Pub Date : 2019-08-01DOI: 10.9758/cpn.2019.17.3.343
Ather Muneer, F. Minhas
Major psychiatric disorders are linked to early mortality and patients afflicted with these ailments demonstrate an increased risk of developing physical diseases that are characteristically seen in the elderly. Psychiatric conditions like major depressive disorder, bipolar disorder and schizophrenia may be associated with accelerated cellular aging, indicated by shortened leukocyte telomere length (LTL), which could underlie this connection. Telomere shortening occurs with repeated cell division and is reflective of a cell’s mitotic history. It is also influenced by cumulative exposure to inflammation and oxidative stress as well as the availability of telomerase, the telomere-lengthening enzyme. Precariously short telomeres can cause cells to undergo senescence, apoptosis or genomic instability; shorter LTL correlates with compromised general health and foretells mortality. Important data specify that LTL may be reduced in principal psychiatric illnesses, possibly in proportion to exposure to the ailment. Telomerase, as measured in peripheral blood monocytes, has been less well characterized in psychiatric illnesses, but a role in mood disorder has been suggested by preclinical and clinical studies. In this manuscript, the most recent studies on LTL and telomerase activity in mood disorders are comprehensively reviewed, potential mediators are discussed, and future directions are suggested. An enhanced comprehension of cellular aging in psychiatric illnesses could lead to their re-conceptualizing as systemic ailments with manifestations both inside and outside the brain. At the same time this paradigm shift could identify new treatment targets, helpful in bringing about lasting cures to innumerable sufferers across the globe.
{"title":"Telomere Biology in Mood Disorders: An Updated, Comprehensive Review of the Literature","authors":"Ather Muneer, F. Minhas","doi":"10.9758/cpn.2019.17.3.343","DOIUrl":"https://doi.org/10.9758/cpn.2019.17.3.343","url":null,"abstract":"Major psychiatric disorders are linked to early mortality and patients afflicted with these ailments demonstrate an increased risk of developing physical diseases that are characteristically seen in the elderly. Psychiatric conditions like major depressive disorder, bipolar disorder and schizophrenia may be associated with accelerated cellular aging, indicated by shortened leukocyte telomere length (LTL), which could underlie this connection. Telomere shortening occurs with repeated cell division and is reflective of a cell’s mitotic history. It is also influenced by cumulative exposure to inflammation and oxidative stress as well as the availability of telomerase, the telomere-lengthening enzyme. Precariously short telomeres can cause cells to undergo senescence, apoptosis or genomic instability; shorter LTL correlates with compromised general health and foretells mortality. Important data specify that LTL may be reduced in principal psychiatric illnesses, possibly in proportion to exposure to the ailment. Telomerase, as measured in peripheral blood monocytes, has been less well characterized in psychiatric illnesses, but a role in mood disorder has been suggested by preclinical and clinical studies. In this manuscript, the most recent studies on LTL and telomerase activity in mood disorders are comprehensively reviewed, potential mediators are discussed, and future directions are suggested. An enhanced comprehension of cellular aging in psychiatric illnesses could lead to their re-conceptualizing as systemic ailments with manifestations both inside and outside the brain. At the same time this paradigm shift could identify new treatment targets, helpful in bringing about lasting cures to innumerable sufferers across the globe.","PeriodicalId":10420,"journal":{"name":"Clinical Psychopharmacology and Neuroscience","volume":"17 1","pages":"343 - 363"},"PeriodicalIF":3.2,"publicationDate":"2019-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47775914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-08-01DOI: 10.9758/cpn.2019.17.3.453
M. Hahm, J. Woo
We report an extremely rare case of a patient with hypoxic-ischemic brain injury who recovered consciousness and motor and cognitive functions due to paradoxical response after zolpidem administration. A 32-year-old woman who had attempted suicide by hanging was admitted. The patient had stabilized in a state of drowsy mentality, quadriparesis, dysphagia, and impaired cognition. Brain magnetic resonance imaging was suggestive of hypoxic ischemic brain injury and unilateral infarction in the right posterior cerebral artery territory. Due to sleep disturbance, zolpidem was administered, and paradoxically consciousness level and function returned to near-normal during the duration of the drug-effect. In addition to previous reports, our case characteristically showed remarkable motor and cognitive function recovery, not only consciousness level. The drug-effect time was gradually decreased after 18 months and absent after 3 years. We have reviewed related literature and discussed possible neuropharmacological and neurobiological mechanism.
{"title":"Paradoxical Motor and Cognitive Function Recovery in Response to Zolpidem in a Patient with Hypoxic-ischemic Brain Injury: A Case Report","authors":"M. Hahm, J. Woo","doi":"10.9758/cpn.2019.17.3.453","DOIUrl":"https://doi.org/10.9758/cpn.2019.17.3.453","url":null,"abstract":"We report an extremely rare case of a patient with hypoxic-ischemic brain injury who recovered consciousness and motor and cognitive functions due to paradoxical response after zolpidem administration. A 32-year-old woman who had attempted suicide by hanging was admitted. The patient had stabilized in a state of drowsy mentality, quadriparesis, dysphagia, and impaired cognition. Brain magnetic resonance imaging was suggestive of hypoxic ischemic brain injury and unilateral infarction in the right posterior cerebral artery territory. Due to sleep disturbance, zolpidem was administered, and paradoxically consciousness level and function returned to near-normal during the duration of the drug-effect. In addition to previous reports, our case characteristically showed remarkable motor and cognitive function recovery, not only consciousness level. The drug-effect time was gradually decreased after 18 months and absent after 3 years. We have reviewed related literature and discussed possible neuropharmacological and neurobiological mechanism.","PeriodicalId":10420,"journal":{"name":"Clinical Psychopharmacology and Neuroscience","volume":"17 1","pages":"453 - 457"},"PeriodicalIF":3.2,"publicationDate":"2019-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46481166","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-08-01DOI: 10.9758/cpn.2019.17.3.388
H. Halis, S. Bitiktaş, O. Baştuğ, B. Tan, Ş. Kavraal, T. Güneş, C. Süer
Objective Hypoxic-ischemic (HI) brain injury in the human perinatal period often leads to significant long-term neurobehavioral dysfunction in the cognitive and sensory-motor domains. Using a neonatal HI injury model (unilateral carotid ligation followed by hypoxia) in postnatal day seven rats, the present study investigated the long-term effects of HI and potential behavioral protective effect of pentoxifylline. Methods Seven-day-old rats underwent right carotid ligation, followed by hypoxia (FiO2 = 0.08). Rats received pentoxifylline immediately after and again 2 hours after hypoxia (two doses, 60–100 mg/kg/dose), or serum physiologic. Another set of seven-day-old rats was included to sham group exposed to surgical stress but not ligated. These rats were tested for spatial learning and memory on the simple place task in the Morris water maze from postnatal days 77 to 85. Results HI rats displayed significant tissue loss in the right hippocampus, as well as severe spatial memory deficits. Low-dose treatment with pentoxifylline resulted in significant protection against both HI-induced hippocampus tissue losses and spatial memory impairments. Beneficial effects are, however, negated if pentoxifylline is administered at high dose. Conclusion These findings indicate that unilateral HI brain injury in a neonatal rodent model is associated with cognitive deficits, and that low dose pentoxifylline treatment is protective against spatial memory impairment.
{"title":"Differential Effects of Pentoxifylline on Learning and Memory Impairment Induced by Hypoxic-ischemic Brain Injury in Rats","authors":"H. Halis, S. Bitiktaş, O. Baştuğ, B. Tan, Ş. Kavraal, T. Güneş, C. Süer","doi":"10.9758/cpn.2019.17.3.388","DOIUrl":"https://doi.org/10.9758/cpn.2019.17.3.388","url":null,"abstract":"Objective Hypoxic-ischemic (HI) brain injury in the human perinatal period often leads to significant long-term neurobehavioral dysfunction in the cognitive and sensory-motor domains. Using a neonatal HI injury model (unilateral carotid ligation followed by hypoxia) in postnatal day seven rats, the present study investigated the long-term effects of HI and potential behavioral protective effect of pentoxifylline. Methods Seven-day-old rats underwent right carotid ligation, followed by hypoxia (FiO2 = 0.08). Rats received pentoxifylline immediately after and again 2 hours after hypoxia (two doses, 60–100 mg/kg/dose), or serum physiologic. Another set of seven-day-old rats was included to sham group exposed to surgical stress but not ligated. These rats were tested for spatial learning and memory on the simple place task in the Morris water maze from postnatal days 77 to 85. Results HI rats displayed significant tissue loss in the right hippocampus, as well as severe spatial memory deficits. Low-dose treatment with pentoxifylline resulted in significant protection against both HI-induced hippocampus tissue losses and spatial memory impairments. Beneficial effects are, however, negated if pentoxifylline is administered at high dose. Conclusion These findings indicate that unilateral HI brain injury in a neonatal rodent model is associated with cognitive deficits, and that low dose pentoxifylline treatment is protective against spatial memory impairment.","PeriodicalId":10420,"journal":{"name":"Clinical Psychopharmacology and Neuroscience","volume":"17 1","pages":"388 - 399"},"PeriodicalIF":3.2,"publicationDate":"2019-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44631925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-08-01DOI: 10.9758/cpn.2019.17.3.364
M. Calabrò, L. Mandelli, C. Crisafulli, Soo-Jung Lee, T. Jun, Sheng-Min Wang, A. Patkar, P. Masand, Changsu Han, C. Pae, A. Serretti
Objective Genetics factors are likely to play a role in the risk, clinical presentation and treatment outcome in major depressive disorder (MDD). In this study, we investigated the role of three candidate genes for MDD; calcium voltage-gated channel subunit alpha1 C (CACNA1C ), cholinergic receptor nicotinic alpha 7 subunit (CHRNA7 ), and mitogen-activated protein kinase 1 (MAPK1). Methods Two-hundred forty-two MDD patients and 326 healthy controls of Korean ancestry served as samples for the analyses. Thirty-nine single nucleotide polymorphisms (SNPs) within CACNA1C, CHRNA7, and MAPK1 genes were genotyped and subsequently tested for association with MDD (primary analysis) and other clinical features (symptoms’ severity, age of onset, history of suicide attempt, treatment outcome) (secondary analyses). Single SNPs, haplotypes and epistatic analyses were performed. Results Single SNPs were not associated with disease risk and clinical features. However, a combination of alleles (haplotype) within MAPK1 was found associated with MDD-status. Secondary analyses detected a possible involvement of CACNA1C haplotype in resistance to antidepressant treatment. Conclusion These data suggest a role for MAPK1 and CACNA1C in MDD risk and treatment resistance, respectively. However, since many limitations characterize the analysis, the results must be considered with great caution and verified.
{"title":"Genes Involved in Neurodevelopment, Neuroplasticity and Major Depression: No Association for CACNA1C, CHRNA7 and MAPK1","authors":"M. Calabrò, L. Mandelli, C. Crisafulli, Soo-Jung Lee, T. Jun, Sheng-Min Wang, A. Patkar, P. Masand, Changsu Han, C. Pae, A. Serretti","doi":"10.9758/cpn.2019.17.3.364","DOIUrl":"https://doi.org/10.9758/cpn.2019.17.3.364","url":null,"abstract":"Objective Genetics factors are likely to play a role in the risk, clinical presentation and treatment outcome in major depressive disorder (MDD). In this study, we investigated the role of three candidate genes for MDD; calcium voltage-gated channel subunit alpha1 C (CACNA1C ), cholinergic receptor nicotinic alpha 7 subunit (CHRNA7 ), and mitogen-activated protein kinase 1 (MAPK1). Methods Two-hundred forty-two MDD patients and 326 healthy controls of Korean ancestry served as samples for the analyses. Thirty-nine single nucleotide polymorphisms (SNPs) within CACNA1C, CHRNA7, and MAPK1 genes were genotyped and subsequently tested for association with MDD (primary analysis) and other clinical features (symptoms’ severity, age of onset, history of suicide attempt, treatment outcome) (secondary analyses). Single SNPs, haplotypes and epistatic analyses were performed. Results Single SNPs were not associated with disease risk and clinical features. However, a combination of alleles (haplotype) within MAPK1 was found associated with MDD-status. Secondary analyses detected a possible involvement of CACNA1C haplotype in resistance to antidepressant treatment. Conclusion These data suggest a role for MAPK1 and CACNA1C in MDD risk and treatment resistance, respectively. However, since many limitations characterize the analysis, the results must be considered with great caution and verified.","PeriodicalId":10420,"journal":{"name":"Clinical Psychopharmacology and Neuroscience","volume":"17 1","pages":"364 - 368"},"PeriodicalIF":3.2,"publicationDate":"2019-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49575566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Attention-deficit hyperactivity disorder (ADHD) is notorious for its debilitating consequences and early age of onset. The need for early diagnosis and intervention has frequently been underscored. Previous studies have attempted to clarify the bidirectional relationship between ADHD and sleep problems, proposing a potential role for sleep problems as early predictors of ADHD. Sleep deprivation, sleep-disordered breathing, and circadian rhythm disturbances have been extensively studied, yielding evidence with regard to their induction of ADHD-like symptoms. Genetic-phenotypic differences across individuals regarding the aforementioned sleep problems have been elucidated along with the possible use of these characteristics for early prediction of ADHD. The long-term consequences of sleep problems in individuals with ADHD include obesity, poor academic performance, and disrupted parent-child interactions. Early intervention has been proposed as an approach to preventing these debilitating outcomes of ADHD, with novel treatment approaches ranging from melatonin and light therapy to myofunctional therapy and adjustments of the time point at which school starts.
{"title":"Sleep Problems as Predictors in Attention-Deficit Hyperactivity Disorder: Causal Mechanisms, Consequences and Treatment","authors":"Y. Um, Seung-Chul Hong, Jong-Hyun Jeong","doi":"10.9758/cpn.2017.15.1.9","DOIUrl":"https://doi.org/10.9758/cpn.2017.15.1.9","url":null,"abstract":"Attention-deficit hyperactivity disorder (ADHD) is notorious for its debilitating consequences and early age of onset. The need for early diagnosis and intervention has frequently been underscored. Previous studies have attempted to clarify the bidirectional relationship between ADHD and sleep problems, proposing a potential role for sleep problems as early predictors of ADHD. Sleep deprivation, sleep-disordered breathing, and circadian rhythm disturbances have been extensively studied, yielding evidence with regard to their induction of ADHD-like symptoms. Genetic-phenotypic differences across individuals regarding the aforementioned sleep problems have been elucidated along with the possible use of these characteristics for early prediction of ADHD. The long-term consequences of sleep problems in individuals with ADHD include obesity, poor academic performance, and disrupted parent-child interactions. Early intervention has been proposed as an approach to preventing these debilitating outcomes of ADHD, with novel treatment approaches ranging from melatonin and light therapy to myofunctional therapy and adjustments of the time point at which school starts.","PeriodicalId":10420,"journal":{"name":"Clinical Psychopharmacology and Neuroscience","volume":"15 1","pages":"9 - 18"},"PeriodicalIF":3.2,"publicationDate":"2017-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45354227","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The characteristic features of Alzheimer’s disease (AD) are the appearance of extracellular amyloid-beta (Aβ) plaques and neurofibrillary tangles in the intracellular environment, neuronal death and the loss of synapses, all of which contribute to cognitive decline in a progressive manner. A number of hypotheses have been advanced to explain AD. Abnormal tau phosphorylation may contribute to the formation of abnormal neurofibrillary structures. Many different structures are susceptible to AD, including the reticular formation, the nuclei in the brain stem (e.g., raphe nucleus), thalamus, hypothalamus, locus ceruleus, amygdala, substantia nigra, striatum, and claustrum. Excitotoxicity results from continuous, low-level activation of N-methyl-D-aspartate (NMDA) receptors. Premature synaptotoxicity, changes in neurotransmitter expression, neurophils loss, accumulation of amyloid β-protein deposits (amyloid/senile plaques), and neuronal loss and brain atrophy are all associated with stages of AD progression. Several recent studies have examined the relationship between Aβ and NMDA receptors. Aβ-induced spine loss is associated with a decrease in glutamate receptors and is dependent upon the calcium-dependent phosphatase calcineurin, which has also been linked to long-term depression.
{"title":"Mechanisms of Alzheimer’s Disease Pathogenesis and Prevention: The Brain, Neural Pathology, N-methyl-D-aspartate Receptors, Tau Protein and Other Risk Factors","authors":"S. Kocahan, Z. Doğan","doi":"10.9758/cpn.2017.15.1.1","DOIUrl":"https://doi.org/10.9758/cpn.2017.15.1.1","url":null,"abstract":"The characteristic features of Alzheimer’s disease (AD) are the appearance of extracellular amyloid-beta (Aβ) plaques and neurofibrillary tangles in the intracellular environment, neuronal death and the loss of synapses, all of which contribute to cognitive decline in a progressive manner. A number of hypotheses have been advanced to explain AD. Abnormal tau phosphorylation may contribute to the formation of abnormal neurofibrillary structures. Many different structures are susceptible to AD, including the reticular formation, the nuclei in the brain stem (e.g., raphe nucleus), thalamus, hypothalamus, locus ceruleus, amygdala, substantia nigra, striatum, and claustrum. Excitotoxicity results from continuous, low-level activation of N-methyl-D-aspartate (NMDA) receptors. Premature synaptotoxicity, changes in neurotransmitter expression, neurophils loss, accumulation of amyloid β-protein deposits (amyloid/senile plaques), and neuronal loss and brain atrophy are all associated with stages of AD progression. Several recent studies have examined the relationship between Aβ and NMDA receptors. Aβ-induced spine loss is associated with a decrease in glutamate receptors and is dependent upon the calcium-dependent phosphatase calcineurin, which has also been linked to long-term depression.","PeriodicalId":10420,"journal":{"name":"Clinical Psychopharmacology and Neuroscience","volume":"15 1","pages":"1 - 8"},"PeriodicalIF":3.2,"publicationDate":"2017-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.9758/cpn.2017.15.1.1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45485969","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-02-01DOI: 10.9758/cpn.2017.15.1.70
Seshadri Sekhar Chatterjee, S. Mitra, S. K. Pal
Wolfram syndrome is a relatively unexplored entity in clinical psychiatry. Historically, the discovery of a specific WFS1 gene had generated huge fanfare regarding specific genetic causations of psychiatric disorders. While the initial enthusiasm has faded now, association of Wolfram syndrome with psychiatric illnesses like schizophrenia, psychosis and suicidal behavior still remain important for understanding biological underpinnings of such disorders. We report a case of Wolfram syndrome presenting with multiple manic episodes, discuss possible genetic underpinnings for the affective symptoms and then discuss certain issues regarding management.
{"title":"Mania in Wolfram’s Disease: From Bedside to Bench","authors":"Seshadri Sekhar Chatterjee, S. Mitra, S. K. Pal","doi":"10.9758/cpn.2017.15.1.70","DOIUrl":"https://doi.org/10.9758/cpn.2017.15.1.70","url":null,"abstract":"Wolfram syndrome is a relatively unexplored entity in clinical psychiatry. Historically, the discovery of a specific WFS1 gene had generated huge fanfare regarding specific genetic causations of psychiatric disorders. While the initial enthusiasm has faded now, association of Wolfram syndrome with psychiatric illnesses like schizophrenia, psychosis and suicidal behavior still remain important for understanding biological underpinnings of such disorders. We report a case of Wolfram syndrome presenting with multiple manic episodes, discuss possible genetic underpinnings for the affective symptoms and then discuss certain issues regarding management.","PeriodicalId":10420,"journal":{"name":"Clinical Psychopharmacology and Neuroscience","volume":"15 1","pages":"70 - 72"},"PeriodicalIF":3.2,"publicationDate":"2017-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42450325","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-02-01DOI: 10.9758/cpn.2017.15.1.53
Jikuang Zhao, Xizheng Wu, S. Nie, Xiang Gao, Jie Sun, Keqin Li, Tiefeng Zhang, Yi Huang
Objective CDKN2B-AS1 polymorphisms were shown to associate with the risk of stroke in European. The goal of this study was to evaluate the contribution of CDKN2B-AS1 rs1333049 to the risk of hemorrhagic stroke (HS) and brain tumor (BT) in Han Chinese. Methods A total of 142 HSs, 115 BTs, and 494 controls were included in the current association study. The genotyping test was performed using the melting temperature shift method. Results We failed to validate the association of CDKN2B-AS1 rs1333049 with the risk of brain disease. Significantly higher levels of low-density lipoprotein cholesterol (LDL-C) (p=0.027), high-density lipoprotein cholesterol (HDL-C) (p<0.001) and total cholesterol (TC) (p<0.001) were found in HSs in the genotype GG/GC carriers, but not the genotype CC carriers (p>0.05). The meta-analysis of 10 studies among 133,993 individuals concluded that rs1333049 of CDKN2B-AS1 gene was likely to increase a 16% incidence rate of cerebrovascular disease (CD) among various populations (odds ratio 1.16, 95% confidence interval 1.08–1.25; p<0.0001, random-effect method). Conclusion Our case-control study identified rs1333049 genotypes showed different association with the concentration of the LDL-C, HDL-C and TC in the HS patients. Meta-analysis supported the association between rs1333049 and CD risk in various populations, although we were unable to observe association between rs1333049 and the risk of HSs in Han Chinese.
{"title":"Association of CDKN2B-AS1 rs1333049 with Brain Diseases: A Case-control Study and a Meta-analysis","authors":"Jikuang Zhao, Xizheng Wu, S. Nie, Xiang Gao, Jie Sun, Keqin Li, Tiefeng Zhang, Yi Huang","doi":"10.9758/cpn.2017.15.1.53","DOIUrl":"https://doi.org/10.9758/cpn.2017.15.1.53","url":null,"abstract":"Objective CDKN2B-AS1 polymorphisms were shown to associate with the risk of stroke in European. The goal of this study was to evaluate the contribution of CDKN2B-AS1 rs1333049 to the risk of hemorrhagic stroke (HS) and brain tumor (BT) in Han Chinese. Methods A total of 142 HSs, 115 BTs, and 494 controls were included in the current association study. The genotyping test was performed using the melting temperature shift method. Results We failed to validate the association of CDKN2B-AS1 rs1333049 with the risk of brain disease. Significantly higher levels of low-density lipoprotein cholesterol (LDL-C) (p=0.027), high-density lipoprotein cholesterol (HDL-C) (p<0.001) and total cholesterol (TC) (p<0.001) were found in HSs in the genotype GG/GC carriers, but not the genotype CC carriers (p>0.05). The meta-analysis of 10 studies among 133,993 individuals concluded that rs1333049 of CDKN2B-AS1 gene was likely to increase a 16% incidence rate of cerebrovascular disease (CD) among various populations (odds ratio 1.16, 95% confidence interval 1.08–1.25; p<0.0001, random-effect method). Conclusion Our case-control study identified rs1333049 genotypes showed different association with the concentration of the LDL-C, HDL-C and TC in the HS patients. Meta-analysis supported the association between rs1333049 and CD risk in various populations, although we were unable to observe association between rs1333049 and the risk of HSs in Han Chinese.","PeriodicalId":10420,"journal":{"name":"Clinical Psychopharmacology and Neuroscience","volume":"15 1","pages":"53 - 58"},"PeriodicalIF":3.2,"publicationDate":"2017-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47647604","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-02-01DOI: 10.9758/cpn.2017.15.1.87
Sujita Kumar Kar, Amit Singh
which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. TO THE EDITOR Restlessness and cramps in legs is a relatively rare phenomenon with antipsychotic olanzapine. If not evaluated, it may cause misdiagnosis or poor treatment adherence. There is no standard guideline for management of olanza-pine induced restlessness and cramps in legs, though ben-zodiazepines and pro-dopaminergic agents are found to be effective. A 20 year-old male had delusions of persecution, third person auditory hallucinations, inappropriate smiling with fluctuating catatonic symptoms (mutism, negati-vism, posturing, and rigidity) for eight months. Earlier, he was diagnosed with schizophrenia and was receiving olanzapine 10 mg/day since three months. Intravenous lorazepam and electroconvulsive therapy was given to which catatonic symptoms responded. As there was persistence of delusion and hallucinations, olanzapine was increased to 15 mg/day, bedtime. Patient reported cramps in both legs resulting in restless leg movements, 2-3 hours following ingestion of olanzapine in night. To get rid of discomfort and cramps in legs, he used to move his legs and even pound it over the bed desperately. The cramps would persist for 1-2 hours, causing sleep disturbance. As delusions and hallucinations were improved after increasing olanzapine, patient was maintained on same anti-psychotic dose. Management of restlessness and cramps in legs, were attempted with analgesics (started with acet-aminophen 500 mg, when not responded tramadol 50 mg had also been tried); however, it persisted causing significant disturbance of sleep. Thus the dosing of olanza-pine was rescheduled to morning time. But the patient complained of restlessness and cramps in legs even during the daytime, 2-3 hours following intake of olanzapine. After this olanzapine was given in divided doses (7.5 mg twice a day); still the patient was complaining of rest-lessness and cramps in legs. Reduction of dose of olanza-pine reduced the severity of leg cramps, but worsening of psychotic symptoms occurred. Patient was investigated for systemic causes that might attribute to restlessness and cramps in legs. All hematological investigation parameters (complete blood count, general blood picture, liver function test, kidney function test, thyroid function test, serum electrolytes, lipid profile as well as blood sugar) and magnetic resonance imaging of brain were within normal limits. Olanzapine was stopped and the patient was shifted to risperidone (started with 2 mg/day and gradually built up to 6 mg/day over a week). The patient was evaluated on Naranjo adverse drug reaction probability scale (score …
{"title":"Management Dilemma in Olanzapine Induced Restlessness and Cramps in Legs","authors":"Sujita Kumar Kar, Amit Singh","doi":"10.9758/cpn.2017.15.1.87","DOIUrl":"https://doi.org/10.9758/cpn.2017.15.1.87","url":null,"abstract":"which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. TO THE EDITOR Restlessness and cramps in legs is a relatively rare phenomenon with antipsychotic olanzapine. If not evaluated, it may cause misdiagnosis or poor treatment adherence. There is no standard guideline for management of olanza-pine induced restlessness and cramps in legs, though ben-zodiazepines and pro-dopaminergic agents are found to be effective. A 20 year-old male had delusions of persecution, third person auditory hallucinations, inappropriate smiling with fluctuating catatonic symptoms (mutism, negati-vism, posturing, and rigidity) for eight months. Earlier, he was diagnosed with schizophrenia and was receiving olanzapine 10 mg/day since three months. Intravenous lorazepam and electroconvulsive therapy was given to which catatonic symptoms responded. As there was persistence of delusion and hallucinations, olanzapine was increased to 15 mg/day, bedtime. Patient reported cramps in both legs resulting in restless leg movements, 2-3 hours following ingestion of olanzapine in night. To get rid of discomfort and cramps in legs, he used to move his legs and even pound it over the bed desperately. The cramps would persist for 1-2 hours, causing sleep disturbance. As delusions and hallucinations were improved after increasing olanzapine, patient was maintained on same anti-psychotic dose. Management of restlessness and cramps in legs, were attempted with analgesics (started with acet-aminophen 500 mg, when not responded tramadol 50 mg had also been tried); however, it persisted causing significant disturbance of sleep. Thus the dosing of olanza-pine was rescheduled to morning time. But the patient complained of restlessness and cramps in legs even during the daytime, 2-3 hours following intake of olanzapine. After this olanzapine was given in divided doses (7.5 mg twice a day); still the patient was complaining of rest-lessness and cramps in legs. Reduction of dose of olanza-pine reduced the severity of leg cramps, but worsening of psychotic symptoms occurred. Patient was investigated for systemic causes that might attribute to restlessness and cramps in legs. All hematological investigation parameters (complete blood count, general blood picture, liver function test, kidney function test, thyroid function test, serum electrolytes, lipid profile as well as blood sugar) and magnetic resonance imaging of brain were within normal limits. Olanzapine was stopped and the patient was shifted to risperidone (started with 2 mg/day and gradually built up to 6 mg/day over a week). The patient was evaluated on Naranjo adverse drug reaction probability scale (score …","PeriodicalId":10420,"journal":{"name":"Clinical Psychopharmacology and Neuroscience","volume":"15 1","pages":"87 - 88"},"PeriodicalIF":3.2,"publicationDate":"2017-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.9758/cpn.2017.15.1.87","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46274939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-02-01DOI: 10.9758/cpn.2017.15.1.47
D. Oh, I. Kim, S. Kim, D. Ahn
Objective The aim of this study was to identify a transcriptomic signature that could be used to classify subjects with autism spectrum disorder (ASD) compared to controls on the basis of blood gene expression profiles. The gene expression profiles could ultimately be used as diagnostic biomarkers for ASD. Methods We used the published microarray data (GSE26415) from the Gene Expression Omnibus database, which included 21 young adults with ASD and 21 age- and sex-matched unaffected controls. Nineteen differentially expressed probes were identified from a training dataset (n=26, 13 ASD cases and 13 controls) using the limma package in R language (adjusted p value <0.05) and were further analyzed in a test dataset (n=16, 8 ASD cases and 8 controls) using machine learning algorithms. Results Hierarchical cluster analysis showed that subjects with ASD were relatively well-discriminated from controls. Based on the support vector machine and K-nearest neighbors analysis, validation of 19-DE probes with a test dataset resulted in an overall class prediction accuracy of 93.8% as well as a sensitivity and specificity of 100% and 87.5%, respectively. Conclusion The results of our exploratory study suggest that the gene expression profiles identified from the peripheral blood samples of young adults with ASD can be used to identify a biological signature for ASD. Further study using a larger cohort and more homogeneous datasets is required to improve the diagnostic accuracy.
{"title":"Predicting Autism Spectrum Disorder Using Blood-based Gene Expression Signatures and Machine Learning","authors":"D. Oh, I. Kim, S. Kim, D. Ahn","doi":"10.9758/cpn.2017.15.1.47","DOIUrl":"https://doi.org/10.9758/cpn.2017.15.1.47","url":null,"abstract":"Objective The aim of this study was to identify a transcriptomic signature that could be used to classify subjects with autism spectrum disorder (ASD) compared to controls on the basis of blood gene expression profiles. The gene expression profiles could ultimately be used as diagnostic biomarkers for ASD. Methods We used the published microarray data (GSE26415) from the Gene Expression Omnibus database, which included 21 young adults with ASD and 21 age- and sex-matched unaffected controls. Nineteen differentially expressed probes were identified from a training dataset (n=26, 13 ASD cases and 13 controls) using the limma package in R language (adjusted p value <0.05) and were further analyzed in a test dataset (n=16, 8 ASD cases and 8 controls) using machine learning algorithms. Results Hierarchical cluster analysis showed that subjects with ASD were relatively well-discriminated from controls. Based on the support vector machine and K-nearest neighbors analysis, validation of 19-DE probes with a test dataset resulted in an overall class prediction accuracy of 93.8% as well as a sensitivity and specificity of 100% and 87.5%, respectively. Conclusion The results of our exploratory study suggest that the gene expression profiles identified from the peripheral blood samples of young adults with ASD can be used to identify a biological signature for ASD. Further study using a larger cohort and more homogeneous datasets is required to improve the diagnostic accuracy.","PeriodicalId":10420,"journal":{"name":"Clinical Psychopharmacology and Neuroscience","volume":"15 1","pages":"47 - 52"},"PeriodicalIF":3.2,"publicationDate":"2017-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.9758/cpn.2017.15.1.47","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48811522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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