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ISSN 2096-0689
CN 11-9363/R (Online)
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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
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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
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Hyaluronic acid hydrogel: a promising scaffold for restoration in the central nervous system
Qunyuan Xu
Journal of Translational Neuroscience    2017, 2 (1): 18-27.   https://doi.org/10-3868/j.issn.2096-0689.2017.01.003
Abstract   PDF (14462KB)
Injury in the central nervous system (CNS), stroke in the brain and trauma in the spinal cord in particular, may result in permanent disability of the patients, since CNS axons do not regenerate appreciably in their native environment due to several inhibitory molecules in the extracellular environment. Therefore,no effective clinical therapies so far are convincingly accepted for CNS injuries. Tissue engineering strategies employing biomaterials are now considered as a promising approach for restoration of these injuries, and hydrogel-based biomaterials are widely employed in this field. Among them, many studies have proven that hyaluronic acid (HA) hydrogel is a reliable and effective biomaterial, which can be a well compatible scaffold with CNS tissue and creating a good microenvironment of neural regeneration in the CNS tissue. The aim of this review is to outline how to use HA-based scaffolds to build up a suitable microenvironment of neural regeneration and restoration after CNS injury, and thereby to indicate the HA hydrogel is a promising scaffold for restoration in the CNS.
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Focusing on neuronal cell-type specific mechanisms for brain circuit organization, function and dysfunction
Lu Li
Journal of Translational Neuroscience    2017, 2 (1): 28-35.   https://doi.org/10-3868/j.issn.2096-0689.2017.01.004
Abstract   PDF (9866KB)
Mammalian brain circuits consist of dynamically interconnected neurons with characteristic morphology, physiology, connectivity and genetics which are often called neuronal cell types. Neuronal cell types have been considered as building blocks of brain circuits, but knowledge of how neuron types or subtypes connect to and interact with each other to perform neuralcomputation is still lacking. Such mechanistic insights are critical not only to our understanding of normal brain functions, such as perception, motion and cognition, but also to brain disorders including Alzheimer’s disease, Schizophrenia and epilepsy, to name a few. Thus it is necessary to carry out systematic and standardized studies on neuronal cell-type specific mechanisms for brain circuit organization and function, which will provide good opportunities to bridge basic and clinical research. Here based on recent technology advancements,we discuss the strategy to target and manipulate specific populations of neurons in vivo to provide unique insights on how neuron types or subtypes behave, interact, and generate emergent properties in a fully connected brain network. Our approach is highlighted by combining transgenic animal models, targeted electrophysiology and imaging with robotics, thus complete and standardized mapping of in vivo properties of genetically defined neuron populations can be achieved in transgenic mouse models, which will facilitate the development of novel therapeutic strategies for brain disorders.
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Animal models and molecular mechanism of major depressive disorder
Di Hu, Lei Liu
Journal of Translational Neuroscience    2017, 2 (2): 25-30.   https://doi.org/10.3868/j.issn.2096-0689.2017.02.004
Abstract   PDF (7661KB)
Major depressive disorder (MDD) has been a devastating neurological problem in modern history.However, therapeutic strategies to relief the disease are inadequate. The limit in understanding of the molecular mechanism of MDD has been holding back discovery of new therapies. Behind this problem is the establishment of animal models to truly reflect human MDD pathology.In this review, we discuss our current understanding of the molecular mechanism of MDD and the strength and weakness of rodent models of depression. Developing new models of MDD and finding new drugable targets are still important steps to discover new therapies against MDD.
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Recommendation for and comparison of three types of dementia: Alzheimer’s disease, subcortical ischemic vascular dementia, and mixed dementia
Lu Shi, Jianping Jia
Journal of Translational Neuroscience    2017, 2 (3): 15-25.   https://doi.org/10.3868/j.issn.2096-0689.2017.03.003
Abstract   PDF (13316KB)
With the progress in global demography of aging, dementia has become a great world health-care issue that require urgent attention and settlement. Dementia can arise from a variety of factors, such as neuronal degeneration for Alzheimer’s disease (AD), vascular risk factors and multiple infarcts for vascular dementia (VaD), and both degeneration and vascular factors for mixed dementia (MD). Pathophysiology of AD includes the amyloid and tau protein hypothesis, and inflammation-related mechanisms are also widespread mentioned. Subcortical ischemic vascular dementia (SIVD), a subtype of VaD, is commonly caused by complete or incomplete lacunar infarction of VaD pathology. MD involves both degeneration and vascular factors, and the interaction between the two results in the complication of the pathological mechanism and clinical phenotype. The clinical manifestations of AD are often divided into four stages according to the progress of the disease, while the phenotypes of SIVD usually has two categories. As for MD, the phenotypes are complex and diverse. Several clinical studies showed that its symptoms and signs are more similar to SIVD than AD. This article aims to analyze and compare the different aspects of the three kinds of dementia.
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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.
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Astroglial anatomy in the times of connectomics
Corrado Calì
Journal of Translational Neuroscience    2017, 2 (4): 31-40.   https://doi.org/10.3868/j.issn.2096-0689.2017.04.004
Abstract   PDF (17516KB)
In contrast to neurons, the role of astrocytes has been matter of debate since their discovery, and mostly because of misconceptions about their role. As a consequence, technologies to study brain physiology have been designed around neurons, to answer one specific question, leaving glia experts with the only possibility to “hack” these techniques to describe astrocytes. As questions to answer about astrocytic functioning are based on factual observations, conclusions are often vague and cryptic, no matter how technically sound the work is. For instance, compelling evidence on calcium elevations has been provided, their dynamics have been studied in detail, but their role is still open for interpretation. Another astrocytic feature that carries a lot of mysteries is their complex morphology. The use of three-dimensional electron microscopy (3DEM) would most certainly be the best approach to unveil hidden features of such complex cells, nevertheless so far 3DEM hasn’t been fully exploited in that sense, nor techniques has been adapted for astrocytic observations in particular. One of the most ambitious neuroscience projects, the connectome, is pushing to their limits electron microscopy, image segmentation and 3D reconstruction and analysis, making it a very good candidate to adapt pipelines and methodologies to the study of astrocytic morphology. Here, we briefly review our current knowledge and technical state of art on 3D glia morphology, and speculate about its future directions.
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Homocysteine and Alzheimer’s disease: a literature review
Jianwei Yang, Jianping Jia
Journal of Translational Neuroscience    2017, 2 (3): 26-30.   https://doi.org/10.3868/j.issn.2096-0689.2017.03.004
Abstract   PDF (5749KB)
Increasing evidence in recent years suggests homocysteine (Hcy) is involved in the pathogenesis of Alzheimer’s disease (AD), and that modifying this risk factor may be an alternative approach to delaying or preventing onset of this disease. However, intervention studies suggest inconsistent effects of folic acid supplementation, with or without vitamin B12, on the prevention of incident AD. Studies with Hcy-lowering therapy show beneficial effects of B vitamins in patients with mild cognitive impairment (MCI), especially in those with high Hcy levels. Further studies are needed to confirm elevated Hcy levels as a potentially treatable risk factor for AD.
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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.
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From Rexed’s laminae to spinal cord connectivity
Gunnar Grant
Journal of Translational Neuroscience    2016, 1 (2): 1-20.   https://doi.org/10-3868/j.issn.2096-0689.2016.02.001
Abstract   PDF (22383KB)
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Optimising validity and translational potential in rodent models of brain disorders
Anthony J Hannan
Journal of Translational Neuroscience    2016, 1 (2): 56-62.   https://doi.org/10-3868/j.issn.2096-0689.2016.02.005
Abstract   PDF (7925KB)
Neurological and psychiatric disorders collectively constitute the greatest burden of disease. However, the human brain is the most complex of biological systems and therefore accurately modeling brain disorders presents enormous challenges. A large range of therapeutic approaches across a diverse collection of brain disorders have been found to show great promise in preclinical testing and then failed during clinical trials. There are a variety of potential reasons for such failures, on both the preclinical and clinical sides of the equation. In this article, I will focus on the key issues of validity in animal models. I will discuss two forms of construct validity, ‘genetic construct validity’ and ‘environmental construct validity’, which model specific aspects of the genome and ‘envirome’ relevant to the disorder in question. The generation of new gene-edited animal models has been facilitated by new technologies, the most notable of which are CRISPR-Cas systems. These and other technologies can be used to enhance construct validity. Finally, I will discuss how face validity can be optimized, via more sophisticated cognitive, affective and motor behavioural tests, translational tools and the integration of molecular, cellular and systems data. Predictive validity cannot yet be assessed for the many preclinical models where we currently lack effective clinical interventions, however this will change as the translational pipeline is honed to deliver therapies for a range of devastating disorders.
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Mapping the synaptic organization by viral cocktails
Jinjin Wu
Journal of Translational Neuroscience    2017, 2 (4): 41-46.   https://doi.org/10.3868/j.issn.2096-0689.2017.04.005
Abstract   PDF (6911KB)
In the past decade, the rapid development of viral tracing techniques, more precisely the neurotropic viral based mono-transsynaptic tracing strategy, provides a powerful tool to map synaptic connectivity in the central and peripheral nervous systems. This mini review provides a brief description of the principles of this tracing method, describe different strategies to trace the neural circuit from defined neuronal populations, and present an update of newly developed viral variants optimizing the method.
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Is autoimmunity in multiple sclerosis secondary to neurodegeneration?
Albert HC Wong, Fang Liu
Journal of Translational Neuroscience    2016, 1 (2): 49-55.   https://doi.org/10-3868/j.issn.2096-0689.2016.02.004
Abstract   PDF (8448KB)
Abstract Multiple sclerosis (MS) is characterized by neurological symptoms that are separated in time and space, which correlate with demyelination and white matter lesions. The conventional pathophysiological model is that an autoimmune reaction against the myelinated nerve sheath results in demyelination, accompanied by axon damage and the death of oligodendrocytes that produce myelin. There is no cure for MS, but current treatments are primarily aimed at suppressing the autoimmune reaction, with the goal of reducing demyelination. These treatments have limited efficacy and developing better treatments for MS remains an important goal. Here we argue that the autoimmune reaction may be secondary to neurodegeneration or neurotoxicity, and that protecting neurons from glutamate-mediated toxicity may be a better therapeutic strategy than targeting the immune system. We have recently demonstrated that a protein-protein interaction between the GluR2 subunit of the AMPA (α-Amino-3-hydroxy-5-methyl-4- isoxazolepropionic acid) glutamate receptor and GAPDH (Glyceraldehyde 3-phosphate dehydrogenase) is elevated in human MS plaques and in an animal model of MS. Disrupting this interaction in a rodent model restores neurological function, preserves myelin, and protects neurons, oligodendrocytes and axons. The peptide we created to block the GluR2-GAPDH interaction also reduces immune system activation, suggesting that autoimmunity is not necessarily the primary etiology in MS. The GluR2-GAPDH interaction may promote cell death via increased calcium influx through non-GluR2-containing AMPA receptors, or through the p53 and Siah1 cell death pathways.
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Disrupted functional connectivity of default mode network and executive control network in patients with vascular cognitive impairment, no dementia
Tan Zhao, Jianping Jia
Journal of Translational Neuroscience    2017, 2 (3): 39-48.   https://doi.org/10.3868/j.issn.2096-0689.2017.03.006
Abstract   PDF (10997KB)
Objective: To investigate functional connectivity within default mode network (DMN) and executive control network (ECN) in vascular cognitive impairment, no dementia (VCIND). Methods: Twenty-eight VCIND patients and sixteen healthy controls were recruited. A seed-based connectivity analysis was performed using data from resting-state functional magnetic resonance imaging (fMRI). Based on previous findings, posterior cingulate cortex (PCC) and dorsolateral prefrontal cortex (DLPFC) were chosen as regions of interest to study these networks. One-sample t-test and two-sample t-test were used for statistical analysis. Results: Compared with the controls, the VCIND group exhibited increased functional activity in such DMN regions as the left inferior temporal gyrus, parahippocampal gyrus, and medial frontal gyrus. The VCIND group had decreased functional connectivity of DMN at right superior frontal gyrus, left mid-cingulate area, the medial part of left superior frontal gyrus, and bilateral medial frontal gyrus. The VCIND group also showed decreased functional connectivity of ECN primarily at left inferior parietal gyrus, right angular gyrus, right middle occipital gyrus, and right middle frontal cortex. Conclusions: Increased functional connectivity within DMN and decreased functional connectivity within ECN suggested dysfunction of these two networks, which might be associated with the cognitive deficits in patients with VCIND. These findings may help us understand the pathogenesis and clinical characteristics of VCIND.
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Perspectives on a collaborative Canada-China research program on diagnostic biomarkers for pre-dementia stages of Alzheimer’s disease
Serge Gauthier, Jianping Jia, Sylvie Belleville, Simon Cloutier, Dessa Sadovnick, Colleen Guimond, Laura Robb, Mario Masellis, Guy A Rouleau, Liyong Wu, Pedro Rosa-Neto
Journal of Translational Neuroscience    2017, 2 (3): 1-6.   https://doi.org/10.3868/j.issn.2096-0689.2017.03.001
Abstract   PDF (5950KB)
As biomarkers are important in the early diagnosis of Alzheimer's disease (AD), the first collaborative work of recruiting early-onset familial AD (EOFAD) families in Canada and China was initiated in 2012. The registration networks have collected hundreds of pedigrees, for which genetic screening, neuropsychological tests and amyloid and tau imaging was used to study diagnostic biomarkers for preclinical and mild cognitive impairment (MCI) stages of AD. Besides identifying pedigrees with novel mutations in presenilins (PSENs)/amyloid precursor protein (APP), the program has benefited training of Chinese research fellows, AD clinical trials for prevention, the ethical concerns for clinical findings, and other collaborative projects with Chinese investigators. Further research of the collaborative program may facilitate the testing and clinical use of novel treatments for EOFAD and late onset AD and contribute to dementia prevention strategies in Canada and China.
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