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The Gut-Brain Axis: The Missing Link in Depression.

Clinical Psychopharmacology and Neuroscience.2015;13(3):239-244. doi:10.9758/cpn.2015.13.3.239

The gut microbiota is essential to human health and the immune system and plays a major role in the bidirectional communication between the gut and the brain. Based on evidence, the gut microbiota is associated with metabolic disorders such as obesity, diabetes mellitus and neuropsychiatric disorders such as schizophrenia, autistic disorders, anxiety disorders and major depressive disorders. In the past few years, neuroscientific research has shown the importance of the microbiota in the development of brain systems. Recent studies showed that the microbiota could activate the immune and central nervous systems, including commensal and pathogenic microorganisms in the gastrointestinal tract. Gut microorganisms are capable of producing and delivering neuroactive substances such as serotonin and gamma-aminobutyric acid, which act on the gut-brain axis. Preclinical research in rodents suggested that certain probiotics have antidepressant and anxiolytic activities. Effects may be mediated via the immune system or neuroendocrine systems. Herein, we present the latest literature examining the effects of the gut microbiota on depression.
Anxiety Disorders ; Axis, Cervical Vertebra* ; Brain ; Central Nervous System ; Depression* ; Depressive Disorder, Major ; Diabetes Mellitus ; gamma-Aminobutyric Acid ; Gastrointestinal Tract ; Humans ; Immune System ; Microbiota ; Neurosecretory Systems ; Obesity ; Probiotics ; Rodentia ; Schizophrenia ; Serotonin

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Classic Studies on the Interaction of Cocaine and the Dopamine Transporter.

Vivek VERMA

Clinical Psychopharmacology and Neuroscience.2015;13(3):227-238. doi:10.9758/cpn.2015.13.3.227

The dopamine transporter is responsible for recycling dopamine after release. Inhibitors of the dopamine transporter, such as cocaine, will stop the reuptake of dopamine and allow it to stay extracellularly, causing prominent changes at the molecular, cellular, and behavioral levels. There is much left to be known about the mechanism and site(s) of binding, as well as the effect that cocaine administration does to dopamine transporter-cocaine binding sites and gene expression which also plays a strong role in cocaine abusers and their behavioral characteristics. Thus, if more light is shed on the dopamine transporter-cocaine interaction, treatments for addiction and even other diseases of the dopaminergic system may not be too far ahead. As today's ongoing research expands on the shoulders of classic research done in the 1990s and 2000s, the foundation of core research done in that time period will be reviewed, which forms the basis of today's work and tomorrow's therapies.
Binding Sites ; Cocaine* ; Dopamine Plasma Membrane Transport Proteins* ; Dopamine* ; Gene Expression ; Parkinson Disease ; Recycling ; Shoulder ; Substance-Related Disorders

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A Case of Very-late-onset Schizophrenia-like Psychosis.

Ji Hyun SON ; Baik Seok KEE

Clinical Psychopharmacology and Neuroscience.2011;9(2):91-93.

This paper presents the case of a 67-year-old woman who visited the Psychiatry Department complaining of persecutory ideas and auditory hallucinations after a buccal cancer operation. On neuropsychological testing, she demonstrated paranoid psychosis and bizarre thoughts. Hospital admission was recommended for supportive care and treatment with antipsychotics. She was initially treated with olanzapine, but this medication had little effect and was replaced with amisulpride, which reduced the residual symptoms. The aim of this report was to discuss the diagnostic process and treatment of very late-onset schizophrenia-like psychosis.
Aged ; Antipsychotic Agents ; Benzodiazepines ; Female ; Hallucinations ; Humans ; Neuropsychological Tests ; Psychotic Disorders ; Sulpiride

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Effects of Sinapic Acid of 4 Vessel Occlusion Model-Induced Ischemia and Cognitive Impairments in the Rat.

Young Ock KIM ; Sang Won LEE ; Myung Sook OH ; Hee Jae LEE

Clinical Psychopharmacology and Neuroscience.2011;9(2):86-90.

OBJECTIVE: Sinapic acid (SA, Sinapine), small naturally occurring hydroxycinnamic acid, has a GABA(A) receptor agonistic property and free radical scavenging activity. We examined potential neuroprotective effects of sinapic acid (SA) using global cerebral ischemia animal model. METHODS: MTT assay was performed to determine cytotoxic effects of SA. To examine the neuroprotective effects of SA, SA was administrated for 14 d before 4-vessel occlusion. Also, to determine whether SA prevents cognitive impairment, Morris water maze was performed. RESULTS: In this study, the efficacy of SA for the prevention of neuronal damage and for the reduction of memory impairment was investigated. CONCLUSION: The results indicate that SA confers significant neuroprotection especially for ischemic hippocampal neurons.
Animals ; Brain Ischemia ; Coumaric Acids ; Glycosaminoglycans ; Hippocampus ; Ischemia ; Maze Learning ; Memory ; Neurons ; Neuroprotective Agents ; Rats ; Receptors, GABA-A

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Effects of Psychotropic Drugs on Quantitative EEG among Patients with Schizophrenia-spectrum Disorders.

June HYUN ; Myung Jae BAIK ; Ung Gu KANG

Clinical Psychopharmacology and Neuroscience.2011;9(2):78-85.

OBJECTIVE: We examined how psychotropic medications affected quantitative EEG (qEEG) results among patients with a schizophrenia-spectrum disorder. METHODS: The drugs were clustered into nine groups depending on their mechanism. We hypothesized that drugs would affect the relative power shown in qEEG results independently and investigated the effect of each drug group on relative power using multiple linear regression analysis and independent samples t-tests. RESULTS: We found that antipsychotics other than clozapine induced an increase in the relative power of alpha activity. Clozapine markedly increased slow waves and decreased alpha activity in the occipital area. The main findings for antidepressants and antiepileptic drugs were the beta increment and lithium increased the power of delta and theta activity. However, we found no evident changes in power due to benzodiazepine. CONCLUSION: Our results are generally consistent with previous pharmaco-EEG studies, despite some differences. Therefore, the EEG effect in each drug group could be singled out even under the polypharmacy condition, with the possible exception of benzodiazepines. Our results support using a new methodological approach to identify the qEEG effects of various psychotropic drugs in clinical settings.
Anticonvulsants ; Antidepressive Agents ; Antipsychotic Agents ; Benzodiazepines ; Clozapine ; Electroencephalography ; Humans ; Linear Models ; Lithium ; Polypharmacy ; Psychotropic Drugs

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The Tolerability of Mirtazapine Augmentation in Schizophrenic Patients Treated with Risperidone: A Preliminary Randomized Placebo-controlled Trial.

Jieun LEE ; Sung Joon CHO ; Kang Soo LEE ; Keunyoung YOOK ; Ah Young CHOE ; Sungjae LEE ; Borah KIM ; Keung Hyang KIM ; Tae Kyou CHOI ; Sang Hyuk LEE

Clinical Psychopharmacology and Neuroscience.2011;9(2):73-77.

OBJECTIVE: Some patients with schizophrenia may need mirtazapine augmentation to improve negative and cognitive symptoms. However there have been a few studies about the tolerability of mirtazapine augmentation to antipsychotics such as akathisia, extrapyramydal symptoms, weight gain, and body mass index (BMI). METHODS: This study was an eight-week double-blind, randomized controlled trial (RCT) of mirtazapine augmentation to risperidone. Twenty-one stabilized participants diagnosed with schizophrenia and undergoing treatment with risperidone were randomized to adjunctive treatment with mirtazapine (15 mg/day for the first two weeks, 30 mg/day for the next six weeks) or placebo. Eleven patients were assigned to the mirtazapine group, and nine patients were given placebo. RESULTS: There was no significant difference between the mirtazapine and placebo groups with respect to Barnes Akathisia rating Scale (BAS) and Sympsom-Angus Scale (SAS). However, the mirtazapine group exhibited a statistically significant increase in weight and BMI (p<0.05). CONCLUSION: These results suggest that mirtazapine augmentation can be tolerable in schizophrenic patients treated with risperidone; however, we should pay attention to the weight gain with mirtazapine. Our results should be replicated in a large-scale lengthy trial.
Antipsychotic Agents ; Body Mass Index ; Humans ; Mianserin ; Neurobehavioral Manifestations ; Psychomotor Agitation ; Risperidone ; Schizophrenia ; Weight Gain

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Rapid Changes in D1 and D2 Dopamine Receptor Binding in Striatal Subregions after a Single Dose of Phencyclidine.

Victoria S DALTON ; Katerina ZAVITSANOU

Clinical Psychopharmacology and Neuroscience.2011;9(2):67-72.

OBJECTIVE: In humans, a single exposure to phencyclidine (PCP) can induce a schizophrenia-like psychosis which can persist for up to two weeks. In rats, an acute dose of PCP increases dopaminergic activity and causes changes in dopamine related behaviours some of which are sexually dimorphic. To better understand the effects of PCP on dopamine receptor adaptations in the short term we examined dopamine D1-like receptors (D1R) and D2-like receptors (D2R) in the mesolimbic and nigrostriatal dopamine pathways, 4 hours after exposure to PCP in female rats. METHODS: Animals received a single dose of 40 mg/kg PCP and were sacrificed 4 hours later. In vitro autoradiography was carried out using [3H] SCH 23390 and [3H] raclopride that target D1R and D2R respectively, in cryostat brain sections. RESULTS: Two way analysis of variance (ANOVA), revealed an overall effect of PCP treatment (F [1,63]=9.065; p=0.004) on D1R binding with an 18% decrease (p<0.01) in binding in the medial caudate putamen. PCP treatment also had an overall effect on D2R binding (F [1,47]=5.450; p=0.024) and a trend for an increase in D2R binding across all the brain regions examined. CONCLUSION: These results suggest opposing D1R and D2R adaptations in striatal subregions of female rats following acute exposure to PCP that may occur through indirect mechanisms.
Animals ; Autoradiography ; Benzazepines ; Brain ; Dopamine ; Female ; Humans ; Phencyclidine ; Psychotic Disorders ; Putamen ; Raclopride ; Rats ; Receptors, Dopamine

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Panel of Genetic Variations as a Potential Non-invasive Biomarker for Early Diagnosis of Alzheimer's Disease.

Suk Ling MA ; Linda Chiu Wa LAM

Clinical Psychopharmacology and Neuroscience.2011;9(2):54-66.

Alzheimer's disease (AD) is the most prevalent form of dementia. Biomarkers such as levels of amyloid beta (Abeta) in cerebrospinal fluid and ApoE genotyping were suggested for the diagnosis of AD, however, the result is either non-conclusive or with invasive procedure. Genome-wide association studies (GWASs) for AD suggested single nucleotide polymorphisms (SNPs) in many genes are associated with the risk of AD, but each only contributed with small effect to the disease. By incorporating a panel of established genetic susceptibility factors, the risk of an individual in getting AD could be better estimated. Further research will be required to reveal if adding to the current well-developed clinical diagnosis protocol, the accuracy and specificity of diagnosis of AD would be greatly improved and if this might also be beneficial in identifying pre-symptomatic AD patients for early diagnosis and intervention of the disease.
Alzheimer Disease ; Amyloid ; Apolipoproteins E ; Biomarkers ; Dementia ; Early Diagnosis ; Genetic Predisposition to Disease ; Genetic Variation ; Genome-Wide Association Study ; Humans ; Polymorphism, Single Nucleotide ; Sensitivity and Specificity

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Second-Generation Antipsychotic Discontinuation in First Episode Psychosis: An Updated Review.

Brian J MILLER ; Chelsea BODENHEIMER ; Krystle CRITTENDEN

Clinical Psychopharmacology and Neuroscience.2011;9(2):45-53.

"All-causes discontinuation" refers to discontinuation of treatment for any reason, and medication adherence is an important component of this measure. Similar to our previous results, we found that almost 30% of patients with first-episode psychosis (FEP) discontinue medication in the first 9 months of treatment, a finding that has important implications for long-term outcomes. Many newer second-generation antipsychotics have not been studied in FEP. The self-reported Drug Attitude Inventory may help identify patients at heightened risk for medication discontinuation. In addition to vigilant monitoring for and adequate treatment of psychopathology and medication side effects, Relapse Prevention Therapy and the use of long-acting injectable agents may be effective interventions decrease discontinuation rates in FEP. There is currently no consensus on how long a patient should remain on an antipsychotic medication following remission of FEP. Studies are needed to identify predictors of which patients in remission from FEP are less likely to relapse when medication is discontinued. Taken together, our findings presented here underscore the importance of addressing medication discontinuation both as a means of preventing long-term morbidity and enhancing remission and functional recovery in FEP.
Antipsychotic Agents ; Consensus ; Humans ; Medication Adherence ; Patient Compliance ; Polytetrafluoroethylene ; Psychopathology ; Psychotic Disorders ; Recurrence ; Schizophrenia

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The Normalization of Brain ¹⁸F-fluorodeoxy-D-glucose Positron Emission Tomography Hypometabolism following Electroconvulsive Therapy in a 55-year-old Woman with Treatment-resistant Late Onset Depression: A Case Report.

Jeongjae BAK ; Sang Mi LEE ; Young Joon KWON ; Se Hoon SHIM ; Joong Il KIM

Clinical Psychopharmacology and Neuroscience.2017;15(1):82-86. doi:10.9758/cpn.2017.15.1.82

Major depressive disorder, especially in later life, has heterogeneous clinical characteristics and treatment responses. Symptomatically, psychomotor retardation, lack of energy, and apathy tends to be more common in people with late-onset depression (LOD). Despite recent advances in psychopharmacologic treatments, 20% to 30% of patients with mood disorders experience inadequate responses to medication, often resulting in a trial of electroconvulsive therapy (ECT). However, the therapeutic mechanism of ECT is still unclear. By using ¹⁸F-fluorodeoxy-D-glucose positron emission tomography-computed tomography (18F-FDG PET/CT), we can obtain the status of brain metabolism in patients with neuropsychiatric disorders and changes during psychiatric treatment course. The object of this case report is evaluating the effect of ECT on brain metabolism in treatment-refractory LOD by PET/CT and understanding the mode of action of ECT. In this case report, we presented a 55-year-old female patient who suffered psychotic depression that was resistant to pharmacological treatment. Several antidepressants and atypical anti-psychotics were applied but there was no improvement in her symptoms. The patient presented not only depressed mood and behaviors but also deficit in cognitive functions. We found decreased diffuse cerebral metabolism in her brain ¹⁸F-FDG PET/CT image. ECT resulted in amelioration of the patients' symptoms and another brain PET imaging 7 weeks after the last ECT course showed that her brain metabolism was normalized.
Antidepressive Agents ; Apathy ; Brain* ; Cognition ; Depression* ; Depressive Disorder, Major ; Electroconvulsive Therapy* ; Electrons* ; Female ; Fluorodeoxyglucose F18 ; Humans ; Metabolism ; Middle Aged* ; Mood Disorders ; Positron-Emission Tomography and Computed Tomography ; Positron-Emission Tomography*

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