Adrián S Elliott, Román D Moreno-Fernández, Patricia Sampedro-Piquero
{"title":"Effects of Alcohol on EEG Activity: A Systematic Review Focused on Sex-Related Differences in Youth.","authors":"Adrián S Elliott, Román D Moreno-Fernández, Patricia Sampedro-Piquero","doi":"10.2174/1570159X23666241106095027","DOIUrl":"10.2174/1570159X23666241106095027","url":null,"abstract":"<p><strong>Background: </strong>Most electroencephalographic (EEG) investigations on alcohol have focused on adults, and scarce data is available about the potential of EEG measurements to detect young people at high-risk, as well as, to understand possible sex differences in alcohol impact on the brain.</p><p><strong>Objective: </strong>This systematic review aimed to explore sex-related differences in EEG among young people with alcohol misuse, alcohol use disorder (AUD), and offspring of families with AUD.</p><p><strong>Methods: </strong>A systematic review of the literature was conducted following PRISMA guidelines. Review protocol was registered in Prospero (ID: CRD42024511471). After article selection process and quality assessment, 25 studies were included in our review. The search included participants between 12 and 30 years old with problematic alcohol consumption, as defined by DSM, AUDIT, or specific alcohol misuse questionnaires.</p><p><strong>Results: </strong>It seems that beta was generally higher in young males with AUD, and they usually exhibited greater interhemispheric connectivity (interHC), whereas young females with AUD tended towards enhanced intraHC. P3 appears to be particularly sensitive to alcohol misuse, with males typically exhibiting a lower amplitude than young females. Other event related potentials (ERPs) such as N415, P640, and the error-related negativity (ERN) lacked sufficient methodological support to draw conclusions regarding sex differences, N340 and P540 suggested avenues for expanding research on memory processing, indicating differences in amplitude between males and females.</p><p><strong>Conclusion: </strong>Considering sex variables in clinical research will enhance our understanding of alterations in brain function and structure with the goal of tailoring treatment strategies for AUD.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142590456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Neuropsychiatric Manifestations of COVID-19 Disease and Post Covid Syndrome: The Role of N Acetyl-cysteine and Acetyl-L-carnitine.","authors":"Tommaso Barlattani, Giuseppe Celenza, Alessandro Cavatassi, Franco Minutillo, Valentina Socci, Carolina Pinci, Riccardo Santini, Francesca Pacitti","doi":"10.2174/011570159X343115241030094848","DOIUrl":"10.2174/011570159X343115241030094848","url":null,"abstract":"<p><p>COVID-19 is associated with neuropsychiatric symptoms, such as anosmia, anxiety, depression, stress-related reactions, and psychoses. The illness can cause persistent cognitive impairment and \"brain fog\", suggesting chronic brain involvement. Clinical entities of ongoing symptomatic COVID-19 and Post COVID Syndrome (PCS) mainly present neuropsychiatric symptoms such as dysgeusia, headache, fatigue, anxiety, depression, sleep disturbances, and post-traumatic stress disorder. The pathophysiology of COVID-19-related brain damage is unclear, but it is linked to various mechanisms such as inflammation, oxidative stress, immune dysregulation, impaired glutamate homeostasis, glial and glymphatic damage, and hippocampal degeneration. Noteworthy is that the metabotropic receptor mGluR2 was discovered as a mechanism of internalisation of SARS-CoV-2 in Central Nervous System (CNS) cells. N-acetylcysteine (NAC) and acetyl-L-carnitine (ALC) are two supplements that have already been found effective in treating psychiatric conditions. Furthermore, NAC showed evidence in relieving cognitive symptomatology in PCS, and ALC was found effective in treating depressive symptomatology of PCS. The overlapping effects on the glutamatergic system of ALC and NAC could help treat COVID-19 psychiatric symptoms and PCS, acting through different mechanisms on the xc-mGluR2 network, with potentially synergistic effects on chronic pain and neuro-astrocyte protection. This paper aims to summarise the current evidence on the potential therapeutic role of NAC and ALC, providing an overview of the underlying molecular mechanisms and pathophysiology. It proposes a pathophysiological model explaining the effectiveness of NAC and ALC in treating COVID-19-related neuropsychiatric symptoms.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142589314","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Tong Nie, Li You, Fang Tang, Yanhui Duan, Eugenie Nepovimova, Kamil Kuca, Qinghua Wu, Wei Wei
{"title":"Microbiota-Gut-Brain Axis in Age-Related Neurodegenerative Diseases.","authors":"Tong Nie, Li You, Fang Tang, Yanhui Duan, Eugenie Nepovimova, Kamil Kuca, Qinghua Wu, Wei Wei","doi":"10.2174/1570159X23666241101093436","DOIUrl":"https://doi.org/10.2174/1570159X23666241101093436","url":null,"abstract":"<p><strong>Background: </strong>Age-related neurodegenerative diseases (NDs) pose a formidable challenge to healthcare systems worldwide due to their complex pathogenesis, significant morbidity, and mortality. Scope and Approach: This comprehensive review aims to elucidate the central role of the microbiotagut- brain axis (MGBA) in ND pathogenesis. Specifically, it delves into the perturbations within the gut microbiota and its metabolomic landscape, as well as the structural and functional transformations of the gastrointestinal and blood-brain barrier interfaces in ND patients. Additionally, it provides a comprehensive overview of the recent advancements in medicinal and dietary interventions tailored to modulate the MGBA for ND therapy.</p><p><strong>Conclusion: </strong>Accumulating evidence underscores the pivotal role of the gut microbiota in ND pathogenesis through the MGBA. Dysbiosis of the gut microbiota and associated metabolites instigate structural modifications and augmented permeability of both the gastrointestinal barrier and the blood-brain barrier (BBB). These alterations facilitate the transit of microbial molecules from the gut to the brain via neural, endocrine, and immune pathways, potentially contributing to the etiology of NDs. Numerous investigational strategies, encompassing prebiotic and probiotic interventions, pharmaceutical trials, and dietary adaptations, are actively explored to harness the microbiota for ND treatment. This work endeavors to enhance our comprehension of the intricate mechanisms underpinning ND pathogenesis, offering valuable insights for the development of innovative therapeutic modalities targeting these debilitating disorders.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142582390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"GRIN2A and Schizophrenia: Scientific Evidence and Biological Mechanisms.","authors":"Xiao-Ming Sheng, Wei Guan","doi":"10.2174/011570159X327712241023084944","DOIUrl":"https://doi.org/10.2174/011570159X327712241023084944","url":null,"abstract":"<p><p>Schizophrenia is a severe psychiatric disorder and a complex polygenic inherited disease that affects nearly 1% of the global population. Although considerable progress has been made over the past 10 years in the treatment of schizophrenia, antipsychotics are not universally effective and may have serious side effects. The hypofunction of glutamate NMDA receptors (NMDARs) in GABAergic interneurons has long been postulated to be the principal pathophysiology of schizophrenia. A recent study has shown that GRIN2A pathogenic variants are closely related to the aetiology of the disorder. GRIN2A encodes the GluN2A protein, which is a subunit of NMDAR. Most GRIN2A variants have been predicted to cause protein truncation, which results in reduced gene expression. Preclinical studies have indicated that GRIN2A mutations lead to NMDAR loss of function and substantially increase the risk of schizophrenia; however, their role in schizophrenia is not well understood. We hypothesise that the heterozygous loss of GRIN2A induces NMDAR hypofunction sufficient to confer a substantial risk of schizophrenia. Therefore, this review focuses on GRIN2A as a target for novel antipsychotics and discusses the mechanisms by which GRIN2A modulates antischizophrenic activities. Moreover, our review contributes to the understanding of the pathophysiology of schizophrenia to facilitate finding treatments for the cognitive and negative symptoms of schizophrenia.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142582385","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Joanna Jastrzębska, Małgorzata Frankowska, Julita Wesołowska, Małgorzata Filip, Irena Smaga
{"title":"Dietary Intervention with Omega-3 Fatty Acids Mitigates Maternal High-Fat Diet-Induced Behavioral and Myelin-Related Alterations in Adult Offspring.","authors":"Joanna Jastrzębska, Małgorzata Frankowska, Julita Wesołowska, Małgorzata Filip, Irena Smaga","doi":"10.2174/1570159X23666241014164940","DOIUrl":"https://doi.org/10.2174/1570159X23666241014164940","url":null,"abstract":"<p><strong>Background: </strong>Maternal high-fat diet (HFD) during pregnancy and lactation induces depression- like phenotype and provokes myelin-related changes in rat offspring in the prefrontal cortex (PFCTX), which persist even to adulthood.</p><p><strong>Objective: </strong>Due to the plasticity of the developing brain, it was decided to analyze whether depressionlike phenotype and myelin-related changes in the early lifetime induced by maternal HFD (60% energy from fat) could be reversed by the omega-3 fatty acid-enriched diet (Ω3D) given from the postweaning period until adulthood (63rd day of life) in offspring.</p><p><strong>Methods: </strong>We analyzed the effect of post-weaning Ω3D on the depressive-like phenotype (assessed by the forced swimming test) and myelin-related changes (measured using RT-qPCR, ELISA, and immunofluorescence staining) in the PFCTX of adult offspring.</p><p><strong>Results: </strong>Ω3D reversed increased immobility time in adult offspring induced by maternal HFD, without affecting the animals' locomotor activity. Molecularly, Ω3D normalized the reduced expression levels of myelin-oligodendrocyte glycoprotein (MOG), as well as myelin and lymphocyte protein (MAL) in males and MOG in females in the PFCTX, changes initially induced by maternal HFD. Additionally, Ω3D normalized the quantity of oligodendrocyte precursor cells and mature oligodendrocytes in the prelimbic, infralimbic, and cingulate cortex in males, which were reduced following maternal HFD exposure. In females, the Ω3D effect was less pronounced, with normalization of oligodendrocyte precursors occurring only in the infralimbic cortex.</p><p><strong>Conclusion: </strong>These findings suggest that Ω3D may play a significant role in correcting behavioral and neurobiological changes caused by adverse prenatal conditions.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142567480","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Antonio Flores-Burgess, Carmelo Millón, Noelia Cantero-García, Juan Pedro Pineda-Gómez, Marta Flores-Gómez, Zaida Díaz-Cabiale
{"title":"A New Augmentation Strategy against Depression Combining SSRIs and the N-terminal Fragment of Galanin (1-15).","authors":"Antonio Flores-Burgess, Carmelo Millón, Noelia Cantero-García, Juan Pedro Pineda-Gómez, Marta Flores-Gómez, Zaida Díaz-Cabiale","doi":"10.2174/1570159X23666241003125019","DOIUrl":"https://doi.org/10.2174/1570159X23666241003125019","url":null,"abstract":"<p><p>Depression is one of the most disabling mental disorders, with the second highest social burden; its prevalence has grown by more than 27% in recent years, affecting 246 million in 2021. Despite the wide range of antidepressants available, more than 50% of patients show treatment-resistant depression. In this review, we summarized the progress in developing a new augmentation strategy based on combining the N-terminal fragment of Galanin (1-15) and SSRI-type antidepressants in animal models.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142557362","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Roberta Zupo, Fabio Castellana, Francesco Panza, Vincenzo Solfrizzi, Madia Lozupone, Roberta Tardugno, Nicola Cicero, Filomena Corbo, Pasquale Crupi, Rodolfo Sardone, Maria Lisa Clodoveo
{"title":"Alzheimer's Disease May Benefit from Olive Oil Polyphenols: A Systematic Review on Preclinical Evidence Supporting the Effect of Oleocanthal on Amyloid-β Load.","authors":"Roberta Zupo, Fabio Castellana, Francesco Panza, Vincenzo Solfrizzi, Madia Lozupone, Roberta Tardugno, Nicola Cicero, Filomena Corbo, Pasquale Crupi, Rodolfo Sardone, Maria Lisa Clodoveo","doi":"10.2174/011570159X327650241021115228","DOIUrl":"https://doi.org/10.2174/011570159X327650241021115228","url":null,"abstract":"<p><strong>Background: </strong>Mediterranean diet may enhance cognitive function and delay the progression of Alzheimer's disease (AD). We conducted a systematic review to investigate the effect of oleocanthal (OC) from extra-virgin olive oil (EVOO) on amyloid-β (Aβ) burden in preclinical models of AD, considering the anti-inflammatory and neuroprotective effects of EVOO biophenols, which are key components of the Mediterranean dietary model.</p><p><strong>Methods: </strong>The literature was searched through six electronic databases until February 2023. Screening of 52 retrieved articles for inclusion criteria resulted in 7 preclinical reports evaluating the effect of an OC-supplemented diet on AD trajectories by means of Aβ load or clearance in affected models. Reports were appraised for risk of bias using the SYRCLE's RoB tool. A protocol was registered on PROSPERO.</p><p><strong>Results: </strong>Case control prevailed over the case-crossover design, and the geographical distribution was uniformly American. The study population mostly included 5xFAD, otherwise TgSwDI or wild-type C57BL/6 mouse models. We found a role of OC in reducing Aβ load in the hippocampal parenchyma and microvessels compared with controls. An increased cerebral clearance of Aβ through the bloodbrain barrier and a substantial improvement in metabolic and behavioral parameters were also reported in preclinical models under an OC-enriched diet. The risk of bias was shown to be moderate overall.</p><p><strong>Conclusion: </strong>Preclinical data are promising about the effects of OC from the Mediterranean diet's EVOO in relieving the burden of Aβ in AD; however, further evidence is needed to corroborate the efficacy of this biophenol and strengthen the speculated causal pathway.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142557363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lin Yang, Jin Li, Fuhong Liu, Xin Chai, Zongping Fang, Xijing Zhang
{"title":"The Biological Changes of Synaptic Plasticity in the Pathological Process of Sepsis-associated Encephalopathy.","authors":"Lin Yang, Jin Li, Fuhong Liu, Xin Chai, Zongping Fang, Xijing Zhang","doi":"10.2174/1570159X23666241028105746","DOIUrl":"https://doi.org/10.2174/1570159X23666241028105746","url":null,"abstract":"<p><p>Sepsis-associated encephalopathy (SAE) is a form of cognitive and psychological impairment resulting from sepsis, which occurs without any central nervous system infection or structural brain injury. Patients may experience long-term cognitive deficits and psychiatric disorders even after discharge. However, the underlying mechanism remains unclear. As cognitive function and mental disease are closely related to synaptic plasticity, it is presumed that alterations in synaptic plasticity play an essential role in the pathological process of SAE. Here, we present a systematic description of the pathogenesis of SAE, which is primarily driven by glial cell activation and subsequent release of inflammatory mediators. Additionally, we elucidate the alterations in synaptic plasticity that occur during SAE and comprehensively discuss the roles played by glial cells and inflammatory factors in this process. In this review, we mainly discuss the synaptic plasticity of SAE, and the main aim is to show the consequences of SAE on inflammatory factors and how they affect synaptic plasticity. This review may enhance our understanding of the mechanism underlying cognitive dysfunction and provide valuable insights into identifying appropriate therapeutic targets for SAE.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142544280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lourdes Álvarez-Sánchez, Mar Peretó, Lorena García-Vallés, Ángel Balaguer, Carmen Peña-Bautista, Laura Ferré-González, Miguel Baquero, Consuelo Cháfer Pericás
{"title":"Fast Declining Prediction in Alzheimer's Disease from Early Clinical Assessment.","authors":"Lourdes Álvarez-Sánchez, Mar Peretó, Lorena García-Vallés, Ángel Balaguer, Carmen Peña-Bautista, Laura Ferré-González, Miguel Baquero, Consuelo Cháfer Pericás","doi":"10.2174/011570159X332930240925095423","DOIUrl":"https://doi.org/10.2174/011570159X332930240925095423","url":null,"abstract":"<p><strong>Intoduction: </strong>The heterogenicity in Alzheimer's Disease (AD) progression hinders individual prognosis. The present work is an observational 2-year longitudinal study in patients with mild cognitive impairment due to AD (n= 52, with positive CSF biomarkers). The aim of this study is to predict which patients are at risk of fast progression. For this, 3 neuropsychological tests based on different domains (clinical dementia, cognition, delayed memory) and the sum of them were used.</p><p><strong>Method: </strong>The tests were performed at diagnosis time (T1) and two years after the diagnosis time (T2). Then, the corresponding progression models were developed using each individual test and their sum as a variable response.</p><p><strong>Results: </strong>As a result, the model based on cognition status to predict fast decline (differences in the Z score (T2-T1) <1.5 were considered fast declining) provided satisfactory performance (AUC 0.74, 83.3% of sensibility and 70.2% of specificity); the models based on clinical dementia and delayed memory to predict fast declining showed low AUC and sensitivity. Nevertheless, the model based on the sum of the 3 tests showed the highest AUC (0.79), low sensitivity (63.6%), and high specificity.</p><p><strong>Conclusion: </strong>The developed progression models could provide useful information to clinicians and AD patients regarding their fast/normal decline in general or specific domains.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142544278","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"NeuropsychopharmARCology: Shaping Neuroplasticity through Arc/Arg3.1 Modulation","authors":"Francesca Mottarlini, Lucia Caffino, Fabio Fumagalli, Francesca Calabrese, Paola Brivio","doi":"10.2174/011570159X338335240903075655","DOIUrl":"10.2174/011570159X338335240903075655","url":null,"abstract":"<p><p>Activity-regulated cytoskeletal associated protein (aka activity-regulated gene Arg3.1) belongs to the effector gene family of the immediate early genes. This family encodes effector proteins, which act directly on cellular homeostasis and function. Arc/Arg3.1 is localized at dendritic processes, allowing the protein local synthesis on demand, and it is considered a reliable index of activitydependent synaptic changes. Evidence also exists showing the critical role of Arc/Arg3.1 in memory processes. The high sensitivity to changes in neuronal activity, its specific localization as well as its involvement in long-term synaptic plasticity indeed make this effector gene a potential, critical target of the action of psychotropic drugs. In this review, we focus on antipsychotic and antidepressant drugs as well as on psychostimulants, which belong to the category of drugs of abuse but can also be used as drugs for specific disorders of the central nervous system (i.e., Attention Deficit Hyperactivity Disorder). It is demonstrated that psychotropic drugs with different mechanisms of action converge on Arc/Arg3.1, providing a means whereby Arc/Arg3.1 synaptic modulation may contribute to their therapeutic activity. The potential translational implications for different neuropsychiatric conditions are also discussed, recognizing that the treatment of these disorders is indeed complex and involves the simultaneous regulation of several dysfunctional mechanisms.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142544279","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}