Progress in brain research最新文献

{"title":"Impact of positive feelings and negative feelings on brain cell regeneration and degeneration.","authors":"Al-Hassan Soliman Wadan, Mohamed Abdelsattar Ahmed, Dana Saeed Abd Elmonem El Gemaie, Nasrollah Moradikor","doi":"10.1016/bs.pbr.2025.02.009","DOIUrl":"10.1016/bs.pbr.2025.02.009","url":null,"abstract":"<p><p>Brain cells intentionally break their DNA as a crucial step in memory formation and learning. This process allows for the expression of specific genes that are essential for these cognitive functions. While our cells are generally adept at repairing this self-inflicted DNA damage, the efficiency of this repair mechanism can decline with age or due to certain genetic factors. The deliberate DNA breakage in neurons enables the activation of rapid response genes, which in turn trigger broader transcriptional programs supporting various behaviors, including learning and memory. This process is a normal part of cellular function and gene expression. However, neurological disorders, certain syndromes, and the aging process can impair this DNA repair ability. When cells struggle to mend the intentional DNA breaks, it can lead to cellular weakening and eventual degeneration. The subsequent discussion will explore how positive and negative emotions influence the processes of brain cell regeneration and degradation.</p>","PeriodicalId":20598,"journal":{"name":"Progress in brain research","volume":"293 ","pages":"1-15"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144182197","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Healthy happiness: The effect of happiness in promoting brain health.","authors":"Matthew-Zane L Broderick, Qadir Khan, Nasrollah Moradikor","doi":"10.1016/bs.pbr.2025.03.004","DOIUrl":"10.1016/bs.pbr.2025.03.004","url":null,"abstract":"<p><p>The Merriam-Webster dictionary defines happiness as \"a state of well-being and contentment\". Psychologically, happiness can be defined as a state of current well-being and positivity resulting from recent stimuli, as well as long-term life satisfaction and peace of mind. This refers to two aspects of happiness discussed in psychology, first coined by Aristotle, pleasurable happiness known as \"hedonia\" and the long-term happiness of living a good life called \"eudaimonia\". These early concepts break down the vaguer and complex idea of happiness into long-term pleasure and positivity. This is where it starts to get more challenging when we try to define happiness in neurobiological terms. Many regions, pathways and circuits in the brain work in tandem to create the conscious and recognized state of happiness we cognitively perceive as humans. However, happiness is a feeling that transcends species boundaries. It is a positive state of emotions that can be expressed in different ways, including contentedness, peace, pleasure, excitement, relief, joy, and more. To do this, happiness must be broken down into constituent parts, localized to specific neuroanatomical regions, and associated with specific projects and structures to really build the anatomical architecture of happiness. Understanding how emotion is quantified and experimentally studied allows the field of neuroscience to build a comprehensive \"neurobiological happiness model\". Here in this chapter, we discuss historical and novel findings into this emotion; we discuss its implication as an evolutionary advantage in the adaptive response, how laughter is associated with happiness, and how a state of positive well-being plays a role in promoting positive brain health.</p>","PeriodicalId":20598,"journal":{"name":"Progress in brain research","volume":"293 ","pages":"127-148"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144181214","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Influence of feelings on the blood-brain barrier (BBB) and drug delivery.","authors":"Omnia Ocab, Hager Adel Saad, Rowan Mashal, Karim Osama, Mahmoud Marzouk, Nabila Hamdi","doi":"10.1016/bs.pbr.2025.03.006","DOIUrl":"10.1016/bs.pbr.2025.03.006","url":null,"abstract":"<p><p>The blood-brain barrier (BBB) is a critical regulator of cerebral homeostasis, displaying high dynamicity of influx and efflux of substances to and from the central nervous system (CNS). In an exploration of the neurochemical pathways through which positive and negative emotions can influence the physiological characteristics of the BBB, this chapter delves into the multifaceted relationship between emotional states and BBB integrity and permeability. Negative emotions exemplified by stress, chronic anxiety, and depression have shown harmful effects on the BBB, suggesting a state of hyperpermeability that compromises the otherwise conferred protection. Few reports in literature examined the exact molecular mechanisms by which negative emotions exhibit signs of damaged and leaky BBB. Although research deciphering those mechanisms is limited, there is consensus that the disruption of tight junction (TJ) protein integrity and expression, along with neuroinflammatory processes, oxidative Stress, and excitotoxicity, plays a role in the induction of BBB damage. Conversely, positive emotions have been shown to exert protective effects, potentially reversing the increased permeability of the BBB. Compared to the research focused on the neural correlates of negative emotions, the neuroscience literature on positive emotions and well-being is still in its infancy. A deeper understanding of the mechanisms by which positive emotions modulate the BBB remains necessary. Additionally, we discuss the therapeutic implications of these findings, considering how emotional well-being can be leveraged in developing treatments for neurological disorders. By integrating neuroscience, psychology, and pharmacology insights, this chapter aims to comprehensively understand the dynamic interplay between emotions and the BBB and its potential to inform novel therapeutic strategies.</p>","PeriodicalId":20598,"journal":{"name":"Progress in brain research","volume":"293 ","pages":"203-242"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144181220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiovascular influence on cognitive decline: The heart's role in neurodegenerative disorders.","authors":"Gargi Gautam, Nasrollah Moradikor","doi":"10.1016/bs.pbr.2025.04.006","DOIUrl":"10.1016/bs.pbr.2025.04.006","url":null,"abstract":"<p><p>Cognitive performance is greatly influenced by cardiovascular health, as vascular integrity and brain perfusion are directly related to diseases including Parkinson's disease, Alzheimer's disease, and vascular dementia. Examining the intricate relationship between the heart and brain, this chapter highlights how atrial fibrillation, diabetes, hypertension, and dyslipidemia affect neurovascular coupling (NVC). Chronic inflammation, oxidative stress, and endothelial dysfunction are some of the risk factors that lead to neurodegeneration. The cerebral microvasculature is further compromised by atherosclerosis and heart failure, which exacerbates neuronal damage and increases the risk of dementia. Supported by clinical and epidemiological data, the discussion delves into the mechanisms behind vascular dementia and the vascular contributions to Alzheimer's disease. Slowing cognitive deterioration requires early intervention through lipid management, blood pressure control, and anticoagulant medication. Additionally, developments in precision medicine and neurovascular-targeted therapies present encouraging paths toward management and prevention. Through the discussion of modifiable cardiovascular risks, this chapter emphasizes how vital vascular health is to maintaining cognitive function and slowing the progression of neurodegenerative diseases.</p>","PeriodicalId":20598,"journal":{"name":"Progress in brain research","volume":"294 ","pages":"33-46"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144668207","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hormetic pathways in environmental enrichment in animal models and humans.","authors":"Maylin Hanampa-Maquera, Rafael Cândido Lourenço, Alexis Bailey, Rosana Camarini","doi":"10.1016/bs.pbr.2025.05.007","DOIUrl":"10.1016/bs.pbr.2025.05.007","url":null,"abstract":"<p><p>Environmental Enrichment (EE), which provides enhanced sensory, cognitive, motor, and social stimulation, has emerged as a powerful paradigm for investigating neuroplasticity and stress resilience. This chapter explores how EE functions through hormetic mechanisms-where multiple mild stimuli trigger adaptive responses that promote beneficial outcomes. Since Hebb's pioneering work on neuronal ensembles, research has demonstrated that EE enhances neurogenesis, synaptic plasticity, and neurotrophic factor expression (BDNF and NGF) while modulating inflammatory processes, epigenetic pathways, and metabolic function. These adaptive responses operate according to biphasic dose-response patterns characteristic of hormesis, where moderate stimulation produces benefits that may diminish or become detrimental with excessive exposure. In animal models, EE has shown remarkable efficacy in mitigating cognitive decline, reducing anxiety-like behaviors, attenuating addiction vulnerability, and protecting against neurodegenerative diseases. The modulation of the hypothalamic-pituitary-adrenal (HPA) axis and the shifts in microglial phenotype observed with EE illustrate its role as a hormetic stimulus, as it can act as a mild stressor that promotes adaptive neuroplasticity, enhancing the organism's ability to cope with future stressors. In humans, analogous enrichments through physical exercise, cognitive challenges, social engagement, and music facilitate neuroplasticity, protect against cognitive decline, and promote stress resilience. The hormetic framework also explains why enrichment must be tailored to individual thresholds-excessive stimulation can overwhelm adaptive capacities, transforming beneficial eustress into harmful distress. By understanding EE as a hormetic intervention, this chapter bridges basic neuroscience with translational applications that may enhance resilience against neuropsychiatric disorders typically prevalent in aging.</p>","PeriodicalId":20598,"journal":{"name":"Progress in brain research","volume":"295 ","pages":"189-227"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144795179","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biomarkers: From early detection to treatment personalization.","authors":"Saman Fatima, Sakshi Tiwari, Bilal Siddiqi, Syed Naved Quadri, M Z Abdin","doi":"10.1016/bs.pbr.2025.08.008","DOIUrl":"10.1016/bs.pbr.2025.08.008","url":null,"abstract":"<p><p>Neurodegenerative disorders (NDs), such as Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS), present increasing issues associated with the unavoidable aging of the world's population. These challenges are further highlighted by the socioeconomic consequences of these diseases. The identification and use of biomarkers for prompt diagnosis, careful observation, and efficient treatment approaches is essential to overcoming these obstacles. The primary methods for diagnosing neurodegenerative illnesses are invasive procedures like lumbar punctures to measure CSF fluid or functional brain imaging methods. Biomarkers for underlying proteinopathy in blood serum and cerebral fluid have been the focus of recent biological research, particularly in vivo. With their ability to provide novel pathways for early detection, illness progression tracking, and individualized treatment plans, biomarkers have become essential instruments in precision medicine. The classification of biomarkers including fluid, digital imaging, and molecular biomarkers is examined in this chapter, with an emphasis on their function in neurodegenerative diseases. In neurodegenerative illnesses and the aging brain, tau, amyloid-β, α-synuclein, and TDP-43 are commonly seen to be deposited together rather than separately. These may be disregarded, and it might be challenging to determine their clinicopathological significance. An overview of illness pathophysiology, diagnostic implications, and the most recent molecular and ultrastructural categories for neurodegenerative disorders are given in this chapter. Addressing these issues through interdisciplinary research and technological advancements will be crucial for the future of biomarker-driven precision medicine. This chapter provides an in-depth overview of the evolving landscape of biomarkers and their transformative impact on the early detection and personalized treatment of neurodegenerative diseases.</p>","PeriodicalId":20598,"journal":{"name":"Progress in brain research","volume":"297 ","pages":"131-153"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145637995","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Future horizons: Innovation, aging, and equity.","authors":"Manoj Kumar Jana, Vishnu Swarup, Suryaprakash Tripathy, Neeraj Mohan Gupta, Sai Sutheertha Chatla, Deepesh Joshi, Subhadeep Mandal, Anushka Giri, Sayantam Jana, Mahesh Narayan, Sirsendu Bikash Maiti, Sudip Das","doi":"10.1016/bs.pbr.2025.08.010","DOIUrl":"10.1016/bs.pbr.2025.08.010","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Precision medicine is on the verge of transforming the treatment of neurodegenerative diseases (NDDs) like Alzheimer's disease (AD) and Parkinson's disease (PD), in response to the intricate interactions of genetic, epigenetic, environmental, and lifestyle factors underlying disease heterogeneity. As the world's aging populations grow, with dementia cases expected to double by 2040 and the costs amounting to over €130 billion a year in Europe alone, there is an urgent need for novel strategies to stem the socioeconomic costs of NDDs. Conventional \"one-drug-fits-all\" strategies that depend on late-stage symptom treatment are progressively insufficient for disorders that are marked by heterogeneous molecular pathways and unpredictable clinical courses. Recent improvements in artificial intelligence (AI), multi-omics integration, and biomarker research now allow patients to be stratified into subpopulations following their genetic risk profiles, neuroimaging signatures, and fluid biomarkers (e.g., amyloid-beta, tau, α-synuclein), enabling early diagnosis and focused treatments. For example, artificial intelligence platforms such as the IHI-PROMINENT project are creating forecasting algorithms to chart disease progression and tailor treatment outcomes, and gene therapy and antisense oligonucleotides (ASOs) address precise mutations in familial AD and PD. These advances are supported by pharmacogenomics, which individualizes drug regimens according to metabolic profiles to reduce side effects and maximize efficacy. Still, translating these advances into practice has major barriers to overcome, such as large-scale biomarker validation, multi-omics standardization, and incorporating real-world evidence from digital health technologies. Aging populations only add complexity to this environment, as comorbidities like diabetes and cardiovascular diseases interact with neurodegenerative pathways, requiring system-based, holistic approaches to care. Equity is still a key challenge: differences in access to sophisticated diagnostics (e.g., PET scans, CSF examination) and expensive therapies (e.g., monoclonal antibodies, CAR-T cell therapy) threaten to worsen global health disparities. In retaliation, initiatives such as the JPND research paradigm advance remote clinical trials and telemedicine platforms for the diverse community in decentralized settings, and policies target reducing financial disincentives through risk-sharing strategies and public-private partnerships. Precision medicine in the treatment of NDDs depends on an integrated network among academia, clinics, and industry, by taking advantage of communal biobanks and AI-enabled big data analysis, for refining the drug development process and validating new targets, e.g., neuroinflammatory signaling and gut-brain axis dysfunction. Innovations, like CRISPR-mediated editing and ambient neuroimaging, have innate or potential power to personalize treatment by identifying early-stage and even pre-","PeriodicalId":20598,"journal":{"name":"Progress in brain research","volume":"297 ","pages":"427-468"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145638060","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-omics integration in disease research.","authors":"Michael Warren Gonzales Ceballos, Florge Francis Arnejo Sy, Amna Akbar, Alishba Taofiq","doi":"10.1016/bs.pbr.2025.08.012","DOIUrl":"10.1016/bs.pbr.2025.08.012","url":null,"abstract":"<p><p>Neurodegenerative diseases, marked by complex molecular mechanisms and diverse clinical features, challenge conventional research approaches. This chapter emphasizes the value of multi-omics integration in understanding the biology of Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis (ALS). Genomic studies reveal risk variants such as APOE ε4 in Alzheimer's and rare mutations in familial forms. Transcriptomics highlights gene expression changes, including synaptic dysfunction in early Parkinson's and alternative splicing errors in TARDBP-related ALS. Proteomics identifies key protein aggregates like amyloid beta and alpha-synuclein, along with modifications such as hyperphosphorylated tau that correlate with cognitive decline. Metabolomics uncovers metabolic alterations, including mitochondrial dysfunction in Parkinson's and lipid peroxidation in ALS, which contribute to disease progression. By combining these layers with high-throughput tools like single-cell sequencing, spatial transcriptomics, and mass spectrometry, researchers can reconstruct molecular networks linking genetic risk, gene regulation, protein dysfunction, and metabolic imbalance. This approach enables patient stratification into molecular subtypes, such as neuroinflammatory clusters defined by microglial gene signatures and cytokine expression. Biomarkers from blood and cerebrospinal fluid allow for minimally invasive disease monitoring. Despite challenges such as data heterogeneity and limited standardization, multi-omics approaches support biomarker discovery and therapeutic development. Integrating these datasets with neuroimaging and digital tools enhances diagnostic precision and guides targeted interventions, such as antisense therapies for SOD1-linked ALS. Multi-omics integration is thus a critical foundation for advancing personalized strategies in neurodegenerative disease research.</p>","PeriodicalId":20598,"journal":{"name":"Progress in brain research","volume":"297 ","pages":"155-189"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145638007","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Global case studies and collaborative frameworks.","authors":"Manoj Kumar Jana, Piyal Mukherjee, Sai Sutheertha Chatla, Prachi Sharma, Jeenal Mistry, Vishnu Swarup, Achal Kumar Srivastava, Sudip Das, Neeraj Mohan Gupta, Anami Ahuja, Snigdha Samanta, Mahesh Narayan","doi":"10.1016/bs.pbr.2025.08.013","DOIUrl":"10.1016/bs.pbr.2025.08.013","url":null,"abstract":"<p><p>As neurodegenerative diseases (NDDs) like Alzheimer's and Parkinson's continue to rise globally, the need for cross-border collaboration in research and treatment has never been more critical. This chapter explores prominent global case studies and collaborative frameworks that exemplify how united efforts are transforming the landscape of NDD research. By pooling expertise, data, and resources, international initiatives are accelerating discoveries in early diagnosis, biomarker identification, and personalized therapies. Highlighting landmark consortia such as the Alzheimer's Disease Neuroimaging Initiative (ADNI) (n.d.), Parkinson's Progression Markers Initiative (PPMI), and emerging multi-omics collaborations, the chapter illustrates how these partnerships overcome the complexity and heterogeneity of NDDs. It delves into technological innovations like artificial intelligence, blockchain data sharing, and real-time patient monitoring, which empower researchers and clinicians to connect genetic, environmental, and lifestyle factors in a holistic manner. Ethical considerations and data privacy frameworks are underscored as pivotal to fostering trust among participants and bridging disparities between regions with varying access to precision medicine. The chapter also sheds light on successful public-private partnerships and patient-focused global networks that place individuals at the center of discovery and care. Challenges such as standardizing protocols across countries, navigating legal frameworks, and securing sustainable funding are discussed alongside future directions for expanding collaborative reach. Ultimately, this comprehensive overview conveys the unprecedented promise held by global cooperation in combating neurodegenerative diseases-offering hope for improved diagnostics, innovative treatments, and enhanced quality of life for millions worldwide.</p>","PeriodicalId":20598,"journal":{"name":"Progress in brain research","volume":"297 ","pages":"377-426"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145638037","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stress and gender differences in brain development.","authors":"Abraham Olufemi Asuku, Priscilla Omobonke Adebayo, Gbonjubola Oyinlola Ogungbangbe","doi":"10.1016/bs.pbr.2025.01.013","DOIUrl":"10.1016/bs.pbr.2025.01.013","url":null,"abstract":"<p><p>This chapter investigates the ways in which male and female brains are differently affected by stress during early development, which in turn affects how susceptible each group is to stress-related illnesses. When examining the structure and function of the brain, gender differences and stress must be taken into account. Male and female brain development differs in response to the prenatal testis's secretion of androgen. It appears that when it comes to responding to stress, encoding memories, feeling emotions, solving specific issues, and making decisions, men and women use distinct areas of the brain. Findings revealed that stress led to specific changes in brain structure and function, with gender-specific differences observed. The prefrontal cortex, the hippocampus, and the amygdala are among the brain regions connected to the stress response. The stress response has been linked to the presentation of numerous mental and psychosomatic conditions. The way men and women respond to stress varies on a biological and psychological level. To gain more insight into the gender differences seen throughout brain development, these disparities must also be investigated. This chapter implies that gender-specific vulnerabilities should be addressed and healthy brain development should be promoted by stress-related interventions.</p>","PeriodicalId":20598,"journal":{"name":"Progress in brain research","volume":"291 ","pages":"319-337"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143980675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}