Home  Journals Subscription Open Access About Us
Just Accepted  |  Online First  |  Current Issue  |  Archive  |  Special Issues  |  Featured Articles  |  Most Downloaded

ISSN 2096-0689
CN 11-9363/R (Online)
  About the Journal
    » Aims & Scope
    » Description
    » Publication Formats
    » Editorial Board
    » Abstracting / Indexing
    » Contact us
    » Online Submission
    » Guidelines for Authors
    » Download Templates
    » Author FAQs
    » Guidelines for Reviewers
    » Online Peer Review
    » To be a Reviewer
    » Acknowledgement
30 Most Downloaded Articles
Published in last 1 year | In last 2 years| In last 3 years| All| Most Downloaded in Recent Month | Most Downloaded in Recent Year|

Please wait a minute...
For Selected: View Abstracts Toggle Thumbnails
The Nobel Prizes in the field of neuroscience—from Camillo Golgi and Ramón y Cajal to John O’Keefe and May-Britt Moser and Edvard I Moser
Gunnar Grant
Journal of Translational Neuroscience.  2016, 1 (1): 1-16.   https://doi.org/10.3868/j.issn.2096-0689.01.001
Abstract   PDF (19289KB)
No less than 17 Nobel Prizes have been awarded the area of neurosocience and no less than 40 laureates. The first prize was given to Camillo Golgi and Ramón y Cajal in 1906 and the last one so far, to John O’Keefe and May-Britt and Edvard I. Moser in 2014.
This presentation of the laureates will not follow the time sequence of the prizes. Instead, I have grouped them in different categories.
Reference | Related Articles | Metrics
Introduction to the Journal of Translational Neuroscience
Xiaomin Wang, Max S Cynader
Journal of Translational Neuroscience.  2016, 1 (1): 0-0.  
Abstract   PDF (562KB)
We are living in the golden age of neuroscience. Spurred on by technological advances in areas as diverse as imaging, genetics, big data, and artificial intelligence. The field of neuroscience is advancing at its fastest pace ever. Individuals with many different skills and backgrounds are pouring into our field and attempting to answer the profound questions about how our brain functions in health and disease.
While we can be justly proud of the advances techniques such as optogenetics, multi-electrode recordings, and new types of brain imaging have brought to our understanding of the brain, the challenge of translating the discoveries that are made at the fundamental neuroscience level to the benefit of society and to patients who suffer from brain diseases continues. There are over one thousand diseases that affect the brain, and the sad truth is that for most of them we still have no effective treatment. Understanding brain function is valuable and important, but to really make a difference to society, we must be able to translate these new understandings to the direct benefit of patients and society. This is the purpose of the Journal of Translational Neuroscience. In this inaugural issue, we begin the long journey of facilitating the publication of world class papers that presage a world in which advances in understanding of brain function can lead to new diagnostics and treatments for brain diseases.
The Journal of Translational Neuroscience is a child of the International Association of Translational Neuroscience(IATN). This organization was founded in 2012 by a group of leading scientists and physicians in China, and is headquartered at the Beijing Institute for Brain Disorders(BIBD). Since inception, it has since grown to encompass about a dozen leading neuroscience centres worldwide. The shared vision of this group includes a commitment to develop new understandings, diagnostics, and treatments around diseases that affect the human brain. Some of the key subjects of inquiry include topics such as neurodegenerative disorders, stroke, brain tumor, mental illness, as well as developmental brain disorders. The journal will accept high quality publications in all of these areas, as well as papers which illuminate technological advances relevant to translational neuroscience.
The last few decades have taken the field of neuroscience from one with great promise to our current status characterized by a huge increase in our understanding of mechanisms of brain function. Now it is time for us to turn these advances and understanding into tangible benefits for patients.
Welcome to the Journal of Translational Neuroscience.

Xiaomin Wang and Max S Cynader
Related Articles | Metrics
The effect of lithium on resting-state brain networks in patients with bipolar depression
Chunhong Liu, Xin Ma, Yuan Zhen, Yu Zhang, Lirong Tang, Feng Li, Changle Tie, Chuanyue Wang
Journal of Translational Neuroscience.  2016, 1 (1): 43-51.   https://doi.org/10.3868/j.issn.2096-0689.01.007
Abstract   PDF (1382KB)
Objective: Although lithium has been a commonly prescribed neurotrophic/neuroprotective mood-stabilizing agents, its effect on spontaneous brain activity in patients with bipolar depression remains unclear. The aim of this study is to reveal the basic mechanism underlying the pathological influences of lithium on resting-state brain function of bipolar depression patients. Methods: 97 subjects including 9 bipolar depression patients with lithium treatment, 19 bipolar depression patients without lithium treatment and 69 healthy controls, were recruited to participate in this study. Amplitude of low-frequency fluctuation (ALFF) and fractional amplitude of low-frequency fluctuation (fALFF) were used to capture the changes of spontaneous brain activity among different groups. In addition, further analysis in terms of Hamilton Depression Rating Scale, the number of depressive episodes, and illness duration in pooled bipolar depression patients were conducted, which combined FLEF and fALEF to identify the basic neural features of bipolar depression patients. Results: It was observed from the imaging results that both the bipolar depression patients receiving lithium treatment and healthy control subjects showed significantly decreased ALFF/fALFF values in the right anterior cingulate cortex and right middle frontal gyrus compared to that from the bipolar depression patients without lithium treatmetn. The ALFF values of the right middle temporal gyrus was also found to be negative related to the number of depressive episode and the total episodes. Conclusions: Our findings suggested that the bipolar depression subjects were identified to have abnormal ALFF/ fALFF in the cortico-limbic systems, including regions like right anterior cingulate cortex, bilateral middle frontal gyrus, right orbital frontal gyrus, and right middle temporal gyrus. In addition, it was also revealed that the decreased ALFF/fALFF in the right anterior cingulate cortex and right middle frontal gyrus might be a biomarker that is related to the lithium effects.
Reference | Related Articles | Metrics
Why sex differences in schizophrenia?
Rena Li, Xin Ma, Gang Wang, Jian Yang, Chuanyue Wang
Journal of Translational Neuroscience.  2016, 1 (1): 37-42.   https://doi.org/10.3868/j.issn.2096-0689.01.006
Abstract   PDF (281KB)
Clinical observation shows that men and women are different in prevalence, symptoms, and responses to treatment of several psychiatric disorders, including schizophrenia. While the etiology of gender differences in schizophrenia is only partially understood, recent genetic studies suggest significant sex-specific pathways in the schizophrenia between men and women. More research is needed to understand the causal roles of sex differences in schizophrenia in order to ultimately develop sex-specific treatment of this serious mental illness. In the present review, we will outline the current evidence on the sex-related factors interaction with disease onset, symptoms and treatment of schizophrenia, and discuss the potential molecular mechanisms that may mediate their cooperative actions in schizophrenia pathogenesis.
Reference | Related Articles | Metrics
Phosphorylation of group I metabotropic glutamate receptors in drug addiction and translational research
Limin Mao, John Q Wang
Journal of Translational Neuroscience.  2016, 1 (1): 17-23.   https://doi.org/10.3868/j.issn.2096-0689.01.002
Abstract   PDF (146KB)
Protein phosphorylation is an important posttranslational modification of group I metabotropic glutamate receptors (mGluR1 and mGluR5 subtypes, mGluR1/5) which are widely distributed throughout the mammalian brain. Several common protein kinases are involved in this type of modification, including protein kinase A, protein kinase C, and extracellular signal-regulated kinase. Through constitutive and activity-dependent phosphorylation of mGluR1/5 at specific residues, protein kinases regulate trafficking, subcellular/subsynaptic distribution, and function of modified receptors. Increasing evidence demonstrates that mGluR1/5 phosphorylation in the mesolimbic reward circuitry is sensitive to chronic psychostimulant exposure and undergoes adaptive changes in its abundance and activity. These changes contribute to long-term excitatory synaptic plasticity related to the addictive property of drugs of abuse. The rapid progress in uncovering the neurochemical basis of addiction has fostered bench-to-bed translational research by targeting mGluR1/5 for developing effective pharmacotherapies for treating addiction in humans. This review summarizes recent data from the studies analyzing mGluR1/5 phosphorylation. Phosphorylation-dependent mechanisms in stimulant-induced mGluR1/5 and behavioral plasticity are also discussed in association with increasing interest in mGluR1/5 in translational medicine.
Reference | Related Articles | Metrics
Cognitive deficits in schizophrenia: from pharmacology to neurocognitive models
Zhemeng Wu, Qian Wang
Journal of Translational Neuroscience.  2018, 3 (1): 1-11.   https://doi.org/10.3868/j.issn.2096-0689.2018.01.001
Abstract   PDF (12883KB)
Schizophrenia is a typical mental disorder characterized by cognitive, social, and emotional impairments and by psychotic symptoms. For nearly a century, there have been ongoing discussions on the anatomical-functional connections between brain abnormalities and symptoms in patients with schizophrenia. Neuroimaging studies in such patients show abnormalities in the prefrontal cortex (PFC), a brain region that acts as an executive center in cognition processing. The disrupted brain connectivity between PFC and other brain structures (such as the limbic system, basal ganglia and thalamus) results in faulty information processing and cognition deficits. Dopamine receptors, which have his torically acted as vital targets in schizophrenia therapies, have complex roles in cognition. Here we reviewed dopamine’s role as a widespread neurotransmitter mediating the PFC-cognitive system. The imbalance of braindopamine level, especially the abnormal D1/D2receptors ratio, leads to dysfunctions in brain connectivity in patients with schizophrenia. Recent neurocognitive modeling studies suggest the imbalance of dopamine receptors affects the internal noise within brain networks, which may lead to reduced signal-to-noise ratio in the PFC neuron populations. Going forward, more researches focusing on the relationship between pharmacology and neurocognitive models are needed, in an effort to identify more effective and efficient ways to treat cognitive impairment in patients with schizophrenia.
Related Articles | Metrics
A review of gut microbiota and Parkinson’s disease
Fengxian Chen, Qinyong Ye
Journal of Translational Neuroscience.  2018, 3 (4): 21-28.   https://doi.org/10.3868/j.issn.2096-0689.2018.04.003
Abstract   PDF (10337KB)
In Parkinson’s disease (PD), the alpha-synuclein (α-syn) pathology occurs both in the enteric nervous system (ENS) and parasympathetic nerves in the early stage of PD, which precedes the central nervous system (CNS) pathology and is related to gastrointestinal dysfunction precedes the onset of motor symptoms in PD. Studies have shown that gut microbiota can affect brain activity through the microbiota-gut-brain axis in PD patients. They can promote the development of PD and might be the origin of PD. There are four communication routes between gut microbiota and brain, which respectively are the gut-brain’s neural network, endocrine system, gut immune system, and barrier paths which include intestinal mucosal barrier and blood-brain barrier (BBB). Based on the alteration of fecal microbiota composition in PD, it is worthwhile to investigate whether microbiota analysis could be used as a biomarker for premotor PD. As a potential therapy, fecal microbiota transplantation (FMT) may be a promising treatment for PD patients. Further studies are needed to elucidate the causal relationship between gut microbiota and PD.
Related Articles | Metrics
International Alliance for Translational Neuroscience
Zhiqing D Xu
Journal of Translational Neuroscience.  2016, 1 (1): 52-55.   https://doi.org/10.3868/j.issn.2096-0689.01.008
Abstract   PDF (1811KB)
The International Alliance for Translational Neuroscience (IATN) is an international multi-institutional organization aimed at achieving decisive advancements in the field of neuroscience and associated disorders by utilizing existing strengths of each institution to promote integration of research, education/training and collaboration of translational neuroscience research activities among the member institutions.
Related Articles | Metrics
Neuroscience at Karolinska Institutet, a medical university in Stockholm
Gunnar Grant
Journal of Translational Neuroscience.  2016, 1 (1): 60-63.   https://doi.org/10.3868/j.issn.2096-0689.01.010
Abstract   PDF (0KB)
Karolinska Institutet is one of the founding members of the International Alliance for Translational Neuroscience, IATN. This alliance was established in Beijing in 2012 and it presently includes seven members worldwide. Karolinska Institutet has a long tradition in research on the nervous system. Early on it was mainly represented by the Department of Neurophysiology and the Nobel Laureate Ragnar Granit, and the Department of Physiology, where Ulf von Euler, also a Nobel Laureate, carried out pioneering work on catecholamines, substance P and prostaglandins (see Grant G: The Nobel Prizes in the Field of Neuroscience which was published in the same issue). Today two departments are specifically devoted to this field, the Department of Neuroscience and the Department of Clinical Neuroscience. In addition, this field of research is explored at the Departments of Physiology and Pharmacology, Cell and Molecular Biology, Medical Biochemistry and Biophysics, as well as at the Department of Neurobiology, Care Sciences and Society. All together neuroscience at Karolinska Institutet represents a very strong discipline.
Related Articles | Metrics
Advancements in pathogenesis studies of Rasmussen's encephalitis
Sichang Chen, Yuguang Guan, Xueling Qi, Guoming Luan
Journal of Translational Neuroscience.  2016, 1 (1): 27-31.   https://doi.org/10.3868/j.issn.2096-0689.01.004
Abstract   PDF (108KB)
Rasmussen's encephalitis (RE), which was first described by Rasmussen in 1958, is a rare, dispersed, and progressive neurological syndrome that is characterized by focal epilepsy, unilateral inflammation of the cerebral cortex, progressive hemiplegia and cognitive deterioration. The etiology of this syndrome remains under investigation, and it is hypothesized and widely accepted that RE is a T-cell-mediated autoimmune response. However, the antigenic epitopes and mechanisms are still unknown. The pathological characteristics of RE are cortical inflammation, neuronal loss, and gliosis that are confined to one cerebral hemisphere. Hemispherectomy remains the only cure for the seizures and cognitive deterioration associated with the disease, but this procedure results in inevitable functional loss in the brain. Compared with surgery, immunomodulatory treatments are expected to cause less neurological deficits, but with limited clinical effect.
Reference | Related Articles | Metrics
A brief history of neuroscience at the University of British Columbia
Max S Cynader, Heather Amos
Journal of Translational Neuroscience.  2016, 1 (1): 56-59.   https://doi.org/10.3868/j.issn.2096-0689.01.009
Abstract   PDF (0KB)
Over the past few decades, the field of neuroscience has grown dramatically and made tremendous progress. From its origins in physics, philosophy and psychology, the field has grown to include among its practitioners talented individuals not only from these founding disciplines but from many others. Though our progress in Neuroscience has been immense, there is still much to be done, and it has become clear that a large number of overlapping complimentary skill sets are required to make progress on the challenging problems that lie ahead. The vision of an interdisciplinary, integrated neuroscience enterprise has characterized our University since the inception of the field. The University of British Columbia is one of the world’s top leading academic institutions, and its Faculty of Medicine is renowned for its broad expertise in research, teaching, and clinical innovation. From the very beginning of the foundation of the University, UBC’s commitment to better understanding the brain was a priority. Just seven years before UBC opened its doors in 1913, the Nobel Prize was awarded to Ramon y Cajal and Camillo Golgi, the scientists who discovered neurons, the amazing, multi-variant, cells that communicate information to, from and within the brain. The study of the brain, was still in its infancy in 1906 when the Nobel Prize was awarded, but one of the first courses offered at UBC was Elementary Psychology, the study of brain and behaviour.
Related Articles | Metrics
Parkinson’s disease: how should we consider the selectivity and progressivity of its neuropathology?
Wei Li, Xiaohan Yu, Shun Yu,
Journal of Translational Neuroscience.  2019, 4 (3): 24-36.   https://doi.org/10.3868/j. issn. 2096-0689. 2019. 03. 003
Abstract   PDF (16284KB)
Parkinson’s disease (PD) is a common age-related neurodegenerative disease characterized by movement disorders. The hallmark pathological lesions of PD are the formation of Lewy pathology in selected populations of neurons throughout the nervous system. Braak and his colleagues created a staging system for PD describing the connection between Lewy pathology and disease severity. They proposed that Lewy pathology might be initially triggered by exogenous pathogens targeting the enteric or olfactory nervous system, then spread in a prion-like propagation manner from the peripheral nerves to the lower brainstem and midbrain, before finally reaching higher cortical structures, causing a sequential occurrence of the non-motor and motor symptoms, depending on the lesioned neurons. However, emerging evidence also supports a functional threshold hypothesis proposed by Engelender and Isacson in which Lewy pathology may occur parallelly in the central and peripheral nervous systems and the symptoms only begin when the functional reserve of the affected neurons (and their connecting brain regions) is unable to allow for network compensation. Consequently, early symptoms of PD reflect the loss of function in the least compensated systems, such as the enteric and olfactory nervous systems, rather than the spread of Lewy pathology from the peripheral to the central nervous systems. The current review article provides a comprehensive overview of the evidence supporting a merged mechanism that the neurodegeneration in PD happens to those neurons that are not only intrinsically vulnerable but also affected by the spread of Lewy pathology.
Related Articles | Metrics
New advances in multiple system atrophy
Lingyu Zhang, Bei Cao, Huifang Shang
Journal of Translational Neuroscience.  2019, 4 (1): 38-49.   https://doi.org/10.3868/j. issn. 2096-0689. 2019. 01. 004
Abstract   PDF (14376KB)
Multiple system atrophy (MSA) is a rapidly progressive neurodegenerative disorder characterized by a variable combination of autonomic failure, parkinsonism with poor response to levodopa, cerebellar ataxia and pyramidal symptoms. The pathological hallmark of MSA is the oligodendrocytic glial cytoplasmic inclusions (GCIs) consisting of α-synuclein, and so MSA, together with Parkinson’s disease (PD) and dementia with Lewy bodies (DLB), is an α-synucleinopathy. Currently few effective biomarkers have been identified for the diagnosis or prognosis of MSA, and there is no established therapy to delay its progression. In this review, we discuss the epidemiology, neuropathology, genetics, clinical presentation and diagnostic biomarkers of MSA, as well as recent advances in its treatment.
Related Articles | Metrics
The role of neuroinflammation in glaucoma
Kojic Ljubomir, Max S Cynader
Journal of Translational Neuroscience.  2017, 2 (4): 1-11.   https://doi.org/10.3868/j.issn.2096-0689.2017.04.001
Abstract   PDF (12781KB)
Glaucoma is a chronic neurodegenerative disorder characterized by progressive damage and loss of retinal ganglion cells (RGCs). It is considered one of the leading causes of irreversible blindness in the older population. There are estimates that glaucoma will affect 80 million individuals worldwide by the end of this decade, and yet we are still not able to identify the signals and the mechanisms that trigger this neurodegenerative disease. Various hypotheses have been generated to address the causes of the progressive RGC death that characterizes the disease. Age and increased intraocular pressure (IOP) have been established as the main risk factors for the development of glaucoma. Recent studies have identified additional factors that play a role in the pathogenesis of this complex multifactorial disease, including inflammation, oxidative stress, vascular dysregulation, disrupted axonal transport of neurotrophic factors, and the release of neurotoxic agents such as glutamate, nitric oxide and free radicals. The currently approved therapies for glaucoma that seek to reduce IOP, including medications, laser treatment, and surgery, are unable to reliably stop RGC loss and functional impairment. Considering the significant personal, medical and socio-economic impacts of glaucoma as a leading cause of blindness, there is a pressing need for new innovative treatment strategies. Here we focus on the role of neuroinflammation in glaucoma and the opportunities that new findings in this area have for the development of future therapeutics.
Related Articles | Metrics
Function and mechanism of traditional Chinese medicine in the prevention and treatment of Parkinson’s disease
Ting Zhang, Ke Wang, Limin Liu, Wei Wang, Li Zhang, Jun Jia, Xiaoli Gong, Xiaomin Wang
Journal of Translational Neuroscience.  2017, 2 (4): 12-23.   https://doi.org/10.3868/j.issn.2096-0689.2017.04.002
Abstract   PDF (14569KB)
Parkinson’s disease (PD) was first discovered 200 years ago. The current gold standard of clinical treatment is still mainly levodopa replacement therapy. Traditional Chinese medicine is the foundation of traditional medicine in China. Chinese herbs and acupuncture both exhibit remarkable efficacy in the treatment of PD. Clinical studies on the treatment of PD using Chinese herbs have confirmed that the combined use of Chinese herbs and the levodopa formulation can significantly increase the treatment effect and reduce toxic side effects. Basic studies further confirmed that various Chinese herbs and their monomeric substances can protect dopaminergic neurons in PD models. The major mechanisms include anti-inflammation, anti-oxidant, anti-apoptosis, neuroprotection, mitochondrial function protection, and regulation of gut microbiota. The function of acupuncture in the treatment of PD has also gradually received extensive attention in China and other countries. Acupuncture not only has peculiar advantages in the improvement of symptoms of PD patients, but also can attenuate adverse drug reactions, delay disease progression, and increase the quality of life of patients. Basic studies further confirmed that acupuncture can improve many motor symptoms in animal models of PD and has cumulative effects and follow-up effects. The major mechanisms include dopaminergic neuron protection functions, anti-inflammation and anti-oxidant effects, and the regulation of related neurotransmitters and neural circuits. The clinical application of acupuncture and Chinese herbs still requires strict randomized, double-blind, controlled design, multi-centre and large-sample sizeevidence-based clinical studies and follow-up observations of long-term efficacy to support the effect. In addition, the multi-target and multi-pathway therapeutic mechanisms need further studies.
Related Articles | Metrics
The biogenesis and biological roles of tRNA-derived short RNAs
Chengjun Wang, Jia Wang, Mingze Wang, Yike Lu, Jizong Zhao
Journal of Translational Neuroscience.  2017, 2 (1): 1-9.   https://doi.org/10-3868/j.issn.2096-0689.2017.01.001
Abstract   PDF (12272KB)
In recent years, next-generation sequencing (NGS) technologies targeting the microRNA (miRNA) transcriptome revealed the existence of tRNA-derived short RNAs: tRNA halves (tiRNAs) and tRNA-derived fragments (tRFs). These small RNAs represent a noveltype of small non-coding RNAs (sncRNAs), which are heterogeneous in size, nucleotide composition and biogenesis, and have been suggested to be involved in translation, cell proliferation, priming of viral reverse transcriptases, regulation of gene expression, modulation of the DNA damage response, tumor suppression and neurological disorders. Herein, we review the mechanism of their biogenesis and discuss in detail the regulatory roles they play in cell physiology. We also point out that the biological function of tRNA-derived short RNAs will be understood better as research moves forward, and that this knowledge will find its way into clinical application in the near future.
Related Articles | Metrics
Comparative effectiveness research and health care reform in China
Yilong Wang, Yongjun Wang
Journal of Translational Neuroscience.  2016, 1 (1): 24-26.   https://doi.org/10.3868/j.issn.2096-0689.01.003
Abstract   PDF (83KB)
China has made significant progress in modernizing its healthcare system in the past 20 years. However, there are some issues that are difficult to solve on the current healthcare status, including the lack of medical care satisfaction in rural areas and urban areas, excessive consumption of medical resources, conflict and tension between the healthcare provider and patients, and the problems caused by the change of model of healthcare. Therefore, the State Council introduced the Opinions of the CPC Central Committee and the State Council on Deepening the Health Care System Reform in 2009 in order to provide basic, safe, effective, convenient and affordable healthcare for all residents. Despite the goals and policies set by the government, how to implement them remains to be challenging. Like evidence-based medicine, comparative effective research (CER) which started in the US in 2000's can provide diagnosis and treatment information for patients, doctors, and health policy makers to make decisions on the effective ways of caring for both individual and population. It also may apply to the conditions of healthcare reform in China. And there are opportunities and challenges of conducting CER in our country. We suggest that the government should establish the national-level CER research institute, CER Leadership Committee and relevant standards, fund the CER projects, and begin CER in certain disciplines.
Reference | Related Articles | Metrics
Brain insulin resistance and Parkinson’s disease
Ge Gao, Hui Yang
Journal of Translational Neuroscience.  2018, 3 (4): 29-37.   https://doi.org/10.3868/j.issn.2096-0689.2018.04.004
Abstract   PDF (10747KB)
Parkinson’s disease (PD) is the second most common neurodegenerative disease. Its most prominent pathological features are the loss of dopaminergic neurons in the substantia nigra pars compacta and the deposition of intraneuronal inclusions named Lewy bodies. Currently, the pathophysiological mechanisms of PD are not fully understood. Growing evidence suggests that insulin resistance, diabetes and PD share similar pathological processes. This raises the possibility that defective insulin signaling pathways contribute to the occurrence and development of PD. In this article, we firstly reviewed the evidence of insulin resistance from epidemiology, PD patients and animal models. We also explained the insulin signal pathways in central nervous system. We then showed the evidence that insulin resistance participates in the pathogenesis of PD via protein aggregation, mitochondrial dysfunction, neural inflammation and cognitive impairment. Finally, we introduced four categories of drugs that facilitate insulin signaling and their effects on neurodegeneration in PD.
Related Articles | Metrics
Translation of basic science into clinical medicine in management for neurogenic bladder
Limin Liao, Guoqing Chen, Fan Zhang
Journal of Translational Neuroscience.  2016, 1 (1): 32-36.   https://doi.org/10.3868/j.issn.2096-0689.01.005
Abstract   PDF (1178KB)
Neurogenic bladder (NB) dysfunction caused by spinal cord injury (SCI) or diseases of the central nervous system or peripheral nerves is a major medical and social problem. Traditional treatments to NB include medication, injection of Botulinum toxin A into the detrusor, neuromodulation and surgery. There are also emerging approaches, such as tissue engineering, stem cell transplantation and gene therapy. In recent years, we have carried out explorations in both therapeutic areas and tried to translate basic research into clinical practice. This paper reviews our work in this regard, and provides references for future research.
Reference | Related Articles | Metrics
Engineering human pluripotent stem cell-derived 3D brain tissues for drug discovery
Ha Nam Nguyen,Hongjun Song,Guoli Ming
Journal of Translational Neuroscience.  2016, 1 (2): 38-48.   https://doi.org/10-3868/j.issn.2096-0689.2016.02.003
Abstract   PDF (12471KB)
Abstract The quest to find novel therapeutics for mental and neurological disorders has been hindered by the lack of access to live human brain samples and relevant experimental models. Conventional 2D human pluripotent stem cell-derived neuronal cultures and animal models do not fully recapitulate many endogenous human biochemical processes and diseasephenotypes. Currently, the majority of candidate drugs obtained from preclinical testing in conventional systems does not usually translate into success and have a high failure rate in clinical trials. Recent advancements in bioengineering and stem cell technologies have resulted in three-dimensional brain-like tissues, such as oragnoids,which better resemble endogenous tissue and are more physiologically relevant than monolayer cultures. These brain-like tissues can bridge the gap between existing models and the patient, and may revolutionize the field of translational neuroscience. Here, we discuss utilities and challenges of using stem cell-derived human brain tissues in basic research and pharmacotherapy
Related Articles | Metrics
Mechanistic roles of the subthalamic nucleus and internal globus pallidus: evidence from local field potentials and deep brain stimulation
Minghong Su, Zheng Ye
Journal of Translational Neuroscience.  2018, 3 (4): 1-14.   https://doi.org/10.3868/j.issn.2096-0689.2018.04.001
Abstract   PDF (15385KB)
Deep brain stimulation (DBS) has become an effective therapeutic option for neurological and psychiatric disorders such as Parkinson’s disease (PD), dystonia, and obsessive-compulsive disorder. The subthalamic nucleus (STN) and internal globus pallidus (GPi) are by far the most commonly used targets for DBS in the treatment of PD. However, STN/GPi stimulation sometimes causes side effects, including motor fluctuations, cognitive declines, and worse emotional experience, which affect patients’ postoperative quality of life. Recent invasive electrophysiological studies are driven by the desire to better understand the mechanisms of therapeutic actions and side effects of STN/GPi stimulation. These studies investigated the function of the STN and GPi in motor, cognitive and affective processes by recording single-neuron firing patterns during the surgery or local field potentials after the surgery. Here we review the relevant studies to provide an integrative picture of the functional roles of the STN and GPi within the basal ganglia loops for motor, cognition, and emotion. Previous studies suggested that STN and GPi gamma oscillations encode the strength and speed of voluntary movements (execution), whereas beta oscillations reflect the effort and demand of potential movements (preparation). In the cognitive domain, oscillatory beta activity in the STN is involved when people have to stop an inappropriate action or to suppress salient but task-irrelevant information, whereas theta/delta activity is associated with the adjustment of decision thresholds and cost-benefit trade-off. In the affective domain, STN activity in the alpha band may represent the valence and arousal of emotional information.
Related Articles | Metrics
Perspectives on mechanisms underlying remote ischemic conditioning against ischemic stroke
Changqing Xia, Xunming Ji
Journal of Translational Neuroscience.  2019, 4 (1): 1-14.   https://doi.org/10.3868/j. issn. 2096-0689. 2019. 01. 001
Abstract   PDF (17092KB)
Ischemic stroke is a major neurological disease with limited effective therapeutic options except for thrombolysis and thrombectomy. Remote ischemic conditioning (RIC) is an approach that promises an alternative to the current treatment portfolio. As an easy-handled, non-invasive regimen, it takes advantage of transient ischemia (currently often made through inflation and deflation of limb blood pressure cuff) to enhance the tolerance of vital organs to ischemia. RIC can be executed before, during and after the onset of stroke. The mechanisms of action of RIC employed at different stroke stages are similar and may involve humoral, neurological and inflammatory pathways. As new mechanisms underlying RIC-induced neuroprotection continue to be revealed, we review in this article some of the latest development in this field, including: ① RIC and RIC-induced fundamental change, hypoxia, as well as the role of hypoxia inducible factors against stroke; ② Potential role of RIC-induced extracellular vesicles in neuroprotection; ③ RIC-induced metabolic changes in tissue protection; ④ Potential effect of RIC on red blood cells (RBC) oxygen delivery; and ⑤ RIC and its anti-inflammatory potential.
Related Articles | Metrics
Genetic factors associated with non-motor symptoms in Parkinson’s disease
Yilun Ge, Kai Li, Chunfeng Liu
Journal of Translational Neuroscience.  2019, 4 (1): 15-29.   https://doi.org/10.3868/j. issn. 2096-0689. 2019. 01. 002
Abstract   PDF (17769KB)
Parkinson’s disease (PD) is the second most common neurodegenerative disorder after Alzheimer’s disease. It is a complex syndrome with heterogeneous aetiologies, pathogenesis and manifestations. Patients with PD may present with motor symptoms and various non-motor symptoms (NMSs). NMSs have been reported in almost every diagnosed case of PD and usually precede motor symptoms. Multiple factors have been proved to be associated with the occurrence of NMSs in PD, among which genetic differentiation is a featured one. With the development of sequencing techniques, an increasing number of NMS-related genetic factors have been identified. This article reviews some of the latest discoveries in this regard.
Related Articles | Metrics
Dendritic spine pathology in autism: lessons learned from mouse models
Qiangge Zhang, Dingxi Zhou, Guoping Feng
Journal of Translational Neuroscience.  2016, 1 (2): 21-37.   https://doi.org/10-3868/j.issn.2096-0689.2016.02.002
Abstract   PDF (20513KB)
Abstract Autism spectrum disorders (ASD) area group of neurodevelopmental disorders that affect up to 1.5% of population in the world. Recent largescale genomic studies show that genetic causes of ASD are very heterogeneous. Gene ontology, pathwayanalysis and animal model studies have revealed several potential converging mechanisms including postsynaptic dysfunction of excitatory synapses. In this review, we focus on the structural and functional specializations of dendritic spines, and describe their defects in ASD.We use Fragile X syndrome, Rett syndrome and Phelan-McDermid syndrome, three of the most studied neurodevelopmental disorders with autism features, as examples to demonstrate the significant contribution made by mouse models towards the understanding of monogenic ASD. We envision that the development and application of new technologies to study the function of dendritic spines in valid animal models will eventually lead to innovative treatments for ASD.
Related Articles | Metrics
Synaptotagmins: links to human disease
Wanru Li, Claire Xi Zhang
Journal of Translational Neuroscience.  2017, 2 (4): 24-30.   https://doi.org/10.3868/j.issn.2096-0689.2017.04.003
Abstract   PDF (8362KB)
Synaptotagmins(Syts) are a large family of integral membrane proteins that regulate synaptic function and membrane trafficking. Emerging evidences show involvement of Syts in human diseases. Here, we review the recent studies of several Syts (Syt1, 2, 7, 11, and 14) in the pathophysiological mechanisms of neurodegeneration disorders such as Alzheimer’s disease, Parkinson’s disease, and attention-deficit/hyperactivity disorder etc. A better understanding of the diverse physiological and pathological functions of different Syt isoforms is needed for potential therapeutic interventions in the future.
Related Articles | Metrics
Recent advances in the molecular mechanism of Janus kinase activation
Yukun Han, Jianliang Zhang
Journal of Translational Neuroscience.  2018, 3 (4): 15-20.   https://doi.org/10.3868/j.issn.2096-0689.2018.04.002
Abstract   PDF (6285KB)
The JAK (Janus kinase) family members play a role in the transmission of signals from extracellular stimuli across the plasma membrane via the cytoplasm to the nucleus in eukaryotes. The JAK family is comprised of JAK1, JAK2, JAK3 and TYK2 (tyrosine kinase 2), and the complexities underlying their activation and regulation are still being investigated. Here, we review the recent advances of their functions and the underlying mechanism of activation. At the molecular level, recent studies have greatly advanced our knowledge of the structures and organization of the JAK proteins, as well as the mechanism of JAK activation, particularly the role of the pseudokinase domain as a suppressor of the adjacent tyrosine kinase domain’s catalytic activity. We also review recent advances in our understanding of the mechanisms of negative regulation exerted by phosphatase and SH2 (Src homology 2) domain-containing proteins. These recent studies highlight the diversity of regulatory mechanisms utilized by the JAK family to maintain signalling fidelity, and shed much light on the potential novel strategies for precise treatment of the associated diseases.
Related Articles | Metrics
Computational fluid dynamics modeling in intracranial atherosclerotic disease
Linfang Lan, Xinyi Leng
Journal of Translational Neuroscience.  2017, 2 (2): 7-15.   https://doi.org/10.3868/j.issn.2096-0689.2017.02.002
Abstract   PDF (10272KB)
Intracranial atherosclerotic disease (ICAD) is an important cause for ischemic stroke and transient ischemic stroke (TIA) throughout the world, especially in Asians, which is not fully appreciated, partly due to its inaccessibility and limitations of current neuroimaging methods. The computational fluid dynamics (CFD) modeling technique provides a novel approach to reveal the hemodynamic characteristics in ICAD, e.g., the distributions of pressure, wall shear stress and flow velocity.In this review article, we aim to provide an overview of the general methodology of CFD modeling in arterial stenotic diseases, the established application of this technique in coronary artery disease, and more importantly,perspectives and challenges of this technique in the investigation of ICAD. Promising findings of preliminary studies using a CFD model for hemodynamic analysis in ICAD warrant verifications. Further studies in this area will help rectify loopholes in the current secondary prevention strategy, and inform individualized treatment for ICAD patients in the near future.
Related Articles | Metrics
Dopamine and cognitive function after global cerebral ischemia-reperfusion: a brief review
Wenzhu Wang, Xu Liu, Yan Yu, Lixu Liu
Journal of Translational Neuroscience.  2018, 3 (3): 9-16.   https://doi.org/10.3868/j.issn.2096-0689.2018.03.002
Abstract   PDF (8862KB)
Global cerebral ischemia/hypoxia may occur due to various causes such as cardiac arrest, shock, and asphyxiation. Even though the patient’s life may be saved after cardiopulmonary resuscitation, cerebral ischemia-reperfusion injury is likely to occur and often results in neurological dysfunction. Apart from motor and speech impediments, patients with such injury may also suffer from impaired higher-level cognitive functions such as learning and memory, placing a heavy burden on families and society. Brain areas associated with the limbic system include the hippocampus, corpus striatum, and amygdala, which are linked with cognitive function. Those brain regions are easily damaged by hypoxia, and since they are connected with the dopaminergic pathway, global cerebral ischemia-reperfusion can damage the dopaminergic pathway as well and affect the projection of dopaminergic neurons in the limbic system. This review article examines the feasibility of using dopamine, a neurotransmitter heavily involved in cognitive function, in experimental research and clinical treatment of global cerebral ischemia-reperfusion injury. Specifically, we examine the effects of dopamine on post-injury cognition and neuronal plasticity, with the ultimate goal of identifying a new tool for clinical treatment.
Related Articles | Metrics
Combination therapy of long-term tumor treating fields with temozolomide and bevacizumab prolongs survival in multifocal glioblastoma diagnosed patient: a case report
Damir Nizamutdinov, Kaiyang Feng, Amanda Johnson, Ekokobe Fonkem
Journal of Translational Neuroscience.  2019, 4 (1): 50-54.   https://doi.org/10.3868/j. issn. 2096-0689. 2019. 01. 005
Abstract   PDF (6876KB)
The multifocal glioblastomas (GBM) are tumors with multiple discrete areas of contrast enhancing tumors which have considerably poorer prognosis than solitary GBM. Median overall survival of diagnosed patients almost twice as less than solitary presentation. We present a case report of multifocal GBM. A 72-year old right-handed male was evaluated at the Neuro-Oncology Clinic of Baylor Scott and White Hospital (Central Division). Patient presented at this hospital because of persistent progressive headaches, confusion, and an incident of fall. Physical evaluation revealed neurological impairments. Brain magnetic resonance imaging (MRI) revealed heterogeneous contrast enhancing lesions with associated vasogenic oedema. Patient underwent a stereotactic biopsy analysis of the larger lesion and pathology evaluation concluded an isocitrate dehydrogenase 1 and 2 wild type GBM with unmethylated O-6-methylguanine-DNA methyltransferase. Treatment remedies: Patient received 4 weeks concurrent radiation therapy along with combination of temozolomide at dose of 75 mg/m2 followed adjuvant temozolomide for 10 cycles with bevacizumab at 10 mg/kg every 2 weeks and Optune treatment. Post treatment evaluation: Repeat MRIs showed near complete resolution of the tumors at 26 months of treatment along with improvement of neurological status. Conclusion: Due to limitations of surgical manipulations in multifocal GBM diagnosed patients, combinational chemo and radiation therapy is the treatment of choice for most cases. Using additional novel treatment with non-invasive therapeutic device proven to be effective is another excellent approach to the established practice. Therefore, combination therapy of Optune plus temozolomide and bevacizumab might be a promising remedy for newly diagnosed multifocal glioblastomas.
Related Articles | Metrics
N-methyl-D-aspartate glutamate receptors (NMDARs) in stroke pathogenesis and treatments
Wenlin Chen, Yang Ge, Yutian Wang
Journal of Translational Neuroscience.  2019, 4 (4): 1-12.   https://doi.org/10.3868/j. issn. 2096-0689. 2019. 04. 001
Abstract   PDF (15844KB)
N-methyl-D-aspartate glutamate receptors (NMDARs) play crucial roles in the pathogenesis of neuronal injuries following a stroke insult; therefore, a plethora of preclinical studies focus on better understanding functions of NMDARs and their associated signaling pathways. Over the past decades, NMDARs have been found to exert dual effects in neuronal deaths signaling and neuronal survival signaling during cerebral ischemia. Moreover, many complex intracellular signaling pathways downstream of NMDAR activation have been elucidated, which provide novel targets for developing much-needed neuro-protectants for patients with stroke. In this review, we will discuss the recent progress in understanding the underlying mechanisms of stroke related to NMDAR activation and the potential therapeutic strategies based on these discoveries.
Related Articles | Metrics
Copyright © 2014 Higher Education Press, All Rights Reserved. Powered by Beijing Magtech Co. Ltd
京ICP备12020869号-1 京ICP证150856号  京公网安备 11010202008535号
Service: 010-58556313 (Technology); 010-58556485 (Subscription) E-mail: subscribe@hep.com.cn