doi.org/10.1016/j.neuint.2024.105904","url":null,"abstract":"<p><p>Traumatic Brain Injury (TBI) is a global healthcare concern with considerable mortality and morbidity. Early diagnosis and timely treatment are critical for optimal clinical prognosis in TBI patients. Injury to the brain tissue following TBI is categorized into primary and secondary injury events, with the former being acute, while the latter evolves over a long period. Although surgical intervention is effective to treat primary injury, secondary injury events that could contribute to long term neurological deterioration, cognitive impairment and neurodegeneration do not have appropriate pharmacotherapy. To address this lacuna, studies based on modern medicine to explore novel drugs in TBI have met with limited success. This has led to focussed efforts to assess natural products capable of targeting multiple pathways in TBI. Complex natural mixtures and isolated phytochemicals capable of targeting redox mechanisms, neuroinflammation, mitochondrial dysfunction, cell death pathways and other specific targets etc. have been characterized. However, the field has met with certain limitations and challenges with inadequate clinical studies and trials being the most important concern. The current review provides an overview of the dietary factors, nutraceuticals, natural extracts, and phytochemicals that could be potentially applied in neuroprotection, TBI therapy and long-term management of cognitive symptoms and other neurological deficits.</p>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":" ","pages":"105904"},"PeriodicalIF":4.4,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142646555","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}

{"title":"Polygonatum sibiricum polysaccharides: A promising strategy in the treatment of neurodegenerative disease","authors":"Xue Jiang ,&nbsp;Yumei Wang ,&nbsp;Zhaochen Lin ,&nbsp;Chao Li ,&nbsp;Qian Wang ,&nbsp;Junyan Zhang ,&nbsp;Xiuhua Liu ,&nbsp;Ziye Li ,&nbsp;Chao Cui","doi":"10.1016/j.neuint.2024.105902","DOIUrl":"10.1016/j.neuint.2024.105902","url":null,"abstract":"<div><div>Neurodegenerative diseases (NDDs), as a neurological disorder characterised by neuronal degeneration and death, are a serious threat to human health and have long attracted attention due to their complex pathogenesis and the ineffectiveness of therapeutic drugs. Existing studies have shown that <em>Polygonatum Sibiricum</em> polysaccharides (PSP) have immunoregulatory, antioxidant, anti-inflammatory and other pharmacological effects, and their neuroprotective effects have been demonstrated in several scientific studies. This paper reviews the main pharmacological effects and mechanisms of PSP in the protection and treatment of NDDs, to provide a reference for the clinical application and basic research of PSP in NDDs.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"181 ","pages":"Article 105902"},"PeriodicalIF":4.4,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142611479","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}

{"title":"The wnt/pyruvate kinase, muscle axis plays an essential role in the differentiation of mouse neuroblastoma cells","authors":"Cheng Lei ,&nbsp;Jiaqi Wang ,&nbsp;Xiaoyu Zhang ,&nbsp;Xuemin Ge ,&nbsp;Wei Zhao ,&nbsp;Xinrong Li ,&nbsp;Wei Jiang ,&nbsp;Mingyu Ma ,&nbsp;Zhenhai Wang ,&nbsp;Shanshan Sun ,&nbsp;Qingfei Kong ,&nbsp;Hulun Li ,&nbsp;Lili Mu ,&nbsp;Jinghua Wang","doi":"10.1016/j.neuint.2024.105901","DOIUrl":"10.1016/j.neuint.2024.105901","url":null,"abstract":"<div><div>Neuronal differentiation and neurite growth are essential processes in nervous system development and are regulated by several factors. Although all-trans retinoic acid (ATRA) has been shown to mediate the differentiation of mouse neuroblastoma cells via the activation of several pathways, including Wnt/β-catenin signaling, the mechanism remains unclear. The pyruvate kinase, muscle (PKM) plays an important role in the glycolysis of neuroblastoma cells and regulates the Wnt signaling pathway in various cancer cells. In this study, we hypothesized that the Wnt/PKM axis regulates the differentiation of neuroblastoma cells (Neuro-2a and N1E-115). To test this hypothesis, we used inhibitors and activators of the Wnt/β-catenin and glycolytic pathways in ATRA-induced differentiated Neuro-2a and N1E-115 cells and established cell lines with silenced or a mutant replacement of Pkm. Western blot and qPCR showed that ATRA treatment activated the Wnt signaling pathway and inhibited PKM-mediated glycolysis. The oxygen consumption rate (indicating oxidative phosphorylation) significantly increased, whereas the extracellular acidification rate (indicating glycolysis) significantly decreased during differentiation; these effects were reversed upon PKM inhibition. The Wnt inhibitor ICG-001 and PKM activator ML-265 inhibited ATRA-induced Neuro-2a and N1E-115 differentiation, whereas RNA interference-mediated Pkm silencing promoted Neuro-2a and N1E-115 differentiation, which was reversed by PKM overexpression. Treatment with the Wnt activator kenpaullone promoted Neuro-2a and N1E-115 differentiation, which was reversed by ML-265 administration. These results indicate that Wnt/β-catenin signaling promotes Neuro-2a and N1E-115 differentiation by inhibiting PKM-mediated glycolysis during ATRA-induced differentiation. These findings may provide a new theoretical basis for the role of glycolysis in nerve differentiation.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"181 ","pages":"Article 105901"},"PeriodicalIF":4.4,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142611483","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}

{"title":"The developing mouse dopaminergic system: Cortical-subcortical shift in D1/D2 receptor balance and increasing regional differentiation.","authors":"Ingvild E Bjerke, Harry Carey, Jan G Bjaalie, Trygve B Leergaard, Jee Hyun Kim","doi":"10.1016/j.neuint.2024.105899","DOIUrl":"https://doi.org/10.1016/j.neuint.2024.105899","url":null,"abstract":"<p><p>The dopaminergic system of the brain is involved in complex cognitive functioning and undergoes extensive reorganization during development. Yet, these changes are poorly characterized. We have quantified the density of dopamine 1- and 2-receptor (D1 and D2) positive cells across the forebrain of male and female mice at five developmental stages using validated transgenic mice expressing green fluorescent protein in cells producing D1 or D2 mRNA. After analyzing >4,500 coronal brain images, a cortico-subcortical shift in D1/D2 balance was discovered, with increasing D1 dominance in cortical regions as a maturational pattern that occurs earlier in females. We describe postnatal trajectories of D1 and D2 cell densities across major brain regions and observe increasing regional differentiation of D1 densities through development. Our results provide the most comprehensive overview of the developing dopaminergic system to date, and an empirical foundation for further experimental and computational investigations of dopaminergic signaling.</p>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":" ","pages":"105899"},"PeriodicalIF":4.4,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142611482","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}

{"title":"An overview of the relationship between inflammation and cognitive function in humans, molecular pathways and the impact of nutraceuticals","authors":"Chusana Mekhora ,&nbsp;Daniel J. Lamport ,&nbsp;Jeremy P.E. Spencer","doi":"10.1016/j.neuint.2024.105900","DOIUrl":"10.1016/j.neuint.2024.105900","url":null,"abstract":"<div><div>Inflammation has been associated with cognitive decline, whether in the peripheral or central nervous systems. The primary mechanism involves the response of microglia, an immune cell in the brain, which generates pro-inflammatory mediators such as cytokines, chemokines, and adhesion molecules. The excessive production of pro-inflammatory mediators may accelerate the damage to neurons, contributing to the development of neurodegenerative diseases such as Alzheimer's disease, mild cognitive impairment, and vascular dementia, as well as a general decline in cognitive function. Various studies have supported the correlation between elevated pro-inflammatory mediators and a decline in cognitive function, particularly in aging and age-related neurodegenerative diseases. Moreover, this association has also been observed in other inflammatory-related conditions, including post-operative cognitive impairment, diabetes, stroke, obesity, and cancer. However, the interaction between inflammatory processes and cognitive function in humans remains unclear and varies according to different health conditions. Therefore, this review aims to consolidate and evaluate the available evidence from original studies as well as meta-analyses in order to provide a greater understanding of the inflammatory process in connection with cognitive function in humans. Furthermore, relevant biological cellular processes, putative inflammatory biomarkers, and the role of nutraceuticals on the interaction between cognitive performance and inflammatory status are outlined.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"181 ","pages":"Article 105900"},"PeriodicalIF":4.4,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142611486","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impairment of neuromotor development and cognition associated with histopathological and neurochemical abnormalities in the cerebral cortex and striatum of glutaryl-CoA dehydrogenase deficient mice","authors":"Ediandra Tissot Castro ,&nbsp;Rafael Teixeira Ribeiro ,&nbsp;Andrey Vinicios Soares Carvalho ,&nbsp;Diorlon Nunes Machado ,&nbsp;Ângela Beatris Zemniaçak ,&nbsp;Rafael Palavro ,&nbsp;Sâmela de Azevedo Cunha ,&nbsp;Tailine Quevedo Tavares ,&nbsp;Diogo Onofre Gomes de Souza ,&nbsp;Carlos Alexandre Netto ,&nbsp;Guilhian Leipnitz ,&nbsp;Alexandre Umpierrez Amaral ,&nbsp;Moacir Wajner","doi":"10.1016/j.neuint.2024.105898","DOIUrl":"10.1016/j.neuint.2024.105898","url":null,"abstract":"<div><div>Patients with glutaric acidemia type I (GA I) manifest motor and intellectual disabilities whose pathogenesis has been so far poorly explored. Therefore, we evaluated neuromotor and cognitive abilities, as well as histopathological and immunohistochemical features in the cerebral cortex and striatum of glutaryl-CoA dehydrogenase (GCDH) deficient knockout mice (<em>Gcdh</em>^{<em>−/−</em>}), a well-recognized model of GA I. The effects of a single intracerebroventricular glutaric acid (GA) injection in one-day-old pups on the same neurobehavioral and histopathological/immunohistochemical endpoints were also investigated. Seven-day-old <em>Gcdh</em>^{<em>−/−</em>} mice presented altered gait, whereas those receiving a GA neonatal administration manifested other sensorimotor deficits, including an abnormal response to negative geotaxis, cliff aversion and righting reflex, and muscle tone impairment. Compared to the WT mice, adult <em>Gcdh−/−</em> mice exhibited motor impairment, evidenced by poor performance in the Rota-rod test. Furthermore, neonatal GA administration provoked long-standing short- and long-term memory impairment in adult <em>Gcdh</em>^{<em>−/−</em>} mice. Regarding the histopathological features, a significant increase in vacuoles and neurodegenerative cells was observed in both the cerebral cortex and striatum of 15- and 60-day-old Gcd<em>h−/−</em> mice and was more pronounced in mice injected with GA. Neuronal loss (decrease of NeuN staining) was also significantly increased in the cerebral cortex and striatum of <em>Gcdh</em>^{<em>−/−</em>} mice, particularly in those neonatally injected with GA. In contrast, immunohistochemistry of MBP, astrocytic proteins GFAP and S100B, and the microglial marker Iba1 was not changed in 60-day-old Gcdh−/− mice, suggesting no myelination disturbance, reactive astrogliosis, and microglia activation, respectively. These data highlight the neurotoxicity of GA and the importance of early treatment aiming to decrease GA accumulation at early stages of development to prevent brain damage and learning/memory disabilities in GA I patients.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"181 ","pages":"Article 105898"},"PeriodicalIF":4.4,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142611499","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}

{"title":"Boron: An intriguing factor in retarding Alzheimer's progression","authors":"Ashmita Das ,&nbsp;Vikas Rajput ,&nbsp;Durlav Chowdhury ,&nbsp;Rajesh Choudhary ,&nbsp;Surendra H. Bodakhe","doi":"10.1016/j.neuint.2024.105897","DOIUrl":"10.1016/j.neuint.2024.105897","url":null,"abstract":"<div><div>Alzheimer's disease (AD) is a neurodegenerative disorder that is the fifth most common cause of mortality worldwide and the second most common cause of death in developed countries. The etiology of AD remains poorly understood; however, it is correlated with the accumulation of proteins in the brain, ultimately leading to cellular damage. Multiple factors, including genetic and environmental factors such as chemicals or food, have been linked to protein aggregation and cell death in AD. Boron is a vital micronutrient that is necessary for plant growth and is abundantly present in various fruits and nuts. Prior research has emphasized the importance of boron as a neuroprotective agent and necessary component for the preservation of brain health and function. However, the precise function of boron in the brain remains poorly understood. This review elucidates the molecular role of boron in the brain by examining existing information about its impact on neurodegenerative diseases and may provide a deeper understanding of the etiology of AD and, ultimately, lead to the development of novel approaches for its treatment.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"181 ","pages":"Article 105897"},"PeriodicalIF":4.4,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142611497","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}

{"title":"Tetramethylpyrazine promotes axonal remodeling and modulates microglial polarization via JAK2-STAT1/3 and GSK3-NFκB pathways in ischemic stroke","authors":"Xuefeng Feng ,&nbsp;Mingcong Li ,&nbsp;Ziyue Lin ,&nbsp;Yun Lu ,&nbsp;Yuming Zhuang ,&nbsp;Jianfeng Lei ,&nbsp;Xiaonan Liu ,&nbsp;Hui Zhao","doi":"10.1016/j.neuint.2023.105607","DOIUrl":"10.1016/j.neuint.2023.105607","url":null,"abstract":"<div><p>Ischemic stroke results in demyelination that underlies neurological disfunction. Promoting oligodendrogenesis will rescue the injured axons and accelerate remyelination after stroke. Microglia react to ischemia/hypoxia and polarize to M1/M2 phenotypes influencing myelin injury and repair. Tetramethylpyrazine (TMP) has neuroprotective effects in treating cerebrovascular disorders. This study aims to evaluate whether TMP promotes the renovation of damaged brain tissues especially on remyelination and modulates microglia phenotypes following ischemic stroke. Here magnetic resonance imaging (MRI)-diffusion tensor imaging (DTI) and histopathological evaluation are performed to characterize the process of demyelination and remyelination. Immunofluorescence staining is used to prove oligodendrogenesis and microglial polarization. Western blotting is conducted to examine interleukin (IL)-6, IL-10, transforming growth factor β (TGF-β) and Janus protein tyrosine kinase (JAK) 2-signal transducer and activator of transcription (STAT) 1/3-glycogen synthase kinase (GSK) 3-nuclear transcription factor κB (NFκB) signals. Results show TMP alleviates the injury of axons and myelin sheath, increases NG2⁺, Ki67⁺/NG2⁺, CNPase⁺, Ki67⁺/CNPase⁺, Iba1⁺/Arg-1⁺ cells and decreases Iba1⁺ and Iba1⁺/CD16⁺ cells in periinfarctions of rats. Particularly, TMP downregulates IL-6 and upregulates IL-10 and TGF-β expressions, besides, enhances JAK2-STAT3 and suppresses STAT1-GSK3-NFκB activation in middle cerebral artery occlusion (MCAo) rats. Then we demonstrate that TMP reverses M1/M2 phenotype via JAK2-STAT1/3 and GSK3-NFκB pathways in lipopolysaccharide (LPS) plus interferon-γ (IFN-γ)-stimulated BV2 microglia. Blocking JAK2 with AG490 counteracts TMP's facilitation on M2 polarization of microglia. This study warrants the promising therapy for stroke with TMP treatment.</p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"170 ","pages":"Article 105607"},"PeriodicalIF":4.2,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0197018623001353/pdfft?md5=ba7c5d6df623ca15adebb8e3ee4e1f53&pid=1-s2.0-S0197018623001353-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10153682","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Involvement of protein L-isoaspartyl methyltransferase in the physiopathology of neurodegenerative diseases: Possible substrates associated with synaptic function","authors":"Sirui Zhou ,&nbsp;Yancheng Zhou ,&nbsp;Wanyu Zhong ,&nbsp;Zhonghao Su ,&nbsp;Zhenxia Qin","doi":"10.1016/j.neuint.2023.105606","DOIUrl":"10.1016/j.neuint.2023.105606","url":null,"abstract":"<div><p><span><span><span>Synaptic dysfunction is a typical pathophysiologic change in neurodegenerative diseases (NDs) such as </span>Alzheimer's disease (AD), </span>Parkinson's disease<span><span> (PD), Hintington's disease (HD) and amyotrophic lateral sclerosis (ALS), which involves protein post-translational modifications (PTMs) including L-isoaspartate (L-isoAsp) formed by </span>isomerization of </span></span>aspartate<span> or deamidation<span> of asparagine<span>. The formation of L-isoAsp could be repaired by protein L-isoaspartyl methyltransferase (PIMT). Some synaptic proteins have been identified as PIMT potential substrates and play an essential role in ensuring synaptic function. In this review, we discuss the role of certain synaptic proteins as PIMT substrates in neurodegenerative disease, thus providing therapeutic synapse-centered targets for the treatment of NDs.</span></span></span></p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"170 ","pages":"Article 105606"},"PeriodicalIF":4.2,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10245136","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}

{"title":"Knockdown of repulsive guidance molecule a promotes polarization of microglia into an anti-inflammatory phenotype after oxygen-glucose deprivation-reoxygenation in vitro","authors":"Guanru Shen ,&nbsp;Hongmei Xiao ,&nbsp;Siyuan Huang,&nbsp;Xiaofan Yuan,&nbsp;Zhang Rongrong,&nbsp;Yue Ma,&nbsp;Xinyue Qin","doi":"10.1016/j.neuint.2023.105546","DOIUrl":"10.1016/j.neuint.2023.105546","url":null,"abstract":"<div><p><span><span>Repulsive guidance molecule<span> a (RGMa) is a glycosylphosphatidylinositol-anchored glycoprotein<span><span> that has been demonstrated to influence neuroinflammatory-related diseases in addition to regulating neuronal differentiation and survival during brain development. However, any function or mechanism of RGMa in the polarization of </span>microglia after </span></span></span>ischemic stroke remains unclear. In the current study, RGMa was found to be expressed at reduced levels in microglia after oxygen-glucose deprivation-reoxygenation (OGD/R) </span><em>in vitro</em><span><span>. RGMa overexpression induced HAPI microglia to predominantly polarize to the M1 phenotype, promoting the release of proinflammatory cytokines<span> and knockdown induced the M2 phenotype, promoting the release of anti-inflammatory cytokines. RGMa overexpression also regulated the polarization of HAPI microglia by inhibiting the transportation of peroxisome proliferator-activated receptor γ (PPARγ) from the nucleus to cytoplasm. The opposite effect resulted from RGMa-knockdown and was reversed by the PPARγ antagonist, GW9662. In addition, RGMa-knockdown HAPI microglial conditioned medium improved the survival of </span></span>oligodendrocytes after OGD/R </span><em>in vitro</em><span>. Thus, inhibition of RGMa may constitute a therapeutic strategy for reducing neuroinflammation after ischemic stroke.</span></p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"170 ","pages":"Article 105546"},"PeriodicalIF":4.2,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10132010","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}