Bandar A. Alyami, Zeeshan Ahmad, Mehreen Ghufran, Mater H. Mahnashi, Abdul Sadiq, Muhammad Ayaz
{"title":"Appraisal of the Neuroprotective Potentials of Isoeugenol Using In-vitro, In-vivo and In-silico Approaches","authors":"Bandar A. Alyami, Zeeshan Ahmad, Mehreen Ghufran, Mater H. Mahnashi, Abdul Sadiq, Muhammad Ayaz","doi":"10.2174/1570159x22666240329125626","DOIUrl":"https://doi.org/10.2174/1570159x22666240329125626","url":null,"abstract":"Background: Alzheimer's disease (AD) is a neurodegenerative condition that affects the elder population and is linked to behavioral instability and cognitive decline. Only a few drugs are approved for clinical management of AD. Volatile oils and their components exhibit diverse pharmacological potentials, including neuroprotective properties. The current study aimed to evaluate isoeugenol's neuroprotective potentials against cognitive impairments caused by scopolamine. Methods: Standard protocols were followed in the in-vitro antioxidant, cholinesterase inhibitory and molecular docking assays. Isoeugenol was initially evaluated for antioxidant potential using DPPH and ABTS free radicals scavenging assays. Subsequently, AChE/BChE inhibition studies were performed following Ellman’s assay. To assess the compound's binding effectiveness at the enzymes' target site, it was docked against the binding sites of cholinesterase. The effect of isoeugenol supplementation on scopolamine-induced amnesia was assessed using Shallow Water Maze (SWM), Y-Maze and Elevated Plus Maze (EPM) tests. Results: In DPPH and ABTS assays, isoeugenol exhibited considerable efficacy against free radicals with IC50 of 38.97 and 43.76 μg/mL, respectively. Isoeugenol revealed 78.39 ± 0.40% and 67.73 ± 0.03% inhibitions against AChE and BChE, respectively, at 1 mg/ml concentration. In docking studies, isoeugenol exhibited a docking score of -12.2390, forming two hydrogen bonds at the active site residues of AChE. Further, with a docking score of -10.1632, isoeugenol binds adequately to theBChE enzyme via two arene-hydrogen interactions and one hydrogen bond. Conclusion: Isoeugenol offered considerable protection against scopolamine-induced memory deficits and improved the special memory of the rodents.","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":"42 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140889342","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}
Md. Ataur Rahman, MD. Hasanur Rahman, Hyewhon Rhim, Bonglee Kim
{"title":"Drug Target to Alleviate Mitochondrial Dysfunctions in Alzheimer’s Disease: Recent Advances and Therapeutic Implications","authors":"Md. Ataur Rahman, MD. Hasanur Rahman, Hyewhon Rhim, Bonglee Kim","doi":"10.2174/1570159x22666240426091311","DOIUrl":"https://doi.org/10.2174/1570159x22666240426091311","url":null,"abstract":": Alzheimer's disease (AD) is a severe progressive neurodegenerative condition associated with neuronal damage and reduced cognitive function that primarily affects the aged worldwide. While there is increasing evidence suggesting that mitochondrial dysfunction is one of the most significant factors contributing to AD, its accurate pathobiology remains unclear. Mitochondrial bioenergetics and homeostasis are impaired and defected during AD pathogenesis. However, the potential of mutations in nuclear or mitochondrial DNA encoding mitochondrial constituents to cause mitochondrial dysfunction has been considered since it is one of the intracellular processes commonly compromised in early AD stages. Additionally, electron transport chain dysfunction and mitochondrial pathological protein interactions are related to mitochondrial dysfunction in AD. Many mitochondrial parameters decline during aging, causing an imbalance in reactive oxygen species (ROS) production, leading to oxidative stress in age-related AD. Moreover, neuroinflammation is another potential causative factor in AD-associated mitochondrial dysfunction. While several treatments targeting mitochondrial dysfunction have undergone preclinical studies, few have been successful in clinical trials. Therefore, this review discusses the molecular mechanisms and different therapeutic approaches for correcting mitochondrial dysfunction in AD, which have the potential to advance the future development of novel drug-based AD interventions.","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":"63 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140889337","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}
Raffaella Nenna, Carla Petrella, Enea Bonci, Paola Papoff, Margherita di Jorgi, Laura Petrarca, Maria Giulia Conti, Christian Barbat, Alessandra Pietrangeli, Marco Fiore, Fabio Midulla, Brome Group
{"title":"Reduced Serum Brain-Derived Neurotrophic Factor in Infants Affected by Severe Bronchiolitis","authors":"Raffaella Nenna, Carla Petrella, Enea Bonci, Paola Papoff, Margherita di Jorgi, Laura Petrarca, Maria Giulia Conti, Christian Barbat, Alessandra Pietrangeli, Marco Fiore, Fabio Midulla, Brome Group","doi":"10.2174/1570159x22999240223153901","DOIUrl":"https://doi.org/10.2174/1570159x22999240223153901","url":null,"abstract":"Background: Bronchiolitis is an acute viral infection of the lower respiratory tract, typical of infants in their first year of life and causing hypoxia in the most serious cases. Bronchiolitis recognizes various demographic risk factors that are associated with greater clinical severity; however, no laboratory factors are yet able to correlate with the clinical severity. Neurotrophins as Brain-Derived Neurotrophic Factor (BDNF) are mediators of neuronal plasticity. BDNF is constitutively expressed in smooth muscle cells and epithelium of the lower respiratory tract, and as it is released during inflammatory conditions, serum levels may have a relevant role in the prognosis of infants with bronchiolitis. Objective: In the present pilot study, we aimed to disclose the presence of serum BDNF in infants hospitalized with bronchiolitis at discharge as a disease severity indicator. Methods and Results: Serum BDNF, measured at hospital discharge, was significantly lower in severe bronchiolitis (expressed as O2-supplemented infants). Furthermore, no changes were disclosed for the Tropomyosin receptor kinase B, the main BDNF receptor and neurofilament light chain, a biomarker of neuronal degeneration. Conclusion: Low serum BDNF in infants with severe bronchiolitis could be associated with a higher utilization by lung cells or with an altered production by lung cells. Therefore, further research is required to study if a decreased production or increased consumption of this biomarker is at the base of the above-mentioned findings.","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":"32 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140586834","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":"Current Insights into the Neurotoxicity of Melamine: A Comprehensive Review","authors":"Reza Naeimi, Fatemeh Safarpour, Hamid Askari, Maryam Ghasemi-Kasman","doi":"10.2174/1570159x22666240320133241","DOIUrl":"https://doi.org/10.2174/1570159x22666240320133241","url":null,"abstract":": Melamine, a heterocyclic nitrogen-rich triazine chemical compound, is widely used in various household products, including furniture, dinnerware, and kitchen appliances. The unauthorized addition of the mixture to various foodstuffs to misrepresent protein content resulted in catastrophic, frequently life-threatening health consequences for kids as well as canines and has garnered international attention. Numerous primary studies and evaluations have been focused on melamine toxicity's implications on kidney function. Despite the profusion of literature on melamine's nephrotoxicity, evidence regarding its toxicity to other organs remains scarce. A number of recent studies suggest melamine can disrupt central nervous system (CNS) function and bring about cognitive impairments, contradicting the commonly held belief that melamine's detrimental effects are limited to the urinary system. The accumulation of melamine in the body is linked to various adverse effects, including depression, impaired synaptic transmission, oxidative stress, and neurodegenerative diseases. Several mechanisms may lead to such complications. However, numerous safeguards against melamine accumulation have been identified. This review could shed light on the potential neurological effects and mechanisms underlying melamine toxicity. Afterward, we will dive into the body's possible protectivemechanisms against melamine-induced toxicity.","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":"1 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140586754","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}
Chang Liang, Resel Pereira, Yan Zhang, Olga L. Rojas
{"title":"Gut Microbiome in Alzheimer’s Disease: from Mice to Humans","authors":"Chang Liang, Resel Pereira, Yan Zhang, Olga L. Rojas","doi":"10.2174/1570159x22666240308090741","DOIUrl":"https://doi.org/10.2174/1570159x22666240308090741","url":null,"abstract":": Alzheimer's disease (AD) is the most prevalent type of dementia, but its etiopathogenesis is not yet fully understood. Recent preclinical studies and clinical evidence indicate that changes in the gut microbiome could potentially play a role in the accumulation of amyloid beta. However, the relationship between gut dysbiosis and AD is still elusive. In this review, the potential impact of the gut microbiome on AD development and progression is discussed. Pre-clinical and clinical literature exploring changes in gut microbiome composition is assessed, which can contribute to AD pathology including increased amyloid beta deposition and cognitive impairment. We also highlight the gut-brain axis and the potential involvement of metabolites produced by the gut microbiome in AD are also highlighted. Furthermore, the potential of antibiotics, prebiotics, probiotics, fecal microbiota transplantation, and dietary interventions as complementary therapies for the management of AD is summarized. This review provides valuable insights into potential therapeutic strategies to modulate the gut microbiome in AD.","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":"84 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140150552","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":"Two Distinct Neuronal Populations in the Rat Parafascicular Nucleus Oppositely Encode the Engagement in Stimulus-driven Reward-seeking","authors":"Mehdi Sicre, Frederic Ambroggi, Julie Meffre","doi":"10.2174/1570159x22666240131114225","DOIUrl":"https://doi.org/10.2174/1570159x22666240131114225","url":null,"abstract":"Background:: The thalamus is a phylogenetically well-preserved structure. Known to densely contact cortical regions, its role in the transmission of sensory information to the striatal complex has been widely reconsidered in recent years. Methods:: The parafascicular nucleus of the thalamus (Pf) has been implicated in the orientation of attention toward salient sensory stimuli. In a stimulus-driven reward-seeking task, we sought to characterize the electrophysiological activity of Pf neurons in rats. Results:: We observed a predominance of excitatory over inhibitory responses for all events in the task. Neurons responded more strongly to the stimulus compared to lever-pressing and reward collecting, confirming the strong involvement of the Pf in sensory information processing. The use of long sessions allowed us to compare neuronal responses to stimuli between trials when animals were engaged in action and those when they were not. We distinguished two populations of neurons with opposite responses: MOTIV+ neurons responded more intensely to stimuli followed by a behavioral response than those that were not. Conversely, MOTIV- neurons responded more strongly when the animal did not respond to the stimulus. In addition, the latency of excitation of MOTIV- neurons was shorter than that of MOTIV+ neurons. Conclusion:: Through this encoding, the Pf could perform an early selection of environmental stimuli transmitted to the striatum according to motivational level","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":"18 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-02-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140010991","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":"Protective Role of Electroacupuncture Against Cognitive Impairment in Neurological Diseases","authors":"Yueyang Xin, Siqi Zhou, Tiantian Chu, Yaqun Zhou, Aijun Xu","doi":"10.2174/1570159x22999240209102116","DOIUrl":"https://doi.org/10.2174/1570159x22999240209102116","url":null,"abstract":": Many neurological diseases can lead to cognitive impairment in patients, which includes dementia and mild cognitive impairment and thus create a heavy burden both to their families and public health. Due to the limited effectiveness of medications in treating cognitive impairment, it is imperative to develop alternative treatments. Electroacupuncture (EA), a required method for Traditional Chinese Medicine, has the potential treatment of cognitive impairment. However, the molecular mechanisms involved have not been fully elucidated. Considering the current research status, preclinical literature published within the ten years until October 2022 was systematically searched through PubMed, Web of Science, MEDLINE, Ovid, and Embase. By reading the titles and abstracts, a total of 56 studies were initially included. It is concluded that EA can effectively ameliorate cognitive impairment in preclinical research of neurological diseases and induce potentially beneficial changes in molecular pathways, including Alzheimer’s disease, vascular cognitive impairment, chronic pain, and Parkinson’s disease. Moreover, EA exerts beneficial effects through the same or diverse mechanisms for different disease types, including but not limited to neuroinflammation, neuronal apoptosis, neurogenesis, synaptic plasticity, and autophagy. However, these findings raise further questions that need to be elucidated. Overall, EA therapy for cognitive impairment is an area with great promise, even though more research regarding its detailed mechanisms is warranted.","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":"77 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139763194","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}
Tommaso Barlattani, Paolo Grandinetti, Alexsander Di Cintio, Alessio Montemagno, Roberta Testa, Chiara D’Amelio, Luigi Olivieri, Carmine Tomasetti, Alessandro Rossi, Francesca Pacitti, Domenico De Berardis
{"title":"Glymphatic System and Psychiatric Disorders: A Rapid Comprehensive Scoping Review","authors":"Tommaso Barlattani, Paolo Grandinetti, Alexsander Di Cintio, Alessio Montemagno, Roberta Testa, Chiara D’Amelio, Luigi Olivieri, Carmine Tomasetti, Alessandro Rossi, Francesca Pacitti, Domenico De Berardis","doi":"10.2174/1570159x22666240130091235","DOIUrl":"https://doi.org/10.2174/1570159x22666240130091235","url":null,"abstract":"Background: Since discovering the glymphatic system, there has been a looming interest in exploring its relationship with psychiatric disorders. Recently, increasing evidence suggests an involvement of the glymphatic system in the pathophysiology of psychiatric disorders. However, clear data are still lacking. In this context, this rapid comprehensive PRISMA-ScR (Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews) scoping review aims to identify and analyze current evidence about the relation between the glymphatic system and psychiatric disorders. Methods: We conducted a comprehensive review of the literature and then proceeded to discuss the findings narratively. Tables were then constructed and articles were sorted according to authors, year, title, location of study, sample size, psychiatric disorder, the aim of the study, principal findings, implications. Results: Twenty papers were identified as eligible, among which 2 articles on Schizophrenia, 1 on Autism Spectrum Disorders, 2 on Depression, 1 on Depression and Trauma-related Disorders, 1 on Depression and Anxiety, 2 on Anxiety and Sleep Disorders, 8 on Sleep Disorders, 2 on Alcohol use disorder and 1 on Cocaine Use Disorder. Conclusion: This review suggests a correlation between the glymphatic system and several psychiatric disorders: Schizophrenia, Depression, Anxiety Disorders, Sleep Disorders, Alcohol Use Disorder, Cocaine Use Disorder, Trauma-Related Disorders, and Autism Spectrum Disorders. Impairment of the glymphatic system could play a role in Trauma-Related Disorders, Alcohol Use Disorders, Cocaine Use Disorders, Sleep Disorders, Depression, and Autism Spectrum Disorders. It is important to implement research on this topic and adopt standardized markers and radio diagnostic tools.","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":"4 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141063536","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}
Alexis E Cullen, Javier Labad, Dominic Oliver, Adam Al-Diwani, Amedeo Minichino, Paolo Fusar-Poli
{"title":"The Translational Future of Stress Neurobiology and Psychosis Vulnerability: A Review of the Evidence.","authors":"Alexis E Cullen, Javier Labad, Dominic Oliver, Adam Al-Diwani, Amedeo Minichino, Paolo Fusar-Poli","doi":"10.2174/1570159X21666230322145049","DOIUrl":"10.2174/1570159X21666230322145049","url":null,"abstract":"<p><p>Psychosocial stress is a well-established risk factor for psychosis, yet the neurobiological mechanisms underlying this relationship have yet to be fully elucidated. Much of the research in this field has investigated hypothalamic-pituitary-adrenal (HPA) axis function and immuno-inflammatory processes among individuals with established psychotic disorders. However, as such studies are limited in their ability to provide knowledge that can be used to develop preventative interventions, it is important to shift the focus to individuals with increased vulnerability for psychosis (i.e., high-risk groups). In the present article, we provide an overview of the current methods for identifying individuals at high-risk for psychosis and review the psychosocial stressors that have been most consistently associated with psychosis risk. We then describe a network of interacting physiological systems that are hypothesised to mediate the relationship between psychosocial stress and the manifestation of psychotic illness and critically review evidence that abnormalities within these systems characterise highrisk populations. We found that studies of high-risk groups have yielded highly variable findings, likely due to (i) the heterogeneity both within and across high-risk samples, (ii) the diversity of psychosocial stressors implicated in psychosis, and (iii) that most studies examine single markers of isolated neurobiological systems. We propose that to move the field forward, we require well-designed, largescale translational studies that integrate multi-domain, putative stress-related biomarkers to determine their prognostic value in high-risk samples. We advocate that such investigations are highly warranted, given that psychosocial stress is undoubtedly a relevant risk factor for psychotic disorders.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":"350-377"},"PeriodicalIF":4.8,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10845079/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9156740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Marco A Ell, Miriam A Schiele, Nicola Iovino, Katharina Domschke
{"title":"Epigenetics of Fear, Anxiety and Stress - Focus on Histone Modifications.","authors":"Marco A Ell, Miriam A Schiele, Nicola Iovino, Katharina Domschke","doi":"10.2174/1570159X21666230322154158","DOIUrl":"10.2174/1570159X21666230322154158","url":null,"abstract":"<p><p>Fear-, anxiety- and stress-related disorders are among the most frequent mental disorders. Given substantial rates of insufficient treatment response and often a chronic course, a better understanding of the pathomechanisms of fear-, anxiety- and stress-related disorders is urgently warranted. Epigenetic mechanisms such as histone modifications - positioned at the interface between the biological and the environmental level in the complex pathogenesis of mental disorders - might be highly informative in this context. The current state of knowledge on histone modifications, chromatin-related pharmacology and animal models modified for genes involved in the histone-related epigenetic machinery will be reviewed with respect to fear-, anxiety- and stress-related states. Relevant studies, published until 30th June 2022, were identified using a multi-step systematic literature search of the Pub- Med and Web of Science databases. Animal studies point towards histone modifications (e.g., H3K4me3, H3K9me1/2/3, H3K27me2/3, H3K9ac, H3K14ac and H4K5ac) to be dynamically and mostly brain region-, task- and time-dependently altered on a genome-wide level or gene-specifically (<i>e.g., Bdnf</i>) in models of fear conditioning, retrieval and extinction, acute and (sub-)chronic stress. Singular and underpowered studies on histone modifications in human fear-, anxiety- or stress-related phenotypes are currently restricted to the phenotype of PTSD. Provided consistent validation in human phenotypes, epigenetic biomarkers might ultimately inform indicated preventive interventions as well as personalized treatment approaches, and could inspire future innovative pharmacological treatment options targeting the epigenetic machinery improving treatment response in fear-, anxiety- and stressrelated disorders.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":"843-865"},"PeriodicalIF":4.8,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10845084/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9156742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}