Thursday, December 29, 2016
Thursday, December 22, 2016
Sunday, December 18, 2016
Friday, December 16, 2016
Friday, December 9, 2016
Friday, December 2, 2016
Thursday, November 10, 2016
Call For Paper
Bentham Science Publishers would like to invite you to submit your research paper for publishing in the Journal of
Thursday, November 3, 2016
Highlighted Article: Mechanisms by which Stress Affects the Experimental and Clinical Inflammatory Bowel Disease (IBD): Role of Brain-Gut Axis
Mechanisms by which Stress Affects the Experimental and Clinical Inflammatory Bowel Disease (IBD): Role of Brain-Gut Axis
Author(s):
Bartosz Brzozowski, Agnieszka Mazur-Bialy, Robert Pajdo, Slawomir Kwiecien, Jan Bilski, Malgorzata Zwolinska-Wcislo, Tomasz Mach and Tomasz Brzozowski Pages 892 - 900 ( 9 )
Abstract:
Background: Stress of different origin is known to alter so called “braingut axis” and contributes to a broad array of gastrointestinal disorders including inflammatory bowel disease (IBD), irritable bowel syndrome (IBS) and other functional gastrointestinal diseases. The stressful situations and various stressors including psychosocial events, heat, hypo- and hyperthermia may worsen the course of IBD via unknown mechanism. The aims of this paper were to provide an overview of experimental and clinical evidences that stress activates the brain-gut axis which results in a mucosal mast cells activation and an increase in the production of proinflammatory cytokines and other endocrine and humoral mediators.
Methods: Research and online content related to effects of stress on lower bowel disorders are reviewed and most important mechanisms are delineated.
Results: Brain conveys the neural, endocrine and circulatory messages to the gut via brain-gut axis reflecting changes in corticotrophin releasing hormone, mast cells activity, neurotransmission at the autonomic nerves system and intestinal barrier function all affecting the pathogenesis of animal colitis and human IBD. Stress triggers the hypothalamus-pituitary axis and the activation of the autonomic nervous system, an increase in cortisol levels and proinflammatory cytokines such as tumor necrosis factor-alpha, interleukin-8, interleukin-1beta and interleukin-6.
Conclusion: The acute or chronic stress enhances the intestinal permeability weakening of the tight junctions and increasing bacterial translocation into the intestinal wall. An increased microbial load in the colonic tissue, excessive cytokine release and a partially blunted immune reactivity in response to stress result in its negative impact on IBD.
Keywords:
Autonomic nervous system, brain-gut axis, cortisol, enteric nervous system, histamine, inflammatory bowel disease, microbiota, proinflammatory cytokines, stress.
Affiliation:
Department of Physiology, Jagiellonian University Medical College, 16 Grzegorzecka Street, 31-531 Cracow, Poland.
For More Information Please Visit Our Website Current Neuropharmacology
Thursday, October 27, 2016
Most Accessed Article: Drug Therapy for Behavioral and Psychological Symptoms of Dementia
Drug Therapy for
Behavioral and Psychological Symptoms of Dementia
Author(s):
Feng Wang, Ting-Yi Feng, Shilin Yang, Maurice
Preter, Jiang-Ning Zhou and Xiao-Ping Wang Pages 307 - 313 ( 7 )
Abstract:
Dementia, which can be induced by diverse
factors, is a clinical syndrome characterized by the decline of cognitive
function. Behavioral and psychological symptoms of dementia (BPSD) include
depression, agitation, and aggression. Dementia causes a heavy burden on
patients and their caregivers. Patients with BPSD should be assessed
comprehensively by practitioners and offered appropriate non-pharmacologic and
pharmacologic therapy. Nonpharmacologic therapy has been recommended as the
basal treatment for BPSD; however, pharmacologic therapy is required under many
situations. Medications, including antipsychotic agents, antidepressants,
sedative and hypnotic agents, mood stabilizers, cholinesterase inhibitors, and
amantadine, are extensively used in clinical practice. We have reviewed the
progression of pharmacologic therapy for BPSD.
Keywords:
Alzheimer’s disease, antipsychotic, behavioral
and psychological symptoms of dementia, dementia, drug, psychiatric symptoms.
Affiliation:
Department of Neurology, Shanghai First
People’s Hospital, Shanghai Jiao-Tong University, China, 200080.
Graphical Abstract:
Thursday, October 20, 2016
Thursday, October 13, 2016
Pharmacological tools to activate microglia and their possible use to study neural network patho-physiology
Current Neuropharmacology, Volume 14 (E-pub ahead of print)
Author(s): Fernando Peña-Ortega.
Affiliation: Departamento de Neurobiología del Desarrollo y Neurofisiología, Instituto de Neurobiología, Universidad Nacional Autónoma de México, Boulevard Juriquilla 3001, Querétaro, 76230, México
Abstract
Background: Microglia are the resident immunocompetent cells of the CNS and also constitute a unique cell type that contributes to neural network homeostasis and function. Understanding microglia cell-signaling not only will reveal their diverse functions but also will help to identify pharmacological and non-pharmacological tools to modulate the activity of these cells. Methods: We undertook a search of bibliographic databases for peer-reviewed research literature to identify microglial activators and their cell-specificity. We also looked for their effects on neural network function and dysfunction. Results: We identified several pharmacological targets to modulate microglial function, which are more or less specific (with the proper control experiments). We also identified pharmacological targets that would require the development of new potent and specific modulators. We identified a wealth of evidence about the participation of microglia in neural network function and their alterations in pathological conditions. Conclusion: The identification of specific microglia-activating signals provides experimental tools to modulate the activity of this heterogeneous cell type in order to evaluate its impact on other components of the nervous system, and it also helps to identify therapeutic approaches to ease some pathological conditions related to microglial dysfunction.Keywords:
Microglia, astrocytes, macrophages, neurons, lipopolysaccharide, complement receptors, scavenger receptors, fractalkine, phosphatidylserine.
Order Eprints Rights and Permissions
Thursday, October 6, 2016
New Issue ::: Current Neuropharmacology, 14 Issue 7
Current Neuropharmacology aims to provide current, timely and comprehensive reviews and guest edited issues of all areas of neuropharmacology and related matters of neuroscience. The reviews cover the fields of molecular, cellular, and systems/behavioural aspects of neuropharmacology and neuroscience.
The journal serves as a comprehensive, multidisciplinary expert forum for neuropharmacologists and neuroscientists.
Articles from the journal Current Neuropharmacology , Volume 14 Issue 7:
- Editorial (Thematic Selection: Inflammatory and Immune Responses in Depression)
- Stress, the Autonomic Nervous System, and the Immune-kynurenine Pathway in the Etiology of Depression
- Inflammation and Immune Regulation as Potential Drug Targets in Antidepressant Treatment
- Animal Models of Maternal Immune Activation in Depression Research
- A Potential Contribution of Chemokine Network Dysfunction to the Depressive Disorders
- Brain-derived Neurotrophic Factor (BDNF)-TrkB Signaling in Inflammation-related Depression and Potential Therapeutic Targets
- Inflammation in Depression and the Potential for Anti-Inflammatory Treatment
- Interferon-Related Depression: A Primer on Mechanisms, Treatment, and Prevention of a Common Clinical Problem
- Systems Genomics Support for Immune and Inflammation Hypothesis of Depression
- Gap Junction Blockers: An Overview of their Effects on Induced Seizures in Animal Models
- Multiple Non-Equivalent Interfaces Mediate Direct Activation of GABAA Receptors by Propofol
For details on the articles, please visit this link :: http://bit.ly/2csqKVy
courtesy by Bentham Insight
Wednesday, October 5, 2016
Current Neuropharmacology Volume 14 Issue 4
Current Neuropharmacology aims to provide current, timely and comprehensive reviews and guest edited issues of all areas of neuropharmacology and related matters of neuroscience. The reviews cover the fields of molecular, cellular, and systems/behavioural aspects of neuropharmacology and neuroscience.
The journal serves as a comprehensive, multidisciplinary expert forum for neuropharmacologists and neuroscientists.
Articles from the journal Current Neuropharmacology, Volume 14 Issue 4:
- Editorial (Thematic Selection: Strategies of Current Drugs and Alternative Treatments for Neurodegenerative Diseases)
- Freezing of Gait in Parkinsonism and its Potential Drug Treatment
- Drug Therapy for Behavioral and Psychological Symptoms of Dementia
- Current Therapy of Drugs in Amyotrophic Lateral Sclerosis
- Current Drug Managements of Wilson’s Disease: From West to East
- Current Treatment Options for Alzheimer’s Disease and Parkinson’s Disease Dementia
- Current Pharmaceutical Treatments and Alternative Therapies of Parkinson’s Disease
- Revisiting the Medical Management of Parkinson’s Disease: Levodopa versus Dopamine Agonist
- AChE Inhibition-based Multi-target-directed Ligands, a Novel Pharmacological Approach for the Symptomatic and Disease-modifying Therapy of Alzheimer’s Disease
- Drug Delivery Systems for Imaging and Therapy of Parkinson’s Disease
- Molecular, Cellular and Clinical Aspects of Intracerebral Hemorrhage: Are the Enemies Within?
For details on the articles, please visit this link :: http://bit.ly/1Zl2So3
courtesy by : Bentham Insight
Friday, August 12, 2016
Brain-derived Neurotrophic Factor (BDNF)-TrkB Signaling in Inflammation-related Depression and Potential Therapeutic Targets
Author(s):
Ji-chun Zhang, Wei Yao and Kenji HashimotoPages 1-10 (10)
Abstract:
Depression is the most prevalent and among the most debilitating of psychiatric disorders. The precise neurobiology of this illness is unknown. Several lines of evidence suggest that peripheral and central inflammation plays a role in depressive symptoms, and that anti-inflammatory drugs canimprove depressive symptoms in patients with inflammation-related depression. Signaling via brain-derived neurotrophic factor (BDNF) and its receptor, tropomycin receptor kinase B (TrkB) plays a key role in the pathophysiology of depression and in the therapeutic mechanisms of antidepressants. A recent paper showed that lipopolysaccharide (LPS)-induced inflammation gave rise to depression-like phenotype by altering BDNF-TrkB signaling in the prefrontal cortex, hippocampus, and nucleus accumbens, areas thought to be involved in the antidepressant effects of TrkB agonist, 7,8-dihydroxyflavone (7,8-DHF) and TrkB antagonist, ANA-12.Here we provide an overview of the tryptophan-kynurenine pathway and BDNF-TrkB signaling in the pathophysiology of inflammation-induced depression, and propose mechanistic actions for potential therapeutic agents.Additionally, the authors discuss the putative role ofTrkB agonists and antagonists as novel therapeutic drugs for inflammation-related depression.
Keywords:
Brain-derived neurotrophic factor (BDNF); Depression;Hippocampus, Inflammation;Nucleus accumbens; Prefrontal cortex; TrkB
Affiliation:
Division of Clinical Neuroscience, Chiba University Center for Forensic Mental Health, 1-8-1 Inohana, Chiba 260-8670, Japan
Read Full-Text article
Animal Models of Maternal Immune Activation in Depression Research
Author(s):
Marianne Ronovsky, Stefanie Berger, Barbara Molz, Angelika Berger and Daniela D. PollakPages 1-16 (16)
Abstract:
Background: Depression and schizophrenia are debilitating mental illnesses with significant socio-economic impact. The high degree of comorbidity between the two disorders, shared symptoms and risk factors, suggest partly common pathogenic mechanisms. Supported by human and animal studies, maternal immune activation (MIA) has been intimately associated with the development of schizophrenia. However, the link between MIA and depression has remained less clear, in part due to the lack of appropriate animal models. Objective: Here we aim to summarize findings obtained from studies using MIA animal models and discuss their relevance for preclinical depression research. Methods: Results on molecular, cellular and behavioral phenotypes in MIA animal models were collected by literature search (PubMed) and evaluated for their significance for depression. Results: Several reports on offspring depression-related behavioral alterations indicate an involvement of MIA in the development of depression later in life. Depression-related behavioral phenotypes were frequently paralleled by neurogenic and neurotrophic deficits and modulated by several genetic and environmental factors. Conclusion: Literature evidence analyzed in this review supports a relevance of MIA as animal model for a specific early life adversity, which may prime an individual for the development of distinct psychopathologies later life. MIA animal models may present a unique tool for the identification of additional exogenous and endogenous factors, which are required for the determination of a specific neuropsychiatric disorder, such as depression, later in life. Hereby, novel insights into the molecular mechanism involved in the pathophysiology of depression may be obtained, supporting the identification of alternative therapeutic strategies.
Affiliation:
Department of Neurophysiology and Neuropharmacology, Center for Physiology and Pharmacology, Medical University of Vienna, Schwarzspanierstrasse 17, A-1090 Vienna, Austria
Read Full-Text article
Freezing of Gait in Parkinsonism and its Potential Drug Treatment
Author(s):
Li-Li Zhang, S. Duff Canning and Xiao-Ping WangPages 302-306 (5)
Abstract:
Freezing of gait (FOG) is a heterogeneous symptom. Studies of treatment for FOG are scarce. Levodopa and monoamine oxidase inhibitors (rasagiline and selegiline) have shown effective improvement for FOG. Other drugs, such as L-threo-3, 4-dihydroxyphenylserine, amantadine, and botulinum toxin have exhibited some beneficial effects. The present review summarizes the potential drug treatment for FOG in Parkinsonism.
Keywords:
Drug treatment, freezing of gait, Levodopa, Parkinson’s disease, Parkinsonism.
Affiliation:
Department of Neurology, Shanghai First People’s Hospital, Shanghai Jiao-Tong University, China. 200080.
Graphical Abstract:
Read Full-Text article
Drug Therapy for Behavioral and Psychological Symptoms of Dementia
Author(s):
Feng Wang, Ting-Yi Feng, Shilin Yang, Maurice Preter, Jiang-Ning Zhou and Xiao-Ping WangPages 307-313 (7)
Abstract:
Dementia, which can be induced by diverse factors, is a clinical syndrome characterized by the decline of cognitive function. Behavioral and psychological symptoms of dementia (BPSD) include depression, agitation, and aggression. Dementia causes a heavy burden on patients and their caregivers. Patients with BPSD should be assessed comprehensively by practitioners and offered appropriate non-pharmacologic and pharmacologic therapy. Nonpharmacologic therapy has been recommended as the basal treatment for BPSD; however, pharmacologic therapy is required under many situations. Medications, including antipsychotic agents, antidepressants, sedative and hypnotic agents, mood stabilizers, cholinesterase inhibitors, and amantadine, are extensively used in clinical practice. We have reviewed the progression of pharmacologic therapy for BPSD.
Keywords:
Alzheimer’s disease, antipsychotic, behavioral and psychological symptoms of dementia, dementia, drug, psychiatric symptoms.
Affiliation:
Department of Neurology, Shanghai First People’s Hospital, Shanghai Jiao-Tong University, China, 200080.
Graphical Abstract:
Read Full-Text article
Current Therapy of Drugs in Amyotrophic Lateral Sclerosis
Author(s):
Haiyan Lu, Wei Dong Le, Ya-Ying Xie and Xiao-Ping WangPages 314-321 (8)
Abstract:
Amyotrophic lateral sclerosis (ALS), commonly termed as motor neuron disease (MND) in UK, is a chronically lethal disorder among the neurodegenerative diseases, meanwhile. ALS is basically irreversible and progressive deterioration of upper and lower motor neurons in the motor cortex, brain stem and medulla spinalis. Riluzole, used for the treatment of ALS, was demonstrated to slightly delay the initiation of respiratory dysfunction and extend the median survival of patients by a few months. In this study, the key biochemical defects were discussed, such as: mutant Cu/Zn superoxide dismutase, mitochondrial protectants, and anti-excitotoxic/ anti-oxidative / antiinflammatory/ anti-apoptotic agents, so the related drug candidates that have been studied in ALS models would possibly be further used in ALS patients.
Keywords:
Amyotrophic lateral sclerosis, motor neuron disease, neurodegenerative disease, SOD1 mutations, riluzole, edaravone, pyrimethamine.
Affiliation:
Department of Neurology, Shanghai First People’s Hospital , Shanghai Jiao-Tong University, China, 200080.
Graphical Abstract:
Read Full-Text article
