Induced Pluripotent Stem Cells as a Novel Tool in Psychiatric Research

Reprogramming of somatic cells into induced pluripotent stem cells (iPSCs) provides a valuable opportunity to study neurodevelopmental and neurodegenerative psychiatric diseases by offering an unlimited source for patient-specific neuronal and glial cells. The present review focuses on the recent advancements in modeling psychiatric disorders such as Phelan-McDermid syndrome, Timothy syndrome, Rett syndrome, schizophrenia, bipolar disorder, and dementia. The treatment effects identified in studies on iPSCs using known therapeutic compounds are also summarized in this review. Here we discuss validation of cellular models and explore iPSCs as a novel drug screening tool. Although there are several limitations associated with the current methods used to study mental disorders, using iPSCs as a model system provides the advantage of rewinding and reviewing the development and degeneration of human neural cells.

A Case of Withdrawal Psychosis from Internet Addiction Disorder

Similar to substance use disorder, patients with Internet addiction disorder (IAD) show excessive use, tolerance and withdrawal symptoms. We report a case of a patient with withdrawal psychosis who showed persecutory delusion and disorganized behaviors in addition to common withdrawal symptoms such as agitation and irritability. A 25-year-old male developed a full-blown psychotic episode within one day after discontinuing an Internet game that he had been playing for at least eight hours a day for two years. Upon admission, he had no abnormal brain imaging findings and laboratory tests. With antipsychotic medication (quetiapine up to 800 mg), his psychotic symptoms rapidly subsided and after four days of treatment, he no longer showed any signs of psychosis. This case report suggests that brief psychosis can develop during withdrawal from long-term excessive use of an Internet and the central pathology beneath the IAD is more likely a form of addiction than impulse control.

NCAM140 and pCREB Expression after Tianeptine Treatment of SH-SY5Y Cells

OBJECTIVE: Antidepressants Modulate Neuronal Plasticity. Tianeptine, An Atypical Antidepressant, Might Be Involved In The Restoration Of Neuronal Plasticity; It Primarily Enhances The Synaptic Reuptake Of Serotonin. Ncam140 Is Involved In Neuronal Development Processes, Synaptogenesis And Synaptic Plasticity. We Investigated The Effect Of Tianeptine On The Expression Of Ncam140 And Its Downstream Signaling Molecule In The Human Neuroblastoma Cell Line Sh-sy5y. METHODS: NCAM protein expression was measured in human neuroblastoma SH-SY5Y cells that were cultivated in serum-free media and treated with 0, 10, or 20 microM tianeptine for 6, 24, or 72 hours. NCAM140 expression in the tianeptine treatment group was confirmed by Western blot, and quantified through measurement of band intensity by absorbance. CREB and pCREB expression was identified after treatment with 20 microM tianeptine for 6, 24, and 72 hours by Western blot. RESULTS: Compared to cells treated for 6 hours, cells treated with 0 or 10 microM tianeptine for 72 hours showed a significant increase in NCAM140 expression and cells treated with 20 microM tianeptine showed a significant increase after 24 and 72 hours. The pCREB level in cells treated with 20 microM tianeptine increased in time-dependent manner. CONCLUSION: Our findings indicated that the tianeptine antidepressant effect may occur by induction of NCAM140 expression and CREB phosphorylation.

Eye Movement Desensitization and Reprocessing for Posttraumatic Stress Disorder in Bipolar Disorder

No abstract available.

Psychiatric Implication for the Regulation of AMPA Receptor

Glutamate receptors are important components of synaptic transmission in the nervous system. Especially, alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors mediate most abundant excitatory synaptic transmission in the brain. There is elaborate mechanism of regulation of AMPA receptors including protein synthesis/degradation, intracellular trafficking, exocytosis/endocytosis and protein modification. In recent studies, it is revealed that functional dysregulation of AMPA receptors are related to major psychiatric disorders. In this review, we describe the structure and function of AMPA receptors in the synapse. We will introduce three steps of mechanism involving trafficking of AMPA receptors to neuronal membrane, lateral diffusion into synapses and synaptic retention by membrane proteins and postsynaptic scaffold proteins. Lastly, we will describe recent studies showing that regulation of AMPA receptors is important pathophysiological mechanism in psychiatric disorders.

Ketamine as a Rapid-Acting Antidepressant

First-line therapy of depression is a pharmacological treatment. Many prescribed antidepressants modulate monoamine neurotransmitters including serotonin, norepinephrine and dopamine. Recently, Ketamine, an N-methyl-D-aspartate receptor antagonist, has received attention and has been investigated for clinical trials and neurobiological studies. Here, I introduce ketamine as a rapid-acting antidepressant.

Another Diagnostic Approach : An Introduction to Research Domain Criteria (RDoC)

The new edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) is published by the American Psychiatric Association. The diagnostic systems for mental disorders have come under criticism for relying on presenting signs and symptoms with the result that they do not adequately reflect relevant neurobiological and behavioral systems. Finally, the National Institute of Mental Health (NIMH) in the United States has suggested the Research Domain Criteria (RDoC) to develop a research classification system based upon dimensions of neurobiology and behavioral aspect. The present review introduces the RDoC as a new reaseach framework.

Psychiatric Implication of Synaptic Adhesion Molecules and Scaffold Proteins

Synaptic adhesion molecules mediate synapse formation, maturation and maintenance. These proteins are localized at synaptic sites in neuronal axons and dendrites. These proteins function as a bridge of synaptic cleft via interaction with another synaptic adhesion molecules in the opposite side. They can interact with scaffold proteins via intracellular domain and recruit many synaptic proteins, signaling proteins and synaptic vesicles. Scaffold proteins function as a platform in dendritic spines or axonal terminals. Recently, many genetic studies have revealed that synaptic adhesion molecules and scaffold proteins are important in neurodevelopmental disorders, psychotic disorders, mood disorders and anxiety disorders. In this review, fundamental mechanisms of synapse formation and maturation related with synaptic adhesion molecules and scaffold proteins are introduced and their psychiatric implications addressed.

Pathogenic Molecular Mechanisms of Glutamatergic Synaptic Proteins in Alzheimer's Disease

Alzheimer's disease(AD) is the most common neurodegenerative disorder and constitutes about two thirds of dementia. Despite a lot of effort to find drugs for AD worldwide, an efficient medicine that can cure AD has not come yet, which is due to the complicated pathogenic pathways and progressively degenerative properties of AD. In its early clinical phase, it is important to find the subtle alterations in synapses responsible for memory because symptoms of AD patients characteristically start with pure impairment of memory. Attempts to find the target synaptic proteins and their pathogenic pathways will be the most powerful alternative strategy for developing AD medicine. Here we review recent progress in deciphering the role of target synaptic proteins related to AD in hippocampal glutamatergic synapses.

Epigenetics and Psychiatric Disorders

In the post-genomic era, the mechanisms controlling activation of genes are thought to be more important. Gene-environment interactions are crucial in both development and treatment of psychiatric disorders as they are complex genetic disorders. Epigenetics is defined as a change of gene expression that occurs without a change of DNA sequence and can be heritable by certain mechanisms. Epigenetic changes play essential roles in control of gene activation. DNA methylation, chromatin remodeling and RNAi act as key mechanisms for epigenetic modifications of genes. Here, we review the basic mechanisms of epigenetics and discuss their potential involvement of human diseases, including psychiatric disorders.