248 research outputs found

    PTSD and Current Translational Research

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    Analysis of Kinase Gene Expression in the Frontal Cortex of Suicide Victims: Implications of Fear and Stress†

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    Suicide is a serious public health issue that results from an interaction between multiple risk factors including individual vulnerabilities to complex feelings of hopelessness, fear, and stress. Although kinase genes have been implicated in fear and stress, including the consolidation and extinction of fearful memories, expression profiles of those genes in the brain of suicide victims are less clear. Using gene expression microarray data from the Online Stanley Genomics Database1 and a quantitative PCR, we investigated the expression profiles of multiple kinase genes including the calcium calmodulin-dependent kinase (CAMK), the cyclin-dependent kinase, the mitogen-activated protein kinase (MAPK), and the protein kinase C (PKC) in the prefrontal cortex (PFC) of mood disorder patients died with suicide (N = 45) and without suicide (N = 38). We also investigated the expression pattern of the same genes in the PFC of developing humans ranging in age from birth to 49 year (N = 46). The expression levels of CAMK2B, CDK5, MAPK9, and PRKCI were increased in the PFC of suicide victims as compared to non-suicide controls (false discovery rate, FDR-adjusted p < 0.05, fold change >1.1). Those genes also showed changes in expression pattern during the postnatal development (FDR-adjusted p < 0.05). These results suggest that multiple kinase genes undergo age-dependent changes in normal brains as well as pathological changes in suicide brains. These findings may provide an important link to protein kinases known to be important for the development of fear memory, stress associated neural plasticity, and up-regulation in the PFC of suicide victims. More research is needed to better understand the functional role of these kinase genes that may be associated with the pathophysiology of suicide

    Startle response related genes

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    The startle reaction (also known as the startle response, the startle reflex, or the alarm reaction) is the psychological and physiological response to a sudden unexpected stimulus, such as a flash of light, a loud noise (acoustic startle reflex), or a quick movement near the face. Abnormalities of startle response have been observed in many stress-related mental disorders, such as schizophrenia and post-traumatic stress disorder (PTSD). However, the molecular mechanisms of startle in stress-associated conditions – for example, whether the startle reaction is associated with any gene variance – is still unknown. In this paper, we will carry out a systematic review by retrieving, assessing, and combining, when applicable, individual studies investigating association of the molecular variation of candidate gene with the startle response. The systematic review is based on the search for numerous publications using the keywords ‘‘startle gene’’ on September 15, 2010 using PubMed, which comprises more than 20 million citations for biomedical literature from MEDLINE and life science journals. A total of 486 publications regarding genes associated with startle have been obtained and reviewed here. There are fewer than 20 publications associating genes with the startle response between 1979, when the first valuable paper was published, and 1999. However, publications have dramatically increase from 2001 and reaches over 70 in 2009. We have characterized them into three categories: startle-associated gene studies in humans, in animals, as well as in both human and animals. This review of research strategy may provide the information for identifying a biomarker for startle response, with the objective of translating research into clinical utility: diagnosis and treatment of stress-induced mental disorders

    Startle response related genes

    Get PDF
    The startle reaction (also known as the startle response, the startle reflex, or the alarm reaction) is the psychological and physiological response to a sudden unexpected stimulus, such as a flash of light, a loud noise (acoustic startle reflex), or a quick movement near the face. Abnormalities of startle response have been observed in many stress-related mental disorders, such as schizophrenia and post-traumatic stress disorder (PTSD). However, the molecular mechanisms of startle in stress-associated conditions – for example, whether the startle reaction is associated with any gene variance – is still unknown. In this paper, we will carry out a systematic review by retrieving, assessing, and combining, when applicable, individual studies investigating association of the molecular variation of candidate gene with the startle response. The systematic review is based on the search for numerous publications using the keywords ‘‘startle gene’’ on September 15, 2010 using PubMed, which comprises more than 20 million citations for biomedical literature from MEDLINE and life science journals. A total of 486 publications regarding genes associated with startle have been obtained and reviewed here. There are fewer than 20 publications associating genes with the startle response between 1979, when the first valuable paper was published, and 1999. However, publications have dramatically increase from 2001 and reaches over 70 in 2009. We have characterized them into three categories: startle-associated gene studies in humans, in animals, as well as in both human and animals. This review of research strategy may provide the information for identifying a biomarker for startle response, with the objective of translating research into clinical utility: diagnosis and treatment of stress-induced mental disorders

    Chemokines as Potential Biomarkers for PTSD in Military Population

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    Post-traumatic stress disorder (PTSD) is a serious mental health concern worldwide among civilians and military personnel. Gaps in our understanding of its biological basis create significant obstacles for accurate diagnosis and assessment of therapeutic interventions. In light of this, investigation of biological factors associated with possible molecular cues of inflammation or neuroimmune disorders, could provide new surrogate markers for PTSD or PTSD treatment response. Analyses to date in deployed military personnel have suggested that sets of chemokines may be useful as biomarkers for PTSD acquired in military operations. Specifically, studies to date suggest that CCL2, CCL15, CCL22, CCL25, CXCL2, and CXCL12 are associated with PTSD onset, while CCL13, CCL20, and CXCL6 are correlated to PTSD risk; CX3CL1 are associated with resilience; CCL3; CXCL11, and CXCL16 are associated with stress response. CCL11, CCL13, CCL20, and CCL25 are correlated with the severity of PTSD symptoms. This chapter reviews the current understanding of potential chemokine markers for PTSD, and the potential chemokines associated with PTSD onset, risk, resilience, as well as stress responses in service members. Although the proposed biomarkers require further validation, these findings may lead to additional knowledge for the education and development of diagnostic and therapeutic approaches for PTSD, not only benefiting military personnel, but civilians as well

    Attention Deficit Hyperactivity Disorder and Risk of Posttraumatic Stress and Related Disorders: A Prospective Longitudinal Evaluation in U.S. Army Soldiers

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    Crossâ sectional associations between attention deficit hyperactivity disorder (ADHD) and posttraumatic stress disorder (PTSD) have been observed, but longitudinal studies assessing this association are lacking. This prospective study evaluated the association between predeployment ADHD and postdeployment PTSD among U.S. Army soldiers. Soldiers who deployed to Afghanistan were surveyed before deployment (T0) and approximately 1 month (T1), 3 months (T2), and 9 months (T3) after their return. Logistic regression was performed to estimate the association between predeployment ADHD and postdeployment (T2 or T3) PTSD among 4,612 soldiers with data at all waves and no record of stimulant medication treatment during the study. To evaluate specificity of the ADHDâ PTSD association, we examined associations among predeployment ADHD, postdeployment major depressive episode (MDE), generalized anxiety disorder (GAD), and suicidal ideation. Weighted prevalence of ADHD predeployment was 6.1% (SE = 0.4%). Adjusting for other risk factors, predeployment ADHD was associated with risk of postdeployment PTSD, adjusted odds ratio (AOR) = 2.13, 95% CI [1.51, 3.00], p < .001, including incidence among soldiers with no predeployment history of PTSD, AOR = 2.50, 95% CI [1.69, 3.69], p < .001. ADHD was associated with postdeployment MDE, AOR = 2.80, 95% CI [2.01, 3.91], p < .001, and GAD, AOR = 3.04, 95% CI [2.10, 4.42], p < .001, but not suicidal ideation. Recognition of associations between predeployment ADHD and postdeployment PTSD, MDE, and GAD may inform targeted prevention efforts. Future research should examine whether treatment of ADHD is protective against PTSD and related disorders in traumaâ exposed individuals.ResumenSpanish Abstracts by Asociación Chilena de Estrés Traumático (ACET)El trastorno de déficit atencional con hiperactividad y el riesgo del trastorno de estrés postraumático y trastornos relacionados: Una evaluación longitudinal prospectiva en soldados del ejército estadounidenseTDAH Y RIESGO DE TEPT EN SOLDADOS DEL EJà RCITO DE EE.UU.Se han observado asociaciones transversales entre el trastorno por déficit de atención con hiperactividad (TDAH) y el trastorno por estrés postraumático (TEPT), pero faltan estudios longitudinales que evalúen esta asociación. Este estudio prospectivo evaluó la asociación entre el TDAH previo al despliegue y el TEPT posterior al despliegue entre los soldados del Ejército de Estados Unidos. Los soldados desplegados en Afganistán fueron encuestados antes del despliegue (T0) y aproximadamente 1 mes (T1), 3 meses (T2), y 9 meses (T3) después de su regreso del despliegue. Se realizó una regresión logística para estimar la asociación entre el TDAH previo al despliegue y el TEPT posterior al despliegue (T2 o T3) en 4.612 soldados con datos en todas las etapas y sin registro de tratamiento con medicamentos estimulantes durante el estudio. Para evaluar la especificidad de la asociación TDAHâ TEPT, examinamos las asociaciones entre el TDAH previo al despliegue, el episodio depresivo mayor posterior al despliegue (EDM), el trastorno de ansiedad generalizada (TAG), y la ideación suicida. La prevalencia ponderada del TDAH previo al despliegue fue de 6.1% (SE = 0.4%). Al controlar los otros factores de riesgo, el TDAH previo al despliegue se asoció con el riesgo de TEPT posterior al despliegue, odds ratio ajustado (AOR en su sigla en inglés) = 2.13, IC del 95% [1.51, 3.00], p <.001, incluida la incidencia entre soldados sin historial previo al despliegue de TEPT, AOR = 2.50, IC del 95% [1.69, 3.69], p <.001. El TDAH se asoció con el EDM posterior al despliegue, AOR = 2.80, IC del 95% [2.01, 3.91], p <.001, y TAG, AOR = 3.04, IC del 95% [2.10, 4.42], p <.001, pero no con ideación suicida. El reconocimiento de las asociaciones entre el TDAH previo al despliegue y el TEPT, el EDM, y el TAG posterior al despliegue puede informar los esfuerzos de prevención específicos. Las investigaciones futuras deberían examinar si el tratamiento del TDAH protege contra el TEPT y los trastornos relacionados en personas expuestas a trauma.æ ½è±¡Traditional and Simplified Chinese Abstracts by the Asian Society for Traumatic Stress Studies (AsianSTSS)ç°¡é« å ç¹ é« ä¸­æ æ ®è¦ ç ±äº æ´²å µå ·å¿ ç ç  ç©¶å­¸æ 翻譯Attention Deficit Hyperactivity Disorder and Risk of Posttraumatic Stress and Related Disorders: A Prospective Longitudinal Evaluation in US Army SoldiersTraditional Chineseæ¨ é¡ : å° æ³¨å ä¸ è¶³æ é åº¦æ´»èº ç è æ £å µå ·å¾ å£ å ç å ç ¸é ç ¾ç ç é¢¨é ª:å° ç¾ å è» äººé ²è¡ ç å ç »ç¸±è²«ç  ç©¶æ ®è¦ : é å¾ ä¸ ç ´æ ç  ç©¶æª¢è¦ å° æ³¨å ä¸ è¶³æ é åº¦æ´»èº ç (ADHD)è å µå ·å¾ å£ å ç (PTSD)ä¹ é ç æ©«æ ·æ §é é £, å ¯æ ¯, æ å ä» æ¬ ç¼ºæª¢è¦ å ©è é é £ç ç¸±è²«ç  ç©¶ã æ ¬å ç »ç  ç©¶æ ¨å ¨é é ç¾ è» æ¨£æ ¬, è© ä¼°æ å½¹å ADHDè· æ å½¹å¾ PTSDç é é £ã æ¨£æ ¬ç ºå å¾ é ¿å¯ æ± æ å½¹ç è» äºº, å ¨æ å½¹å (T0)å å® æ æ å½¹å¾ ç´ 1å æ (T1)ã 3å æ (T2)å 9å æ (T3)æ ¥å èª¿æ ¥ã æ å 以é 輯迴歸å æ å æ æ 波段ç æ ¸æ , ä¼°è¨ 4,612å è» äººæ å½¹å ADHDè· æ å½¹å¾ (T2 æ T3)PTSDç é é £ã ç  ç©¶ä¸­, æ¨£æ ¬ä¸¦ç ¡æ ç ¨è å¥®è ¥ç ©ã ç ºäº è§£ADHDâ PTSDç ç ¹æ® é é £, æ å æª¢è¦ ä»¥ä¸ é  ç ®ä¹ é ç é é £:æ å½¹å ADHDã å® æ æ å½¹å¾ ç å ´é æ é¬±ç¯ æ®µ(MDE)ã å»£æ³ æ §ç ¦æ ®ç (GAD)ã è ªæ®ºæ 念ã æ å½¹å ADHDæ ®é åº¦ç º6.1% (SE = 0.4%)ã å° å ¶ä» é¢¨é ªå  ç´ ä½ èª¿ç¯ å¾ , æ å½¹å ADHDè· æ å½¹å¾ æ £PTSDç é¢¨é ªæ æ é é £(å·²èª¿ç¯ å ç® æ¯ (AOR) = 2.13, 95% CI [1.51, 3.00], p < .001), ç ¶ä¸­å æ ¬æ å½¹å ä¸¦ç ¡PTSDç è» äºº(AOR = 2.50, 95% CI [1.69, 3.69], p < .001)ã ADHDè· å® æ æ å½¹å¾ æ £MDEç (AOR = 2.80, 95% CI [2.01, 3.91], p < .001)å GAD(AOR = 3.04, 95% CI [2.10, 4.42] p < .001)é ½æ é , ä½ è· è ªæ®ºæ å¿µç ¡é ã äº è§£æ å½¹å ADHDè· æ å½¹å¾ PTSDã MDEå GADç é é £, å ¯è ½æ å ©ç ¼å± é å° æ §ç é  é ²å·¥ä½ ã æ ªä¾ ç  ç©¶æ æª¢è¦ å° å å µäººå£«æ ä¾ ADHDæ²»ç , æ ¯å ¦å° å ¶PTSDå ç ¸é ç ¾ç æ ä¿ è­·æ æ ã Simplified Chineseæ  é¢ : ä¸ æ³¨å ä¸ è¶³æ è¿ åº¦æ´»è· ç ä¸ æ £å 伤å å å ç å ç ¸å ³ç ¾ç ç é£ é ©:å¯¹ç¾ å ½å äººè¿ è¡ ç å ç »çºµè´¯ç  ç©¶æ ®è¦ : è¿ å¾ ä¸ ç ´æ ç  ç©¶æ£ è§ ä¸ æ³¨å ä¸ è¶³æ è¿ åº¦æ´»è· ç (ADHD)ä¸ å 伤å å å ç (PTSD)ä¹ é ´ç æ¨ªæ ­æ §å ³è¿ , å ¯æ ¯, æ ä»¬ä» æ¬ ç¼ºæ£ è§ ä¸¤è å ³è¿ ç çºµè´¯ç  ç©¶ã æ ¬å ç »ç  ç©¶æ ¨å ¨é è¿ ç¾ å æ ·æ ¬, è¯ ä¼°æ å½¹å ADHDè· æ å½¹å PTSDç å ³è¿ ã æ ·æ ¬ä¸ºå å¾ é ¿å¯ æ± æ å½¹ç å 人, å ¨æ å½¹å (T0)å å® æ æ å½¹å 约1个æ (T1)ã 3个æ (T2)å 9个æ (T3)æ ¥å è° æ ¥ã æ ä»¬ä»¥é »è¾ å å½ å æ å æ æ 波段ç æ °æ ®, 估计4,612å å 人æ å½¹å ADHDè· æ å½¹å (T2 æ T3)PTSDç å ³è¿ ã ç  ç©¶ä¸­, æ ·æ ¬å¹¶æ  æ ç ¨å ´å¥ è ¯ç ©ã ä¸ºäº è§£ADHDâ PTSDç ç ¹æ® å ³è¿ , æ ä»¬æ£ è§ ä»¥ä¸ é¡¹ç ®ä¹ é ´ç å ³è¿ :æ å½¹å ADHDã å® æ æ å½¹å ç 严é æ é è 段(MDE)ã å¹¿æ³ æ §ç ¦è ç (GAD)ã è ªæ æ 念ã æ å½¹å ADHDæ ®é 度为6.1% (SE = 0.4%)ã å¯¹å ¶ä» é£ é ©å  ç´ ä½ è° è å , æ å½¹å ADHDè· æ å½¹å æ £PTSDç é£ é ©æ æ å ³è¿ (å·²è° è è ç® æ¯ (AOR) = 2.13, 95% CI [1.51, 3.00], p < .001), å½ ä¸­å æ ¬æ å½¹å å¹¶æ  PTSDç å 人(AOR = 2.50, 95% CI [1.69, 3.69], p < .001)ã ADHDè· å® æ æ å½¹å æ £MDEç (AOR = 2.80, 95% CI [2.01, 3.91], p < .001)å GAD(AOR = 3.04, 95% CI [2.10, 4.42] p < .001)é ½æ å ³, ä½ è· è ªæ æ å¿µæ  å ³ã äº è§£æ å½¹å ADHDè· æ å½¹å PTSDã MDEå GADç å ³è¿ , å ¯è ½æ å ©å å± é å¯¹æ §ç é¢ é ²å·¥ä½ ã æ ªæ ¥ç  ç©¶åº æ£ è§ å¯¹å å 人士æ ä¾ ADHDæ²»ç , æ ¯å ¦å¯¹å ¶PTSDå ç ¸å ³ç ¾ç æ ä¿ æ ¤æ åº ãPeer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/146971/1/jts22347_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146971/2/jts22347.pd
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