A review of epigenetic contributions to post-traumatic stress disorder
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Post-traumatic stress disorder (PTSD) is a syndrome which serves as a classic example of psychiatric disorders that result from the intersection of nature and nurture, or gene and environment. By definition, PTSD requires the experience of a traumatic exposure, and yet data suggest that the risk for PTSD in the aftermath of trauma also has a heritable (genetic) component. Thus, PTSD appears to require both a biological (genetic) predisposition that differentially alters how the individual responds to or recovers from trauma exposure. Epigenetics is defined as the study of changes in organisms caused by modification of gene expression rather than alteration of the genetic code itself, and more recently it has come to refer to direct alteration of DNA regulation, but without altering the primary sequence of DNA, or the genetic code. With regards to PTSD, epigenetics provides one way for environmental exposure to be "written" upon the genome, as a direct result of gene and environment (trauma) interactions. This review provides an overview of the main currently understood types of epigenetic regulation, including DNA methylation, histone regulation of chromatin, and noncoding RNA regulation of gene expression. Furthermore, we examine recent literature related to how these methods of epigenetic regulation may be involved in differential risk and resilience for PTSD in the aftermath of trauma.
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El trastorno de estrés postraumático (TEPT) constituye un síndrome que sirve como ejemplo clásico de los trastornos psiquiátricos que resultan de la intersección entre la naturaleza y la crianza, o el gen y el medio ambiente. Aunque por definición, el TEPT requiere la experiencia de una exposición traumática, los datos sugieren que el riesgo de TEPT después del trauma tiene también un componente hereditario (genético). Por lo tanto, el TEPT parece requerir de una predisposición biológica (genética) que altere de manera diferencial la forma en que el individuo responde o se recupera de la exposición traumática. La epigenética se define como el estudio de los cambios en los organismos causados por la modificación de la expresión génica en lugar de la alteración del código genético en sí mismo, y más recientemente se ha referido a la alteración directa de la regulación del ADN, pero sin cambios en la secuencia primaria del ADN o en el código genético. En relación con el TEPT, la epigenética constituye una forma de "escritura" de la exposición ambiental sobre el genoma, como resultado directo de las interacciones genéticas y ambientales (trauma). En esta revisión se entrega una visión general de los principales tipos de regulación epigenética conocidos en la actualidad, como la metilación del ADN, la regulación de la histona de la cromatina y la regulación de la expresión génica del ARN no codificante. Además, se examina la literatura reciente relacionada con la forma en que estos métodos de regulación epigenética pueden estar involucrados en el riesgo diferencial y en la resiliencia para el TEPT después del trauma.

Le syndrome de stress post-traumatique (SSPT) est un exemple classique de trouble psychiatrique résultant du croisement de l'inné et de l'acquis, ou du gène et de l'environnement. Par définition, le SSPT sous-entend une exposition à un traumatisme et cependant, d'après certaines données, le risque de SSPT dans les suites d'un traumatisme a aussi une composante héritable (génétique). Le SSPT semble donc nécessiter une prédisposition biologique (génétique) qui modifie différemment la façon dont la personne répond à ou guérit d'une exposition à un traumatisme. L'épigénétique se définit comme l'étude des changements dans l'organisme provoqués par une modification de l'expression des gènes plus que par une modification du code génétique lui-même ; plus récemment, l'épigénétique renvoie à une modification directe de la régulation de l'ADN mais sans changement de la séquence primaire de l'ADN ou du code génétique. Dans le cadre d'un SSPT, l'épigénétique permet d' « inscrire ¼ l'exposition à l'environnement dans le génome, en tant que résultat direct des interactions du gène et de l'environnement (traumatisme). Cet article propose une vision globale des principaux modes de régulation épigénétique actuellement compris, dont la méthylation de l'ADN, la régulation de la chromatine par les histones et la régulation de l'expression génique par l'ARN non codant. En outre, nous analysons la littérature récente qui étudie la façon dont ces méthodes de régulation épigénétique sont impliquées dans les différents risques et résilience pour le SSPT à la suite d'un traumatisme.

Recent Genetics and Epigenetics Approaches to PTSD.

PURPOSE OF REVIEW: Following a life-threatening traumatic exposure, about 10% of those exposed are at considerable risk for developing posttraumatic stress disorder (PTSD), a severe and disabling syndrome characterized by uncontrollable intrusive memories, nightmares, avoidance behaviors, and hyperarousal in addition to impaired cognition and negative emotion symptoms. This review will explore recent genetic and epigenetic approaches to PTSD that explain some of the differential risk following trauma exposure. RECENT FINDINGS: A substantial portion of the variance explaining differential risk responses to trauma exposure may be explained by differential inherited and acquired genetic and epigenetic risk. This biological risk is complemented by alterations in the functional regulation of genes via environmentally induced epigenetic changes, including prior childhood and adult trauma exposure. This review will cover recent findings from large-scale genome-wide association studies as well as newer epigenome-wide studies. We will also discuss future "phenome-wide" studies utilizing electronic medical records as well as targeted genetic studies focusing on mechanistic ways in which specific genetic or epigenetic alterations regulate the biological risk for PTSD.

Hydroxyl radical and superoxide dismutase in blood of patients with Parkinson's disease: relationship to clinical data.

Hydroxyl radical (.OH) levels in blood, superoxide dismutase (SOD) activity in plasma (plasma-SOD) and in red blood cells (RBC) relative to Cu,Zn-SOD (SOD1) protein (RBC-SOD/SOD1), SOD1 protein in RBC (SOD1/RBC) and plasma (SOD1/plasma), and Mn-SOD protein in plasma (SOD2/plasma) were measured in patients with Parkinson's disease (PD), multiple-system atrophy (MSA) with parkinsonism, and in control subjects. Patients with PD had significantly higher.OH and plasma-SOD values and significantly lower RBC-SOD/SOD1 and SOD1/RBC values than the corresponding MSA and control values. In PD, RBC-SOD/SOD1 values were significantly lower in older patients and were negatively correlated with age.OH levels were significantly higher in PD patients with early onset, a long period of illness or severe Yahr stage, and were negatively correlated with onset and positively correlated with duration of illness. RBC-SOD/SOD1 values in PD patients who received pergolide therapy were significantly higher than those in PD patients who received neither pergolide nor bromocriptine therapy. Therefore, the higher.OH level and the lower SOD1 activity may play a role in the onset and progression of PD, and pergolide may act neuroprotectively by inducing SOD1 activity.

Senile delirium with special reference to situational factors and recurrent delirium.

Factors initiating senile delirium were examined in 129 elderly inpatients (65 years or older). Sixty-eight patients were males and 61 females, with a mean age of 76.3 years. Delirium developed in most cases on the first two days of admission in the hospital, and the admission appeared to be a key factor precipitating delirium in about 30% of the patients. Delirium resolved or improved in 80% of the patients, but usually persisted in patients with dementia. Senile delirium tended to reappear repeatedly in patients whose episode of delirium lasted for more than 2 weeks, was associated with dementia, or had a prior history of delirium.