Publisher: BMC (Biomed Central)   (Total: 310 journals)

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Showing 201 - 310 of 310 Journals sorted alphabetically
Italian J. of Pediatrics     Open Access   (Followers: 2, SJR: 0.685, CiteScore: 2)
J. for ImmunoTherapy of Cancer     Open Access   (Followers: 6, SJR: 2.798, CiteScore: 6)
J. of Angiogenesis Research     Open Access   (Followers: 2)
J. of Animal Science and Biotechnology     Open Access   (Followers: 7, SJR: 1.228, CiteScore: 3)
J. of Animal Science and Technology     Open Access   (Followers: 3)
J. of Biological Engineering     Open Access   (Followers: 3, SJR: 1.34, CiteScore: 4)
J. of Biological Research - Thessaloniki     Open Access   (SJR: 0.32, CiteScore: 2)
J. of Biomedical Semantics     Open Access   (Followers: 2, SJR: 0.952, CiteScore: 2)
J. of Cardiothoracic Surgery     Open Access   (Followers: 5, SJR: 0.607, CiteScore: 1)
J. of Cardiovascular Magnetic Resonance     Open Access   (Followers: 1, SJR: 2.292, CiteScore: 5)
J. of Clinical Movement Disorders     Open Access   (Followers: 3)
J. of Congenital Cardiology     Open Access   (Followers: 4)
J. of Cotton Research     Open Access  
J. of Diabetes and Metabolic Disorders     Open Access   (Followers: 8, SJR: 0.818, CiteScore: 2)
J. of Eating Disorders     Open Access   (Followers: 9, SJR: 0.693, CiteScore: 1)
J. of Environmental Health Science & Engineering     Open Access   (Followers: 1, SJR: 0.802, CiteScore: 3)
J. of Ethnobiology and Ethnomedicine     Open Access   (SJR: 0.693, CiteScore: 3)
J. of Experimental & Clinical Cancer Research     Open Access   (Followers: 3, SJR: 2, CiteScore: 6)
J. of Foot and Ankle Research     Open Access   (Followers: 5, SJR: 0.873, CiteScore: 2)
J. of Health, Population and Nutrition     Open Access   (Followers: 9, SJR: 0.875, CiteScore: 2)
J. of Hematology & Oncology     Open Access   (Followers: 3, SJR: 2.292, CiteScore: 6)
J. of Inflammation     Open Access   (Followers: 2, SJR: 1.101, CiteScore: 3)
J. of Intensive Care     Open Access   (Followers: 6, SJR: 1.137, CiteScore: 3)
J. of Medical Case Reports     Open Access   (Followers: 1, SJR: 0.331, CiteScore: 1)
J. of Molecular Psychiatry     Open Access   (Followers: 9, SJR: 0.355, CiteScore: 0)
J. of Nanobiotechnology     Open Access   (Followers: 4, SJR: 1.38, CiteScore: 5)
J. of Negative Results in BioMedicine     Open Access   (SJR: 0.483, CiteScore: 1)
J. of Neurodevelopmental Disorders     Open Access   (SJR: 1.71, CiteScore: 4)
J. of NeuroEngineering and Rehabilitation     Open Access   (Followers: 14, SJR: 1.515, CiteScore: 5)
J. of Neuroinflammation     Open Access   (Followers: 2, SJR: 2.336, CiteScore: 5)
J. of Occupational Medicine and Toxicology     Open Access   (Followers: 13, SJR: 0.591, CiteScore: 2)
J. of Orthopaedic Surgery and Research     Open Access   (Followers: 7, SJR: 0.751, CiteScore: 2)
J. of Otolaryngology - Head and Neck Surgery     Open Access   (Followers: 10, SJR: 0.827, CiteScore: 2)
J. of Ovarian Research     Open Access   (SJR: 1.008, CiteScore: 3)
J. of Pharmaceutical Policy and Practice     Open Access   (Followers: 4, SJR: 0.545, CiteScore: 1)
J. of Physiological Anthropology     Open Access   (Followers: 8, SJR: 0.514, CiteScore: 2)
J. of the Intl. AIDS Society     Open Access   (Followers: 9, SJR: 2.092, CiteScore: 4)
J. of the Intl. Society of Sports Nutrition     Open Access   (Followers: 58, SJR: 0.775, CiteScore: 2)
J. of Therapeutic Ultrasound     Open Access   (SJR: 0.906, CiteScore: 3)
J. of Translational Medicine     Open Access   (Followers: 4, SJR: 1.565, CiteScore: 4)
J. of Trauma Management & Outcomes     Open Access   (Followers: 6, SJR: 0.398, CiteScore: 1)
J. of Venomous Animals and Toxins including Tropical Diseases     Open Access   (Followers: 1, SJR: 0.573, CiteScore: 2)
Kidney Disease and Transplantation     Open Access   (Followers: 4)
Lipids in Health and Disease     Open Access   (SJR: 0.915, CiteScore: 2)
Longevity & Healthspan     Open Access   (Followers: 1)
Malaria J.     Open Access   (Followers: 8, SJR: 2.082, CiteScore: 3)
Marine Biodiversity Records     Open Access   (Followers: 4, SJR: 0.354, CiteScore: 1)
Measurement Instruments for the Social Sciences     Open Access  
Microbial Cell Factories     Open Access   (Followers: 8, SJR: 1.443, CiteScore: 4)
Military Medical Research     Open Access   (Followers: 3, SJR: 0.601, CiteScore: 2)
Mobile DNA     Open Access   (SJR: 3.783, CiteScore: 5)
Molecular Autism     Open Access   (Followers: 9, SJR: 2.377, CiteScore: 5)
Molecular Brain     Open Access   (Followers: 3, SJR: 1.805, CiteScore: 4)
Molecular Cancer     Open Access   (Followers: 4, SJR: 2.778, CiteScore: 7)
Molecular Cytogenetics     Open Access   (Followers: 1, SJR: 0.623, CiteScore: 1)
Molecular Neurodegeneration     Open Access   (Followers: 2, SJR: 3.418, CiteScore: 7)
Movement Ecology     Open Access   (Followers: 10, SJR: 2.242, CiteScore: 4)
Multidisciplinary Respiratory Medicine     Open Access   (Followers: 4, SJR: 1.13, CiteScore: 2)
Multiple Sclerosis and Demyelinating Disorders     Open Access   (Followers: 5)
Neural Development     Open Access   (Followers: 2, SJR: 1.821, CiteScore: 2)
NeuroMetals     Open Access  
Neuropsychiatric Electrophysiology     Open Access  
Neurovascular Imaging     Open Access  
Nutrition & Metabolism     Open Access   (Followers: 10)
Nutrition J.     Open Access   (Followers: 7, SJR: 1.447, CiteScore: 4)
Orphanet J. of Rare Diseases     Open Access   (Followers: 1, SJR: 1.413, CiteScore: 3)
Particle and Fibre Toxicology     Open Access   (Followers: 2, SJR: 2.253, CiteScore: 8)
Patient Safety in Surgery     Open Access   (Followers: 4, SJR: 0.525, CiteScore: 1)
Pediatric Rheumatology     Open Access   (Followers: 7, SJR: 0.729, CiteScore: 2)
Philosophy, Ethics, and Humanities in Medicine     Open Access   (Followers: 1, SJR: 0.285, CiteScore: 1)
Pilot and Feasibility Studies     Open Access   (Followers: 1)
Plant Methods     Open Access   (Followers: 2, SJR: 1.885, CiteScore: 4)
PMC Biophysics     Open Access  
Population Health Metrics     Open Access   (Followers: 6, SJR: 1.954, CiteScore: 3)
Porcine Health Management     Open Access  
Proteome Science     Open Access   (Followers: 1, SJR: 0.792, CiteScore: 2)
Public Health Reviews     Open Access   (Followers: 2, SJR: 0.454, CiteScore: 1)
Radiation Oncology     Open Access   (Followers: 6, SJR: 1.293, CiteScore: 3)
Renal Replacement Therapy     Open Access   (Followers: 4)
Reproductive Biology and Endocrinology     Open Access   (Followers: 4, SJR: 1.203, CiteScore: 3)
Reproductive Health     Open Access   (Followers: 2, SJR: 1.228, CiteScore: 2)
Research Involvement and Engagement     Open Access  
Respiratory Research     Open Access   (Followers: 1, SJR: 1.644, CiteScore: 4)
Retrovirology     Open Access   (SJR: 1.855, CiteScore: 3)
Safety in Health     Open Access   (Followers: 63)
Scandinavian J. of Trauma, Resuscitation and Emergency Medicine     Open Access   (Followers: 12, SJR: 0.618, CiteScore: 2)
Scoliosis     Open Access   (Followers: 3)
Scoliosis and Spinal Disorders     Open Access   (Followers: 1, SJR: 0.843, CiteScore: 2)
Skeletal Muscle     Open Access   (Followers: 1, SJR: 2.32, CiteScore: 4)
Source Code for Biology and Medicine     Open Access   (SJR: 0.784, CiteScore: 2)
Sports Medicine, Arthroscopy, Rehabilitation, Therapy & Technology     Open Access   (Followers: 17)
Standards in Genomic Sciences     Open Access   (SJR: 0.768, CiteScore: 2)
Stem Cell Research & Therapy     Open Access   (Followers: 10, SJR: 1.685, CiteScore: 5)
Substance Abuse Treatment, Prevention and Policy     Open Access   (Followers: 8, SJR: 1.108, CiteScore: 2)
Sustainable Earth     Open Access  
Systematic Reviews     Open Access   (Followers: 11, SJR: 1.794, CiteScore: 4)
Theoretical Biology and Medical Modelling     Open Access   (Followers: 1, SJR: 0.783, CiteScore: 2)
Thrombosis J.     Open Access   (Followers: 4, SJR: 1.009, CiteScore: 3)
Thyroid Research     Open Access   (Followers: 1, SJR: 0.329, CiteScore: 1)
Tobacco Induced Diseases     Open Access   (Followers: 9, SJR: 0.716, CiteScore: 2)
Translational Neurodegeneration     Open Access   (Followers: 1, SJR: 1.901, CiteScore: 5)
Trials     Open Access   (Followers: 4, SJR: 1.291, CiteScore: 2)
Tropical Diseases, Travel Medicine and Vaccines     Open Access   (Followers: 1)
Vascular Cell     Open Access   (SJR: 1.349, CiteScore: 4)
Veterinary Research     Open Access   (Followers: 12)
Virology J.     Open Access   (Followers: 7, SJR: 1.053, CiteScore: 2)
Women's Midlife Health     Open Access   (Followers: 1)
World Allergy Organization J.     Open Access   (Followers: 1, SJR: 1.936, CiteScore: 6)
World J. of Emergency Surgery     Open Access   (Followers: 5, SJR: 1.098, CiteScore: 3)
World J. of Surgical Oncology     Open Access   (Followers: 1, SJR: 0.688, CiteScore: 2)

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Journal of Molecular Psychiatry
Journal Prestige (SJR): 0.355
Number of Followers: 9  

  This is an Open Access Journal Open Access journal
ISSN (Online) 2049-9256
Published by BMC (Biomed Central) Homepage  [310 journals]
  • Unified theory of Alzheimer’s disease (UTAD): implications for
           prevention and curative therapy

    • Abstract: Abstract The aim of this review is to propose a Unified Theory of Alzheimer’s disease (UTAD) that integrates all key behavioural, genetic and environmental risk factors in a causal chain of etiological and pathogenetic events. It is based on three concepts that emanate from human’s evolutionary history: (1) The grandmother-hypothesis (GMH), which explains human longevity due to an evolutionary advantage in reproduction by trans-generational transfer of acquired knowledge. Consequently it is argued that mental health at old-age must be the default pathway of humans’ genetic program and not development of AD. (2) Therefore, mechanism like neuronal rejuvenation (NRJ) and adult hippocampal neurogenesis (AHN) that still function efficiently even at old age provide the required lifelong ability to memorize personal experiences important for survival. Cumulative evidence from a multitude of experimental and epidemiological studies indicate that behavioural and environmental risk factors, which impair productive AHN, result in reduced episodic memory performance and in reduced psychological resilience. This leads to avoidance of novelty, dysregulation of the hypothalamic–pituitary–adrenal (HPA)-axis and cortisol hypersecretion, which drives key pathogenic mechanisms of AD like the accumulation and oligomerization of synaptotoxic amyloid beta, chronic neuroinflammation and neuronal insulin resistance. (3) By applying to AHN the law of the minimum (LOM), which defines the basic requirements of biological growth processes, the UTAD explains why and how different lifestyle deficiencies initiate the AD process by impairing AHN and causing dysregulation of the HPA-axis, and how environmental and genetic risk factors such as toxins or ApoE4, respectively, turn into disease accelerators under these unnatural conditions. Consequently, the UTAD provides a rational strategy for the prevention of mental decline and a system-biological approach for the causal treatment of AD, which might even be curative if the systemic intervention is initiated early enough in the disease process. Hence an individualized system-biological treatment of patients with early AD is proposed as a test for the validity of UTAD and outlined in this review.
      PubDate: 2016-07-15
       
  • αT-catenin in restricted brain cell types and its potential
           connection to autism

    • Abstract: Background Recent genetic association studies have linked the cadherin-based adherens junction protein alpha-T-catenin (αT-cat, CTNNA3) with the development of autism. Where αT-cat is expressed in the brain, and how its loss could contribute to this disorder, are entirely unknown. Methods We used the αT-cat knockout mouse to examine the localization of αT-cat in the brain, and we used histology and immunofluorescence analysis to examine the neurobiological consequences of its loss. Results We found that αT-cat comprises the ependymal cell junctions of the ventricles of the brain, and its loss led to compensatory upregulation of αE-cat expression. Notably, αT-cat was not detected within the choroid plexus, which relies on cell junction components common to typical epithelial cells. While αT-cat was not detected in neurons of the cerebral cortex, it was abundantly detected within neuronal structures of the molecular layer of the cerebellum. Although αT-cat loss led to no overt differences in cerebral or cerebellar structure, RNA-sequencing analysis from wild type versus knockout cerebella identified a number of disease-relevant signaling pathways associated with αT-cat loss, such as GABA-A receptor activation. Conclusions These findings raise the possibility that the genetic associations between αT-cat and autism may be due to ependymal and cerebellar defects, and highlight the potential importance of a seemingly redundant adherens junction component to a neurological disorder.
      PubDate: 2016-06-21
       
  • De novo POGZ mutations in sporadic autism disrupt the DNA-binding activity
           of POGZ

    • Abstract: Background A spontaneous de novo mutation is a new mutation appeared in a child that neither the parent carries. Recent studies suggest that recurrent de novo loss-of-function mutations identified in patients with sporadic autism spectrum disorder (ASD) play a key role in the etiology of the disorder. POGZ is one of the most recurrently mutated genes in ASD patients. Our laboratory and other groups have recently found that POGZ has at least 18 independent de novo possible loss-of-function mutations. Despite the apparent importance, these mutations have never previously been assessed via functional analysis. Methods Using wild-type, the Q1042R-mutated, and R1008X-mutated POGZ, we performed DNA-binding experiments for proteins that used the CENP-B box sequence in vitro. Data were statistically analyzed by one-way ANOVA followed by Tukey-Kramer post hoc tests. Results This study reveals that ASD-associated de novo mutations (Q1042R and R1008X) in the POGZ disrupt its DNA-binding activity. Conclusions Here, we report the first functional characterization of de novo POGZ mutations identified in sporadic ASD cases. These findings provide important insights into the cellular basis of ASD.
      PubDate: 2016-04-21
       
  • Prevalence of mental distress and associated factors among caregivers of
           patients with severe mental illness in the outpatient unit of Amanuel
           Hospital, Addis Ababa, Ethiopia, 2013: Cross-sectional study

    • Abstract: s Background Caregivers like family members or other relatives are central and provide not only practical help and personal care but also give emotional support, and they are suffering from plenty of challengeable tasks. These, eventually, cast out family caregivers into multidimensional problems prominently for mental distress like depression, anxiety, sleep problem and somatic disorder which are followed by physiologic changes and impaired health habits that ultimately lead to illness and possibly to death. Numerous studies demonstrate that mental distress of caregivers are two times compared to general populations. Despite it was not uncommon to observe manifestations of caregivers’ mental distress, yet there was no study on this area. Therefore, this study was intended to assess the prevalence of mental distress and associated factors among the caregivers of persons with severe mental illness in the out patients unit of Amanuel Hospital, Ethiopia. Methods Institutional based cross sectional study was conducted from May 1 to 31, 2013 at Amanuel Hospital, Addis Ababa, Ethiopia. Systematic random sampling technique with “k” interval of 13 was employed to withdraw a total of 423 participants from study population. Five psychiatric nurses carried out interview by using standardized and validated Self Reported Questionnaire (SRQ 20). Descriptive statistics, binary and multivariate logistic regression analysis were conducted. Results This study revealed that the overall prevalence of mental distress was found to be 221(56.7 %). The factors like missed social support, two or more times admission of patient, care giving for psychotic patient, being farmer and being female were found to be predictors for mental distress of caregivers with this [AOR 95 % CI = 9.523(5.002, 18.132)], 3.293(1.474, 3.3560), 2.007(1.109, 3.634), 2.245(1.129, 4.463) and 3.170(1.843, 5.454)] respectively. Conclusions In this respect the study observed that there was a higher level of mental distress experienced by caregivers of patients with severe mental illness in Amanuel Hospital, and social support are strongly associated with mental distress besides to other variables. Effectively planned interventions have to be targeted at alleviating mental distress and actions like on-going psycho-education and mutual support that could expand social support should be implemented in Amanuel hospital health service delivery system.
      PubDate: 2015-10-08
       
  • Preparation for teacher collaboration in inclusive classrooms – stress
           reduction for special education students via acceptance and commitment
           training: A controlled study

    • Abstract: Background The education system in Germany is beginning to witness a sea change, lately, owing to the country’s ratification of the United Nation’s Convention on the Rights of Persons with Disabilities. The enactment is aiming at making provision for special education teachers to share the same teaching platform and institution with other teachers for teaching children from all backgrounds, irrespective of their needs. While promoting the benefits of collaborative teaching, this provision would also effectively establish role demarcation among teachers. However, the level of participation and adaptiveness displayed by individual teachers would play a major role in determining the success or failure of the intended collaborative framework. Collaboration also becomes challenging due to the level of stress involved in the teaching profession. The fact that only 65 % of teachers in Germany reach retirement age while still in service, primarily due to psychiatric illness, has posed questions on adopting the collaborative framework for teachers from diverse backgrounds. In other words, it can be stated that the process of collaborating with teachers from different professional backgrounds and with varying levels of skills will potentially lead to further stress. The stress-related psychological states, developed through the collaborative processes, might affect the biological stress-response systems of the participating teachers. With stress-response contributing directly to the pathogenesis of stress-related diseases and disorders in the long term, it would be important to contain the ripple effect of collaborative framework that the enactment intends to establish between SEN (special educational needs) teachers and others. Methods In addition to impacting the long-term health of teachers, the collaborative framework is also suggestive of having similar effects on students studying special education (SEN students). A study was conducted to examine the stress levels associated with the collaborative framework. An expression in terms of two (group affiliation) × 2 (measurement time) between subjects design was implemented to examine the effects of an Acceptance and Commitment Training on the subjective tension of a sample (N = 68) of SEN students. The sample was split into an intervention and a control group (IG and CG). The effects of the training on collaborative competence were examined using the Chi-square test. Questionnaire and role plays were used to assess the collaborative competence and the subjective tension. Results The participants had significant stress levels and displayed an uncooperative attitude during the initial assessment. However, these results reversed after the Acceptance and Commitment Training. Significant decrease in stress levels and improved cooperation were evident among the participants in the intervention group, as opposed to the participants of the control group. Conclusions The findings of this study show that the Acceptance and Commitment Training is an appropriate medium to establish and develop collaboration skills, and an effective technique to reduce high levels of subjective stress. Furthermore, the training evaluation and feedback indicate that it is well-accepted by all participants. The training is also endorsed as a practically relevant medium to help SEN students collaborate and combat stress.
      PubDate: 2015-09-28
       
  • Insights into the origin of DNA methylation differences between
           monozygotic twins discordant for schizophrenia

    • Abstract: Background DNA methylation differences between monozygotic twins discordant for schizophrenia have been previously reported. However, the origin of methylation differences between monozygotic twins discordant for schizophrenia is not clear. The findings here argue that all DNA methylation differences may not necessarily represent the cause of the disease; rather some may result from the effect of antipsychotics. Methods Methylation differences in rat brain regions and also in two pairs of unrelated monozygotic twins discordant for schizophrenia have been studied using genome-wide DNA methylation arrays at Arraystar Inc. (Rockville, Maryland, USA). The identified gene promoters showing significant alterations to DNA methylation were then further characterized using ingenuity pathway analysis (Ingenuity System Inc, CA, USA). Results Pathway analysis of the most significant gene promoter hyper/hypomethylation revealed a significant enrichment of DNA methylation changes in biological networks and pathways directly relevant to neural development and psychiatric disorders. These included HIPPO signaling (p = 3.93E-03) and MAPK signaling (p = 4.27E-03) pathways involving hypermethylated genes in schizophrenia-affected patients as compared to their unaffected co-twins. Also, a number of significant pathways and networks involving genes with hypomethylated gene promoters have been identified. These included CREB signaling in neurons (p = 1.53E-02), Dopamine-DARPP32 feedback in cAMP signaling (p = 7.43E-03) and Ephrin receptors (p = 1.13E-02). Further, there was significant enrichment for pathways involved in nervous system development and function (p = 1.71E-03-4.28E-02). Conclusion The findings highlight the significance of antipsychotic drugs on DNA methylation in schizophrenia patients. The unique pathways affected by DNA methylation in the two pairs of monozygotic twins suggest that patient-specific pathways are responsible for the disease; suggesting that patient-specific treatment strategies may be necessary in treating the disorder. The study reflects the need for developing personalized medicine approaches that take into consideration epigenetic variations between patients.
      PubDate: 2015-06-26
       
  • Characterization of cognitive deficits in spontaneously hypertensive rats,
           accompanied by brain insulin receptor dysfunction

    • Abstract: Background The spontaneously hypertensive rat (SHR) has been used to model changes in the central nervous system associated with cognitive-related disorders. Recent human and animal studies indicate a possible relationship between cognitive deficits, insulin resistance and hypertension. We aimed to investigate whether cognitively impaired SHRs develop central and/or peripheral insulin resistance and how their cognitive performance is influenced by the animal’s sex and age as well as strains used for comparison (Wistar and Wistar-Kyoto/WKY). Methods Three and seven-month-old SHR, Wistar, and WKY rats were studied for their cognitive performance using Morris Water Maze (MWM) and Passive Avoidance tests (PAT). Plasma glucose and insulin were obtained after oral glucose tolerance tests. Cerebral cortex, hippocampus, and striatum status of insulin-receptor (IR) β-subunit and glycogen synthase kinase-3β (GSK3β) and their phosphorylated forms were obtained via ELISA. Results SHRs performed poorly in MWM and PAT in comparison to both control strains but more pronouncedly compared to WKY. Females performed poorer than males and 7-month-old SHRs had poorer MWM performance than 3-month-old ones. Although plasma glucose levels remained unchanged, plasma insulin levels were significantly increased in the glucose tolerance test in 7-month-old SHRs. SHRs demonstrated reduced expression and increased activity of IRβ-subunit in cerebral cortex, hippocampus, and striatum with different regional changes in phospho/total GSK3β ratio, as compared to WKYs. Conclusion Results indicate that cognitive deficits in SHRs are accompanied by both central and peripheral insulin dysfunction, thus allowing for the speculation that SHRs might additionally be considered as a model of insulin resistance-induced type of dementia.
      PubDate: 2015-06-04
       
  • Behavioral disorders and cognitive impairment associated with cerebellar
           lesions

    • Abstract: Abstract In the last decade evidence has accumulated that suggests that the cerebellum is involved not only in motor but also in behavioral and cognitive functions. A myriad of anatomical, clinical and imaging studies support that assumption. The lengthened survival of patients with cerebellar tumors has also brought an increased awareness of neurocognitive deficits to the neurooncological community. Although evidence from neurosurgical case series exists that clearly demonstrates that patients afflicted from posterior fossa tumors are at high risk for long-term cognitive or adaptive deficits, there is still a lack of systematic translational review on this issue. Accordingly a systematic review was conducted to summarize the impact of cerebellar lesions on behavior and cognition. The findings and clinical implications are discussed in the light of the recent advances in neuroimaging techniques.
      PubDate: 2015-05-15
       
  • A systematic review of agomelatine-induced liver injury

    • Abstract: Abstract Agomelatine is an antidepressant with a unique mechanism of action. Since its marketing in 2009, concerns have been raised regarding its potential to induce liver injury. The authors therefore address the need to comprehensively evaluate the potential risk posed by agomelatine of inducing liver injury by reviewing data from published and unpublished clinical trials in both the pre- and postmarketing settings, as well as data from non-interventional studies, pharmacovigilance database reviews and one case report. Recommendations for clinicians are also provided. In this review, agomelatine was found to be associated with higher rates of liver injury than both placebo and the four active comparator antidepressants used in the clinical trials for agomelatine, with rates as high as 4.6% for agomelatine compared to 2.1% for placebo, 1.4% for escitalopram, 0.6% for paroxetine, 0.4% for fluoxetine, and 0% for sertraline. The review also provides evidence for the existence of a positive relationship between agomelatine dose and liver injury. Furthermore, rates of liver injury were found to be lower in non-interventional studies. Findings from pharmacovigilance database reviews and one case report also highlight the risk of agomelatine-induced liver injury. As agomelatine does pose a risk of liver injury, clinicians must carefully monitor liver function throughout treatment. However, agomelatine’s unique mechanism of action and favourable safety profile render it a valuable treatment option. A quantitative analysis of agomelatine-induced liver injury is lacking in the literature and would be welcomed.
      PubDate: 2015-04-21
       
  • Effects of physical exercise on central nervous system functions: a review
           of brain region specific adaptations

    • Abstract: Abstract Pathologies of central nervous system (CNS) functions are involved in prevalent conditions such as Alzheimer’s disease, depression, and Parkinson’s disease. Notable pathologies include dysfunctions of circadian rhythm, central metabolism, cardiovascular function, central stress responses, and movement mediated by the basal ganglia. Although evidence suggests exercise may benefit these conditions, the neurobiological mechanisms of exercise in specific brain regions involved in these important CNS functions have yet to be clarified. Here we review murine evidence about the effects of exercise on discrete brain regions involved in important CNS functions. Exercise effects on circadian rhythm, central metabolism, cardiovascular function, stress responses in the brain stem and hypothalamic pituitary axis, and movement are examined. The databases Pubmed, Web of Science, and Embase were searched for articles investigating regional brain adaptations to exercise. Brain regions examined included the brain stem, hypothalamus, and basal ganglia. We found evidence of multiple regional adaptations to both forced and voluntary exercise. Exercise can induce molecular adaptations in neuronal function in many instances. Taken together, these findings suggest that the regional physiological adaptations that occur with exercise could constitute a promising field for elucidating molecular and cellular mechanisms of recovery in psychiatric and neurological health conditions.
      PubDate: 2015-04-18
       
  • Metabolite profiling in posttraumatic stress disorder

    • Abstract: Background Traumatic stress does not only increase the risk for posttraumatic stress disorder (PTSD), but is also associated with adverse secondary physical health outcomes. Despite increasing efforts, we only begin to understand the underlying biomolecular processes. The hypothesis-free assessment of a wide range of metabolites (termed metabolite profiling) might contribute to the discovery of biological pathways underlying PTSD. Methods Here, we present the results of the first metabolite profiling study in PTSD, which investigated peripheral blood serum samples of 20 PTSD patients and 18 controls. We performed liquid chromatography (LC) coupled to Quadrupole/Time-Of-Flight (QTOF) mass spectrometry. Two complementary statistical approaches were used to identify metabolites associated with PTSD status including univariate analyses and Partial Least Squares Discriminant Analysis (PLS-DA). Results Thirteen metabolites displayed significant changes in PTSD, including four glycerophospholipids, and one metabolite involved in endocannabinoid signaling. A biomarker panel of 19 metabolites classifies PTSD with 85% accuracy, while classification accuracy from the glycerophospholipid with the highest differentiating ability already reached 82%. Conclusions This study illustrates the feasibility and utility of metabolite profiling for PTSD and suggests lipid-derived and endocannabinoid signaling as potential biological pathways involved in trauma-associated pathophysiology.
      PubDate: 2015-02-08
       
  • Sleep hygiene awareness: its relation to sleep quality and diurnal
           preference

    • Abstract: Background Sleep hygiene is a core component for psychological treatments of insomnia and essential for maintaining a satisfactory sleep. Our study aimed to measure the sleep hygiene awareness and the self-reported quality of sleep among three age groups (young adults, adults and middle-aged adults) and to determine their relation. We also measured their relation with diurnal preference. Methods Using an online questionnaire, we surveyed six hundred fifty two participants, recruited nationwide from the community and from the students in three main cities in Romania. Results Sleep hygiene awareness was moderate on the whole and significantly worse in young adults (compared to the other age groups) and in those complaining of poor sleep (compared to those with good sleep). Sleep quality was average and linked positively with diurnal preference (the more evening oriented, the poorer the sleep). Diurnal preference was not found to play a role regarding sleep hygiene awareness. Conclusions Our results suggest that better sleep hygiene awareness does not necessarily guarantee better sleep quality and that it may actually be an indicator of dissatisfaction with the obtained sleep.
      PubDate: 2015-01-31
       
  • Mitochondrial complex I and III gene mRNA levels in schizophrenia, and
           their relationship with clinical features

    • Abstract: Background The etiology of schizophrenia is not precisely known; however, mitochondrial function and cerebral energy metabolism abnormalities were determined to be possible factors associated with the etiology of schizophrenia. Impaired mitochondrial function negatively affects neuronal plasticity, and can cause cognitive deficits and behavioral abnormalities observed during the clinical course of schizophrenia. The present study aimed to investigate the relationship between the clinical features of schizophrenia, and mitochondrial complex activation, based on measurement of mRNA levels in the NDUFV1, NDUFV2, NDUFS1, and UQCR10 genes involved in the peripheral mitochondrial complex. Methods The study included 138 schizophrenia patients and 42 healthy controls. The schizophrenia group was divided into a chronic schizophrenia subgroup (n = 84) and a first-episode schizophrenia subgroup (n = 54). The symptoms profile and severity of disorder were evaluated using the Scale for the Assessment of Negative Symptoms (SANS), Scale for the Assessment of Positive Symptoms (SAPS), and Brief Psychiatric Rating Scale (BPRS). Results The level of mRNA expression of NDUFV1, NDUFV2, and NDUFS1 was significantly higher in the schizophrenia group than in the control group. The mRNA level of NDUFV2 was positively correlated with BPRS and SAPS scores in the first-episode schizophrenia subgroup. Conclusion The findings showed that there was a positive correlation between gene mRNA levels and psychotic symptomatology, especially positive symptoms. Our results suggest that mRNA levels of the NDUFV1, NUDFV2, and NDUFS1 genes of complex I of the mitochondrial electron transport chain might become a possible peripheral marker for the diagnosis of schizophrenia.
      PubDate: 2014-12-10
       
  • Sluggish cognitive tempo and its neurocognitive, social and emotive
           correlates: a systematic review of the current literature

    • Abstract: Objectives Since the elimination of items associated with Sluggish Cognitive Tempo (SCT) during the transition from DSM-III to DSM-IV from the diagnostic criteria of Attention-deficit Hyperactivity Disorder (ADHD), interest in SCT and its associated cognitive as well as emotional and social consequences is on the increase. The current review discusses recent findings on SCT in clinical as well as community based ADHD populations. The focus is further on clinical correlates of SCT in populations different from ADHD, SCT’s genetic background, SCT’s association with internalizing and other behavioral comorbidities, as well as SCT’s association with social functioning and its treatment efficacy. Method A systematic review of empirical studies on SCT in ADHD and other pathologies in PsycInfo, SocIndex, Web of Science and PubMed using the key terms “Sluggish Cognitive Tempo”, “Cognitive Tempo”, “Sluggish Tempo” was performed. Thirty-two out of 63 studies met inclusion criteria and are discussed in the current review. Results/Conclusion From the current literature, it can be concluded that SCT is a psychometrically valid construct with additive value in the clinical field of ADHD, oppositional defiant disorder (ODD), internalizing disorders and neuro-rehabilitation. The taxonomy of SCT has been shown to be far from consistent across studies; however, the impact of SCT on individuals’ functioning (e.g., academic achievement, social interactions) seems remarkable. SCT has been shown to share some of the genes with ADHD, however, related most strongly to non-shared environmental factors. Future research should focus on the identification of adequate SCT measurement to promote symptom tailored treatment and increase studies on SCT in populations different from ADHD.
      PubDate: 2014-08-05
       
  • The relationship between irritable bowel syndrome and psychiatric
           disorders: from molecular changes to clinical manifestations

    • Abstract: Abstract Irritable bowel syndrome (IBS) is a functional syndrome characterized by chronic abdominal pain accompanied by altered bowel habits. Although generally considered a functional disorder, there is now substantial evidence that IBS is associated with a poor quality of life and significant negative impact on work and social domains. Neuroimaging studies documented changes in the prefrontal cortex, ventro-lateral and posterior parietal cortex and thalami, and implicate alteration of brain circuits involved in attention, emotion and pain modulation. Emerging data reveals the interaction between psychiatric disorders including generalized anxiety disorder, panic disorder, major depressive disorder, bipolar disorder, and schizophrenia and IBS, which suggests that this association should not be ignored when developing strategies for screening and treatment. Psychological, social and genetic factors appear to be important in the development of IBS symptomatology through several mechanisms: alteration of HPA axis modulation, enhanced perception of visceral stimuli or psychological vulnerability. Elucidating the molecular mechanisms of IBS with or without psychiatric comorbidities is crucial for elucidating the pathophysiology and for the identification of new therapeutical targets in IBS.
      PubDate: 2014-06-27
       
  • Centenary of Karl Jaspers’s general psychopathology: implications
           for molecular psychiatry

    • Abstract: Abstract Modern molecular psychiatry benefits immensely from the scientific and technological advances of general neuroscience (including genetics, epigenetics, and proteomics). This “progress” of molecular psychiatry, however, will be to a degree “unbalanced” and “epiphytic” should the development of the corresponding theoretical frameworks and conceptualization tools that allow contextualization of the individual neuroscientific findings within the specific perspective of mental health care issues be neglected. The General Psychopathology, published by Karl Jaspers in 1913, is considered a groundbreaking work in psychiatric literature, having established psychopathology as a space of critical methodological self-reflection, and delineating a scientific methodology specific to psychiatry. With the advance of neurobiology and molecular neuroscience and its adoption in psychiatric research, however, a growing alienation between current research-oriented neuropsychiatry and the classical psychopathological literature is evident. Further, consensus-based international classification criteria, although useful for providing an internationally accepted system of reliable psychiatric diagnostic categories, further contribute to a neglect of genuinely autonomous thought on psychopathology. Nevertheless, many of the unsolved theoretical problems of psychiatry, including those in the areas of nosology, anthropology, ethics, epistemology and methodology, might be fruitfully addressed by a re-examination of classic texts, such as Jaspers’s General Psychopathology, and their further development and adaptation for 21st century psychiatry.
      PubDate: 2014-05-16
       
  • HIV-associated neurocognitive disorders

    • Abstract: Abstract Currently, neuropsychological impairment among HIV+ patients on antiretroviral therapy leads to a reduction in the quality of life and it is an important challenge due to the high prevalence of HIV-associated neurocognitive disorders and its concomitant consequences in relation to morbidity and mortality- including those HIV+ patients with adequate immunological and virological status. The fact that the virus is established in CNS in the early stages and its persistence within the CNS can help us to understand HIV-related brain injury even when highly active antiretroviral therapy is effective. The rising interest in HIV associated neurocognitive disorders has let to development new diagnostic tools, improvement of the neuropsychological tests, and the use of new biomarkers and new neuroimaging techniques that can help the diagnosis. Standardization and homogenization of neurocognitive tests as well as normalizing and simplification of easily accessible tools that can identify patients with increased risk of cognitive impairment represent an urgent requirement. Future efforts should also focus on diagnostic keys and searching for useful strategies in order to decrease HIV neurotoxicity within the CNS.
      PubDate: 2014-03-04
       
  • Association study in siblings and case-controls of serotonin- and
           oxytocin-related genes with high functioning autism

    • Abstract: Background Autism spectrum disorder (ASD) is heritable and neurodevelopmental with unknown causes. The serotonergic and oxytocinergic systems are of interest in autism for several reasons: (i) Both systems are implicated in social behavior, and abnormal levels of serotonin and oxytocin have been found in people with ASD; (ii) treatment with selective serotonin reuptake inhibitors and oxytocin can yield improvements; and (iii) previous association studies have linked the serotonin transporter (SERT; SLC6A4), serotonin receptor 2A (HTR2A), and oxytocin receptor (OXTR) genes with ASD. We examined their association with high functioning autism (HFA) including siblings and their interaction. Methods In this association study with HFA children (IQ > 80), siblings, and controls, participants were genotyped for four single nucleotide polymorphisms (SNPs) in OXTR (rs2301261, rs53576, rs2254298, rs2268494) and one in HTR2A (rs6311) as well as the triallelic HTTLPR (SERT polymorphism). Results We identified a nominal significant association with HFA for the HTTLPR s allele (consisting of S and LG alleles) (p = .040; odds ratio (OR) = 1.697, 95% CI 1.191–2.204)). Four polymorphisms (HTTLPR, HTR2A rs6311, OXTR rs2254298 and rs53576) in combination conferred nominal significant risk for HFA with a genetic score of ≥4 (OR = 2.09, 95% CI 1.05–4.18, p = .037). The resulting area under the receiver operating characteristic curve was 0.595 (p = .033). Conclusions Our findings, combined with those of previous reports, indicate that ASD, in particular HFA, is polygenetic rather than monogenetic and involves the serotonergic and oxytocin pathways, probably in combination with other factors.
      PubDate: 2014-01-24
       
  • Neurotrophin levels at admission did not change significantly upon alcohol
           deprivation and were positively correlated with the BMI and LDL levels

    • Abstract: Background The neurotrophins brain-derived neurotrophic factor (BDNF) and neurotrophic factor 3 (NT3) could play a role in addictive behavior. Interactions between BDNF and dopamine transmission influence the alcohol intake. It has been hypothesized that extensive alcohol consumption leads to diminished circulating BDNF levels and impaired BDNF-mediated protective mechanisms. What is more, alcohol dependency causes changes in lipid metabolism which in turn may influence the neurotrophin system. Methods In this study, we tested the hypothesis that alcohol withdrawal increases the serum levels of BDNF in alcoholic patients and investigated correlations between serum BDNF and NT3 and alcohol in breath as well as with the body-mass-index (BMI), lipoprotein profiles and lifestyle factors in 110 male in-patients diagnosed with alcohol addiction on the first day after admission and at discharge. Results The intoxication level (alcohol in breath at admission) was significantly correlated with liver enzymes and BDNF concentrations (R = .28; p = .004). Patients with positive breath-alcohol test at admission had about 9 times higher NT3 levels and higher liver enzyme concentration levels than nonintoxicated subjects. Alcohol intoxicated patients with pathological aspartate aminase (ASAT) levels had even higher NT3 level (F = 5.41; p = .022). The concentration of NT3 was positively associated with the (BMI) (admission R = .36; p = .004; discharge R = .33; p = .001), and the obese patients had 3 to 5 times higher NT3 concentration than the others. Low-density lipoprotein (LDL) concentration levels were found to positively correlate with NT3 concentration levels (admission R = .025; p = .015 discharge R = .24; p = .23). Conclusion Other than expected, the levels of NT3 and to a lesser extent BDNF levels, were found to be significantly increased in acute alcohol abuse. Alcohol deprivation did not significantly change the serum neurotrophin levels at admission. NT3 levels were positively correlated with the BMI and LDL levels. Because of expected difference between genders, we recommend investigating these correlations further in patients of both genders.
      PubDate: 2013-12-02
       
  • Olanzapine induced DNA methylation changes support the dopamine hypothesis
           of psychosis

    • Abstract: Background The dopamine (DA) hypothesis of schizophrenia proposes the mental illness is caused by excessive transmission of dopamine in selected brain regions. Multiple lines of evidence, including blockage of dopamine receptors by antipsychotic drugs that are used to treat schizophrenia, support the hypothesis. However, the dopamine D2 receptor (DRD2) blockade cannot explain some important aspects of the therapeutic effect of antipsychotic drugs. In this study, we hypothesized that antipsychotic drugs could affect the transcription of genes in the DA pathway by altering their epigenetic profile. Methods To test this hypothesis, we examined the effect of olanzapine, a commonly used atypical antipsychotic drug, on the DNA methylation status of genes from DA neurotransmission in the brain and liver of rats. Genomic DNA isolated from hippocampus, cerebellum, and liver of olanzapine treated (n = 2) and control (n = 2) rats were analyzed using rat specific methylation arrays. Results Our results show that olanzapine causes methylation changes in genes encoding for DA receptors (dopamine D1 receptor, dopamine D2 receptor and dopamine D5 receptor), a DA transporter (solute carrier family 18 member 2), a DA synthesis (differential display clone 8), and a DA metabolism (catechol-O-methyltransferase). We assessed a total of 40 genes in the DA pathway and found 19 to be differentially methylated between olanzapine treated and control rats. Most (17/19) genes showed an increase in methylation, in their promoter regions with in silico analysis strongly indicating a functional potential to suppress transcription in the brain. Conclusion Our results suggest that chronic olanzapine may reduce DA activity by altering gene methylation. It may also explain the delayed therapeutic effect of antipsychotics, which occurs despite rapid dopamine blockade. Furthermore, given the common nature of epigenetic variation, this lends insight into the differential therapeutic response of psychotic patients who display adequate blockage of dopamine receptors.
      PubDate: 2013-11-04
       
 
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