Genetic variability in the neurobiology of nicotine dependence: effects on smoking behavior / A variabilidade genética na neurobiologia da adição à nicotina: reflexos no comportamento tabágico

Abstract Background Smoking dependence is a chronic disease and a public health problem. The neurobiology of nicotine addiction can explain smoking behavior. This system has genetic variability that has been associated with vulnerability to dependence. Genetic variability in the neurobiology of smoking can help to understand why individuals exposed to drugs may or may not become addicted. Objective This study aims to address genetic variability in the neurobiology of smoking addiction with a focus on polymorphic genes related to the nicotinic response and the dopaminergic reward pathway. Method This work involved a search of the main scientific research on genetic variability in the neurobiology of smoking and its effects on smoking behavior. One hundred and five studies were selected, most of which highlighted polymorphisms in the genes of nicotinic receptors, dopamine receptors, and nicotine metabolism. Results The majority of studies have focused on genes related to the activation of the dopaminergic reward system by nicotine. Combinations between different polymorphisms were also highlighted, showing that interactions can determine a genetic profile of predisposition to smoking addiction. Additionally, gender and ethnicity were identified as relevant factors. Conclusion Knowledge of the genetic bases involved in the individual response to smoking can enable a better understanding of inter-individual differences in smoking behavior, and contribute to improving the treatment of addiction.

Resumo Introdução A dependência nicotínica é uma doença crônica e um problema de saúde pública. O comportamento tabágico pode ser explicado pela neurobiologia da adição, cujas variações genéticas têm sido associadas à dependência. A variabilidade genética na neurobiologia do tabagismo pode ajudar a entender por que indivíduos expostos a drogas podem ou não se tornar viciados. Objetivo Este estudo tem como objetivo abordar a variabilidade genética na neurobiologia do tabagismo com foco em genes polimórficos relacionados à resposta nicotínica e à via de recompensa dopaminérgica. Método Uma pesquisa foi realizada nas principais bases de dados científicos sobre a variabilidade genética na neurobiologia do tabagismo e seus efeitos no comportamento do tabagismo. 105 estudos foram selecionados, em sua maioria destacando polimorfismos nos genes de receptores nicotínicos, receptores de dopamina e de metabolismo da nicotina. Resultados A maioria dos estudos concentrou-se em genes relacionados à ativação do sistema de recompensa dopaminérgico pela nicotina. Determinadas combinações entre genótipos de diferentes polimorfismos também se destacaram, mostrando que interações gênicas podem determinar um perfil genético de predisposição ao tabagismo. Além disso, gênero e etnia foram identificados como fatores relevantes. Conclusão O conhecimento das bases genéticas envolvidas na resposta individual ao tabagismo pode permitir uma melhor compreensão das diferenças interindividuais no comportamento tabágico e contribuir para melhoria dos tratamentos disponíveis para a dependência.

Un acercamiento al conocimiento de la presencia de marcadores neurobiológicos en la génesis del suicidio / An approach to the knowledge of the presence of neurobiological markers in the genesis of suicide / Uma abordagem para o conhecimento da presença de marcadores neurobiológicos nagênese do suicídio

RESUMEN El suicidio ha constituido desde siempre uno de los grandes enigmas de la humanidad. El presente trabajo tiene como objetivo abordar los elementos más actuales de la génesis neurobiológica de la conducta suicida que puedan contribuir a su prevención. Se realizaron diversas búsquedas en materiales impresos y digitales a partir de las consultas del catálogo online de la biblioteca virtual de Infomed, en bases de datos multidisciplinarias así como las revistas digitales certificadas. Entre los marcadores neurobiológicos descritos en la actualidad más destacados están bajos niveles del 5-HIAA en el líquido cefalorraquídeo (LCR), aumento de la densidad de los receptores 5-HT1A en la corteza pre- frontal, disminución de los sitios de unión del receptor serotoninérgico en la misma región, modificación del sistema GABA-érgico y los receptores benzodiazepínicos entre otros. A modo de conclusión se puede decir que los marcadores neurobiológicos y los factores psicopatológicos- de interacción familiar- de stress psicosocial descritos buscan identificar aquellos individuos con potencial riesgo de suicidio para establecer medidas de prevención, lo cual exige su detección e intervención a tiempo buscando evitar la ocurrencia del primer intento y a su vez la repetición del acto que conlleve al desenlace fatal.

ABSTRACT Suicide has always been one of the great enigmas of humanity. The present work aims to address the most current elements of the neurobiological genesis of suicidal behavior that can contribute to its prevention. Various searches were made of printed and digital materials based on queries in the online catalog of the Infomed virtual library, in multidisciplinary databases as well as certified digital journals. Among the most prominent neurobiological markers currently described are low levels of 5-HIAA in cerebrospinal fluid (CSF), increased density of 5-HT1A receptors in the prefrontal cortex, decreased receptor binding sites serotonergic in the same region, decrease in platelet serotonin receptors, modification of the GABA-ergic system and benzodiazepine receptors, among others. Suicide has multidimensional qualities and a multifactorial etiopathogenesis, therefore, in the consummation of the suicidal act, genetic factors -neurobiological - psychopathological - family interaction - psychosocial stress should be considered. By way of conclusion, the neurobiological and psychosocial markers described seek to identify those individuals with a potential risk of suicide to establish a prevention measure, which requires their detection and intervention in time, seeking to avoid the occurrence of the first attempt and, in turn, the repetition of the act that entails to the fatal outcome.

RESUMO O suicídios em prefoium dos grandes enigmas da humanidade. O presente trabalho visa abordar os elementos maisatuais da gênese neurobiológica do comportamento suicida que podem contribuir para sua prevenção. Foram realizadas várias pesquisas em materiais impressos e digitais do catálogo online da biblioteca virtual Infomed, em bases de dados multidisciplinares e também em revistas digitais certificadas. Entre os marcadores neurobiológicos mais proeminentes atualmente descritos estão baixos níveis de 5-HIAA no líquido cefalorraquidiano (LCR), aumento da densidade de receptores 5-HT1A no córtex pré-frontal, diminuição dos sítios de ligação do receptor serotonérgicona mesma região, modificação do GABA- sistema ergico e receptores de benzodiazepina, entre outros. A título de conclusão, pode-se dizer que os marcadores neurobiológicos e fatores psicopatológicos - de interação familiar - do estresse psicossocial descritos buscam identificar aqueles indivíduos com potencial risco de suicídio para estabelecer medidas de prevenção, o que requer sua detecção e intervenção em tempo, visando evitar a ocorrência da primeira tentativa e, por sua vez, a repetição do ato que leva ao resultado fatal.

Research progress on anhedonia and its measurement methods / 中国药理学通报

Anhedonia, or markedly diminished interest or pleas-ure, is a hallmark symptom of depression.As a psychopathological symptom, anhedonia was first noted in the early 19th century.The neurobiological mechanisms that underline anhedonia and its role in diagnosing depression disorder or evaluating antidepressant response have long been aroused attention for nearly a century.Consequently, there are many measuring methods established in both the animal study and human research, which would be reviewed in the present study.

The formation and erasure of drug addiction memories / 复旦学报（医学版）

Psychoactive substance abuse has been a public health and social problem in the world.The essence of psychoactive substance addiction is a pathological memory (addiction memory) based on alterations in gene expression and synapticplasticity.Here we summarize recent findings in the neurobiological mechanisms of psychoactive substance addiction.

Cognitive-behavioral therapy for schizophrenia: an overview on efficacy, recent trends and neurobiological findings / Terapia cognitivo-comportamental para esquizofrenia: uma revisão sobre eficácia, avanços recentes e achados neurobiológicos

OBJECTIVE: Cognitive Behavioral Therapy (CBT) has been recommended by several international guidelines as the gold-standard treatment to address the needs of patients with schizophrenia. This review provides an overview on recent advances regarding CBT for schizophrenia. METHODS: An electronic search was performed on PubMed/MEDLINE, Web of Science and Cochrane Database, using the key-words: "schizophrenia", "psychosis", "cognitive-behavioral therapy", "CBT" and "psychotherapy". RESULTS: Numerous systematic reviews support the immediate and long-term efficacy of Cognitive Behavioral Therapy to reduce positive and negative symptoms in patients with schizophrenia. In the last decade, CBT for schizophrenia has been applied to clinical high-risk subjects and delivered using innovative approaches (low intensity, web-based and self-guided). Brain regions and networks which support high-level cognitive functions have been associated with CBT responsiveness. There is preliminary evidence indicating that CBT induces a prefrontal dependent increase in the top-down modulation of social threat activation. CONCLUSION: In the last decade, CBT for schizophrenia has explored new treatment outcomes, targeted acute and pre-clinical populations and provided alternative methods to reach more patients and reduce intervention costs. The patients' neurocognitive profile seems to play a critical role in treatment response and combining CBT with cognitive remediation may allow to enhance therapeutic effects. Although CBT for schizophrenia is widely established as a gold-standard practice, future studies using innovative CBT protocols, exploring brain-related predictors and treatment outcomes may allow this intervention to be more effective, personalized and to reach a wider number of patients.

INTRODUÇÃO: A terapia cognitivo-comportamental (TCC) tem sido recomendada em diversas guidelines internacionais como a intervenção psicoterapêutica padrão de ouro para pacientes com esquizofrenia. Esta revisão tem como objetivo fornecer uma visão global sobre os avanços recentes da TCC na esquizofrenia. MÉTODOS: Para esta revisão narrativa foi realizada uma busca eletrônica na PubMed/MEDLINE, Web of Science e Cochrane Database utilizando as palavras-chave: "schizophrenia", "psychosis", "cognitive-behavioral therapy", "CBT" e "psychotherapy". RESULTADOS: Várias revisões sistemáticas suportam a eficácia da TCC na redução a curto e longo prazo dos sintomas positivos e negativos da esquizofrenia. Na última década, a TCC tem sido aplicada a indivíduos com alto risco de psicose, sendo também exploradas abordagens inovadoras na sua utilização (curta duração, web-based, autogestão). Redes neurais responsáveis por funções cognitivas de nível superior têm sido associadas a respostas positivas após TCC para esquizofrenia. Existe ainda evidência preliminar que a TCC promove a ativação de zonas pré-frontais responsáveis pela modulação top-down face a ameaças sociais. CONCLUSÃO: Na última década, a TCC para esquizofrenia tem explorado novos desfechos, intervindo em populações agudas e pré-clínicas e utilizado métodos alternativos para alcançar mais pacientes e reduzir custos O perfil neurocognitivo dos pacientes aparenta ter um papel crítico na resposta ao tratamento, pelo que combinar a TCC com reabilitação cognitiva poderá potenciar os seus efeitos terapêuticos. Apesar da TCC ser uma prática recomendada para a esquizofrenia, estudos futuros usando protocolos inovadores e explorando preditores e desfechos relacionados com o cérebro poderão possibilitar que esta intervenção seja mais eficaz, personalizável e alcance o máximo número de pacientes possível.

Factores de riesgo en la aparición del trastorno por déficit de atención e hiperactividad en pacientes con epilepsia infantil de reciente diagnóstico / Risk factors in the emergence of attention deficit hyperactivity disorder in patients with diagnosis child recent epilepsy

Resumen: Antecedentes: la epilepsia y el trastorno por déficit de atención e hiperactividad (TDAH) son frecuentes de la infancia; se han reportado como comorbilidades. Se estima que aproximadamente 40% de los pacientes con epilepsia pueden presentar TDAH; sin embargo, hay pocas evidencias de si es acompañante o producto de la actividad epiléptica anormal, efectos secundarios de los fármacos o un proceso multigenético asociado. Objetivos: describir qué factores neurobiológicos tiene mayor relevancia en la aparición del trastorno por déficit de atención e hiperactividad en pacientes con epilepsia infantil de reciente diagnóstico. Materiales y métodos: se evaluó pacientes con epilepsia recién diagnosticada, entre los 4 y 16 años de edad durante el período comprendido entre octubre de 2011 y abril de 2012 con un seguimiento prospectivo de 6 meses, estableciendo desde el inicio si existían criterios de TDAH y midiendo factores tanto biológicos como asociados para el desarrollo de TDAH. Se completó los estudios para el abordaje de epilepsia. Resultados: se evaluaron 32 pacientes en los que se observó que el 40% tenía criterios de TDAH del subtipo inatento; además, se determinó que en el sexo masculino las epilepsias parciales representan el 63.2%, y en el femenino las epilepsias generalizadas el 53.8%. Los fármacos utilizados más frecuentes fueron el AVP (72%) y CBZ (28%). Conclusiones: consideramos que es muy frecuente el subtipo de TDAH inatento, lo que sustenta la idea de que sus síntomas son una disfunción neurológica causada por la epilepsia que por un trastorno biológico asociado. Esto realza la importancia de diagnosticar y tratar la epilepsia en sí, y evaluar después de un tiempo, la necesidad de complementar los tratamientos que controlen el TDAH. Palabras claves: factores neurobiológicos, epilepsia infantil de reciente diagnóstico, trastorno de déficit de atención e hiperactividad (TDAH).

Background: Epilepsy and ADHD are neurological disorders frequently seen in childhood, and have been reported as comorbidities. It is estimated that about 40% of patients with epilepsy may have ADHD, however, there is little evidence that if this disorder is or companion product of the abnormal epileptic activity, drug side effects or process associated multigenic. Objective: Describe which of the neurobiological factors have greater relevance in the development of attention deficit disorder and hyperactivity in patients with newly diagnosed childhood epilepsy. Materials and methods: We evaluated patients with newly diagnosed epilepsy, between 4 and 16 years of age in the period between October 2011 and April 2012 with a prospective monitoring six months from start setting if were no criteria for ADHD and measuring both biological factors associated with development of ADHD. Were completed relevant studies for addressing epilepsy. Results: We evaluated more than 32 patients, where it was observed that 40% of the sample had ADHD criteria for inattentive subtype, also was determined that in males partial epilepsies represent 63.2% and in women the epilepsy represents 53,8% overall. Among the most common drugs used were VPA by 72% and 28% CBZ. Conclusions: We believe it is very common subtype of ADHD is found the inattentive, so supports the idea that many of the symptoms of ADHD represent a more neurological dysfunction that epilepsy associated with a biological disorder, This enhances the importance of a diagnosis and treatment of epilepsy itself and to assess after a while, the need to supplement with control treatments for ADHD.

Neurobiological Mechanism of Memory

Memory is one of the most important mental mechanisms which is crucial for us to adapt to environmental surroundings and to maintain our identity. The neurobiological mechanisms for memory are based upon the synaptic plasticity that involve both functional and structural changes at the synapses in the neural circuits participating in learning and memory. Memory is not a single process but has two forms of short-term and long-term memory that are two independent but overlapping processes that blend into one another. The short-term memory depends upon the functional change of synaptic strength but the long-term memory requires anatomic changes of synapses in the neural circuit. Memory storage seems to use elements of a common genetic switch, involving cyclic adenosine monophospate (cAMP)-dependent protein kinase, mitogen activated protein kinase, and cAMP response element-binding protein, to convert short-term memory into long-term memory.

Understanding of the sensorimotor-cognitive difficulties in attention deficit and hyperactivity disorders children / 中华实用儿科临床杂志

Attention deficit and hyperactivity disorders (ADHD),a neurodevelopmental disability with core symptoms of inattention,hyperactivity and impulsivity increases the risk of many cognitive problems.However,the brain structures and pathways involved in the interplays between the core symptoms,such as activity deficits,and cognitive impairments have remained unknown over the past decades.This article review the academic developments in recent years that elucidate the neural mechanisms involved in the sensorimotor-cognitive difficulties at systematic,circuitry,cellular,and molecular levels.The treatment potentials of physical activity enhancement were addressed,as a new alternative and supplementary therapeutic strategy for ADHD,based on our current understanding of the neurobiology of cognitive-sensorimotor interaction.

Comparison of the neurobiological effects of attribution retraining group therapy with those of selective serotonin reuptake inhibitors

The aim of this study was to compare the effectiveness of attribution retraining group therapy (ARGT) with selective serotonin reuptake inhibitors (SSRIs) in the treatment of major depressive disorder (MDD), generalized anxiety disorder (GAD), and obsessive-compulsive disorder (OCD). Subjects were sequentially recruited and randomized into two groups, one receiving ARGT (n = 63) and the other SSRIs (n = 66) for 8 weeks. Fifty-four ARGT outpatients with MDD (n = 19), GAD (n = 19), and OCD (n = 16) and 55 SSRI outpatients with MDD (n = 19), GAD (n = 19), and OCD (n = 17) completed the study. All subjects were assessed using the Hamilton Depression Scale and Hamilton Anxiety Scale before and after treatment. The 10-item Yale-Brown Obsessive Compulsive Scale was employed only for OCD subjects. Plasma levels of serotonin, norepinephrine, cortisol, and adrenocorticotropic hormone were also measured at baseline and 8 weeks after completion of treatment. Symptom scores were significantly reduced (P < 0.001) in both the ARGT and SSRI groups at the end of treatment. However, MDD, GAD and OCD patients in the ARGT group had significantly lower plasma cortisol concentrations compared to baseline (P < 0.05), whereas MDD and OCD patients receiving SSRIs showed significantly increased plasma levels of serotonin (P < 0.05). These findings suggest that ARGT may modulate plasma cortisol levels and affect the hypothalamus-pituitary-adrenal axis as opposed to SSRIs, which may up-regulate plasma serotonin levels via a different pathway to produce an overall improvement in the clinical condition of the patients.

Attributional retraining group therapy versus selective serotonin reuptake inhibitors: neurobiological effects / 中华行为医学与脑科学杂志

Objective To compare the effects on neurobiological factors of attributional retraining group therapy (ARGT) or selective serotonin reuptake inhibitors (SSRI) for major depressive disorder (MDD),anxiety disorder (AD) and obsessive-compulsive disorder (OCD).Methods Outpatients with MDD,AD and OCD were divided into ARGT group (n =63) and SSRI group (n =66) according to the sequence of entering the study.MDD,AD and OCD patients were respectively measured with Hamilton Depression Scale (HAMD),Hamilton Anxiety Scale (HAMA),and Yale-Brown Obsessive Compulsive Scale (Y-BOCS) before and after 8 weeks treatment.All subjects were detected of plasma serotonin,norepinephrine,cortisol and adrenocorticotropic hormone by radioimmunoassay before and after treatment.Results After treatment,HAMD scores of MDD patients were reduced significantly in both ARGT group (t =18.411,P =0.000) and SSRI group (t =20.092,P =0.000) ; HAMA scores of GAD patients were reduced significantly in both ARGT group (t =13.989,P=0.000) and SSRI group (t=15.815,P=0.000) ;Y-BOCS scores of OCD patients were reduced significantly in both ARGT group (t =5.465,P =0.000)and SSRI group (t =4.792,P =0.000).In ARGT group,MDD (t =3.145,P =0.006),AD (t =2.785,P =0.012) and OCD patients (t =2.877,P =0.011) decreased plasma cortisol concentrations significantly.In SSRI group,MDD (t =-2.923,P =0.010) and OCD patients (t =-2.301,P =0.035) improved plasma serotonin significantly and MDD patients (t =-2.333,P =0.033) improved plasma norepinephrine significantly.Conclusion ARGT can modulate plasma cortisol level.SSRI can up-modulate plasma serotonin level.The two therapies take effect by different biological ways.

Frecuencia de riesgo neurobiológico en recién nacidos / Neurobiological risk frequency on newborns

Introducción: Los niños de alto riesgo o vulnerabilidad neurobiológica son aquellos que por sus antecedentes pre, peri o postnatales tienen una mayor probabilidad de presentar alteraciones en su desarrollo psicomotor. La evidencia sugiere que estos niños deben ingresar a Programas de Atención Temprana. objetivo: Describir la frecuencia de niños de alto riesgo neurobiológico que nacieron en hospitales públicos del Servicio de Salud Vina del Mar Quillota, durante al ano 2008. Paciente y Método: Se utilizó un diseno descriptivo a partir del análisis de información existente en los libros de registros de los servicios de maternidad y neonatología, del universo de niños nacidos vivos en hospitales públicos de la red de este servicio. Resultados: Los niños de alto riesgo representaron un 21,01 por ciento del total de recién nacidos vivos. Los factores de riesgo biológico más frecuentes fueron la prematurez (11,4 por ciento), el retardo de crecimiento intrauterino (9,0 por ciento) y el bajo peso de nacimiento (7,8 por ciento). Conclusión: Este estudio epidemiológico, representa el punto de partida para explorar la necesidad existente de disponer de registros estadísticos de los distintos factores de riesgo biológico y contar con espacios formales para realizar atención temprana en el servicio de salud Vina del Mar Quillota con el propósito de prevenir y tratar alteraciones del desarrollo psicomotor en todos los niños con riesgo neurobiológico.

Introduction: High-risk or neurobiological vulnerable children are those who are more likely to have alterations in their psychomotor development during their pre-, peri-, or post-natal periods. Evidence suggests that these children must have early medical care. objective: To describe the frequency of high-risk neuro-biological infants born during 2008 in Vina del Mar Quillota public health hospitals. Methods: A descriptive design was used based on the analysis of existing information in the maternity and neonatology record books regarding live births in public hospitals of this service network. Results: The high-risk children accounted for 21.01 percent of all live births. The most frequent biological risk factors were prematurity (11.4 percent), intrauterine growth retardation (9.0 percent) and low birth weight (7.8 percent). Conclusion: This epidemiological study represents the starting point for exploring the existing need to have statistical records of the various risk factors as well as have formal spaces for early treatment in the Quillota Vina del Mar health service to prevent and treat abnormal psychomotor development in all children with neurobiological risk.

Neuropsychological and neurobiological markers of the preclinical stage of Alzheimer's disease

Dementia, especially Alzheimer's disease, has a high prevalence in the elderly population. Therefore, identifying individuals who are at a high risk for early diagnosis is crucial to allow both pharmacological and behavioral therapeutic interventions, which in some cases can delay the progression of dementia. This paper describes neuropsychological and neurobiological markers for the early diagnosis of Alzheimer's disease and presents the main risk factors, including neuropathological, neuroanatomical, neurofunctional, genetic, and neuropsychological. The literature shows that the combination of these markers is the best method for predicting Alzheimer's disease, years before its clinical manifestation. The most prevalent neurobiological and neuropsychological risk factors include (1) senile plaques and neurofibrillary tangles in the medial temporal lobe and cortical regions, (2) low concentrations of Aâ1-42 peptide and high concentrations of total tau protein and phosphorylated tau protein in cerebrospinal fluid, (3) reduced global cerebral volume, increased ventricular volume, and atrophy in the hippocampal formation and entorhinal cortex, (4) global reductions in cerebral metabolism and perfusion in the temporoparietal junction, temporal, parietal, and frontal lobes, hippocampal formation, and posterior cingulate cortex, (5) the presence of the apolipoprotein E å4 allele, and (6) verbal anterograde episodic long-term memory impairment and executive dysfunction. The present review discusses the evidence for markers that identify individuals who are at a high risk of developing Alzheimer's disease and the importance of longitudinal studies in this context.

Neurobiological and Clinical Characteristics According to Lesch's Typology in Alcohol Dependence

OBJECTIVES: Many studies have suggested different neurobiological findings and clinical courses in alcoholism. Recently, subtyping in alcohol dependence has become essential to overcome the heterogeneity of patients. Among several criteria of subtypes, Lesch's typology is proposed to integrate biological, social, and psychological factors. This review provides neurobiological findings and treatment-responses of alcohol dependence according to Lesch's typology. METHOD: We searched the international published medical literature using the search terms 'Lesch's typology' and 'alcohol dependence' and using the limits 'human'. RESULTS: We identified 17 studies with subjects of alcohol dependence according to Lesch's typology. CONCLUSION: They indicated that each subtype of Lesch's typology can have specific neurobiological factors and different clinical responses as follows. Lesch's subtype 1 is characterized by severe withdrawal symptoms and associated with elevated glutamate and homocysteine. Lesch's subtype 2 is defined by individuals who drink alcohol as self-medication for anxiety. Their craving has significant positive correlations with prolactin, leptin level, or intake-volume (vasopressin). Lesch's subtype 4 is related to cerebral dysfunction and associated with increased glutamate and left-handedness. Clinical trials showed that naltrexone was effective in Lesch's subtype 3 and 4 patients, while acamprosate was effective in the subtypes 1 and 2.

Bases neurobiológicas de vulnerabilidad psiquiátrica a lo largo de las etapas de la vida hormonal de la mujer / Neurobiological bases of psychiatric vulnerability through the female hormonal stages

Women are about twice more likely than men to suffer from depression, it has been hypothesized that reproductive events (i.e., premenstrual, pre and postpartum, menopausal transition) may represent vulnerability periods for depression, in part because of a heightened sensitivity to intense hormonal fluctuations. 1) Most women report physical or emotional symptoms premenstrually, some being severe enough to be diagnosed as premenstrual dysphoric disorder (PMDD); some recent studies suggest that PMDD is biologically different from major depression; 2) While pregnancy does not increase the risk for depression, women with a past history of depression are at risk for recurrent episodes or relapse if antidepressant medications are discontinued; 3) Hormonal changes during the postpartum period may trigger symptoms of postpartum depression; 4) Almost half of perimenopausal women are clinically depressed, and over a third experience their first episode of depression in the perimenopausal period. The increase in major depressive episodes during this period has been linked to erratic gonadal hormonal changes.

Las mujeres poseen alrededor del doble de posibilidades que los hombres de sufrir depresión. Se ha planteado como hipótesis que los eventos reproductivos (ej. premenstrual, pre y postparto, transición menopáusica) pueden representar periodos de vulnerabilidad para la depresión, en parte, debido a la elevada sensibilidad a las intensas fluctuaciones hormonales. 1) La mayoría de las mujeres informan síntomas físicos o emocionales premenstruales, siendo algunos suficientemente severos para ser diagnosticados como trastorno disfórico premenstrual (TDPM); algunos estudios recientes sugieren que el TDPM es biológicamente diferente de la depresión mayor; 2) Mientras que el embarazo no aumenta el riesgo para la depresión, las mujeres con una historia pasada de depresión están en riesgo para episodios recurrentes o recaída si se discontinúan los medicamentos antidepresivos; 3) Los cambios hormonales durante el período del postparto pueden gatillar síntomas de depresión postparto; 4) Casi la mitad de las mujeres perimenopáusicas están clínicamente deprimidas y sobre un tercio experimenta su primer episodio de depresión en el período perimenopáusico. El aumento de los episodios depresivos mayores durante este período se ha relacionado con cambios erráticos de las hormonas gonadales.

Teoría de la mente: una revisión acerca del desarrollo del concepto / Theory of the mind: a review about the development of the concept

El término "Teoría de la Mente" se refiere a una habilidad cognitiva compleja, que permite que un individuo atribuya estados mentales a sí mismo y a otros. Es un sistema de conocimientos que permite inferir creencias, deseos, sentimientos, y de esta manera conseguir interpretar, explicar o comprender los comportamientos propios y de otros, así como predecirlos y controlarlos. Para cumplir con el objetivo propuesto de exponer el desarrollo del término, se abordarán teóricos que precedieron el concepto y otros posteriores a su desarrollo.. Todos ellos han colaborado de manera directa o indirecta a la consolidación y desarrollo de esta propuesta teórica. La Teoría de la Mente ha sido objeto de un considerable esfuerzo de investigación y se ha convertido en un importante constructo teórico que ha dado lugar a una serie de posturas que la caracterizan, dentro de las cuales se encuentran: teoría-teoría; teorías de módulos innatos, teorías de simulación, la construcción social de la mente y teorías neurobiológicas.

The term "Theory of Mind" refers to a complex cognitive skill that allows an individual to attribute mental states to himself and others, is a system of knowledge that we infer beliefs, desires, feelings and thus achieve interpret, explain or understand, as if to predict and control the behavior of themselves and others. According to the goal of exposing the development of the term, addressing theoretical concept that proceeded and later to him, they have collaborated in a direct or indirect consolidation and development of this theoretical proposal. The theory of the mind has been the subject of considerable research effort and has become an important theoretical construct that led to a series of positions among which are: theory-theory, theory of innate modules, theories simulation, the social construction of the mind, neurobilogical theories.*

Neurobiological basis for learning disorders with a special emphasis on reading disorders / 소아과

Learning disorders are diagnosed when the individual's achievement on standardized tests in reading, mathematics, or written expression is substantially below that expected for age, schooling, and level of intelligence. Subtypes of learning disorders may be classified into two groups, language-based type learning disorders including reading and writing disorder, and nonverbal type learning disorder (NLD) such as those relating to mathematics & visuospatial skills, and those in the autism spectrum. Converging evidence indicates that reading disorder represents a disorder within the language system and more specifically within a particular subcomponent of that system, phonological processing. Recent advances in neuroimaging technology, particularly the development of fMRI, provide evidences of a neurobiological basis for reading disorder, specifically a disruption of two left hemisphere posterior brain systems, one parieto-temporal, the other occipito-temporal. The former is the reading system for beginner reading, the latter for skilled reading. Compensatory engagement of anterior systems around the inferior frontal gyrus(Broca's area) and a posterior(right occipito-temporal) system is noted in persistent poor readers in long-term follow up study. The theoretical model proposed to explain NLD's source is not right hemisphere damage, but rather the white matter model. The working hypothesis of the white matter model is that the underdevelopment of, damage to, or dysfunction of cerebral white matter(long myelinated fibers) is the source of this disorder. The role of an evidence-based effective intervention in the remediation of children with learning disorder is discussed.

Understanding Stress by Neuroscience

Stress can be defined generally as reponses to stressors on the body or in a definition more focused on the central nervous system, it can be defined as alterations in neuro-psychological homeostatic processes. There is a psychological aspect to stress, related to issues such as memory, emotion, arousal, and also a biological aspect which included activation of specific brain and endocrine circuits. This article reviews a series of neurobiological mechanisms aimed at understanding what are pathways by which stress is perceived, processed, and transduced into a neuroendocrine response. Multiple brain structures are involved in the organization of responses to stressful stimuli. Among them the hypothalamus, septohippocampal structures, amygdala, cingulate and prefrontal cortices, hindbrain regions such as the brainstem catecholamine cell body group (A2/C2 cell groups in the nucleus of the tractus solitaris; A1/C1 cell groups in the ventrolateral medulla; A6 cell groups in the locus ceruleus), the parabrachial nucleus, cuneiform nucleus, and dorsal raphe nucleus are prominent structures. We reviewed with the focus on the classic stress circuits: the limbic- hypothalamic-pituitary- adrenal axis (LHPA) and locus ceruleus-norepinephrine (LC-NE) system. Our review indicates that the LHPA stress circuit and LC- NE system are the complex systems with multiple control mechanisms and that these mechanisms are altered in pathological states, such as chronic stress and depression. The holistic features described in this reviews can provide insight into the nature and location of brain circuits and neurotransmitter receptors involved in stress and the treatment of stress-related disorders.

Neurobiological Mechanism of Nicotine Dependence / 대한정신약물학회지

Nicotine, the primary psychoactive components of tobacco smoke, produce diverse neurophysiological and behavioral effects through several brain regions and neurochemical pathways. It acts as an agonist to activate and desensitize nicotinic acetylcholine receptors. Nicotinic signaling leads to activation of reward centers in the CNS, including the mesoaccumbens dopamine system, which ultimately leads to behavioral reinforcement and addiction. Indeed, the actions of nicotine on many systems, including brainstem cholinergic, GABAergic, glutaminergic, noradrenergic, and serotonergic systems, may help to mediate nicotine effects related to addiction. And many years of smoking induces neuroadaptations in acetylcholine and dopamine systems. Moreover, the long-term synaptic changes results in learned behaviors and memory which are associated with smoking. We reviewed the nicotinic synaptic mechanisms in midbrain dopaminergic areas. In summary, nicotine as obtained from tobacco interacts with multiple nicotinic acetylcholine receptor subtypes on dopamine, GABA, glutaminergic neuron to produce not only the acute positive reinforcement but also the synaptic changes associated with learning and memory.

Genetic and Neurobiological Etiologies of Alcohol Dependence / 신경정신의학

The etiologies of alcohol dependence may be divided into three factors:biological, psychological, and social factors. Among these, many of the current articles deal with the genetic factors, due to rapid developments in methodology and so on. Because of these reasons, it is thought that it would be worthful to review the articles related to the genetic etiologies and other neurobiological etiologies of alcohol dependence at this point. Because alcohol dependence is a complicated and heterogenous disease, it is not likely to be associated with a single gene polymorphism. And as it is still early times in identifying its genetic etiology, I think it is not easy to make conclusion in this field now. However, I believe that many recent studies using endophenotype and haplotype will give us more promising results. The fact that unlike other substances, alcohol dose not act on only one or two neurotransmitter receptors makes neurobiological research to be not easy one. It is interesting that some of the articles reported in this fields recently dose not confined to brain reward system but extended to CRF or molecular biology.

Post-Stroke Apathy and Anxiety

This paper reviews the frequency, clinical and neurobiological correlates, and treatments of apathy and anxiety following stroke. Apathy is defined as diminished motivation not attributable to decreased level of consciousness, cognitive impairment, or emotional distress. Apathy is a common neuropsychiatric manifestation following stroke, affecting up to 22.5-50% of patients. Post-stroke apathy frequently coexists with depression and is positively correlated with advancing aging. It was reported that poor ADL and cognitive function was related with apathy, while even greater impairment was associated with the presence of both apathy and depression. It has been suggested that apathy in stroke patients may be mediated by posterior limb of internal capsule, frontal subcortical pathway, or corticolimbic-reticular subsystem. Recently the possibility of pharmacological treatment of apathy following apathy has been raised, although there was no controlled trials addressing the issue. Generalized anxiety disorder (GAD), the most common form of anxiety after stroke, occurs in up to 26.9-28% of stroke patients. Many patients with GAD also have depression. It was reported that GAD following stroke had usually chronic course and negative impact to the physical and social recovery of patient. Post-stroke anxiety cannot be explained only by the psychological reaction to stroke and its possible physical complication, but is likely to be significantly associated with the pathophysiological mechanism caused by brain injury. Lorazepam, buspirone and some antidepressants, such as SSRI, SNRI, and nonsedating TCA, can be tried, although there was no controlled trials addressing the treatment of anxiety following stroke. In conclusion, apathy and anxiety are very common neuropsychiatric manifestation following stroke and seem to have negative influences to the functional recovery of patients. Therefore, it is needed to apply active treatments, especially including pharmacological approaches, to them.