Alterations in the Immune Response, Apoptosis and Synaptic Plasticity in Posttraumatic Stress Disorder: Molecular Indicators and Relation to Clinical Symptoms

Posttraumatic stress disorder (PTSD) (ICD-10 codes: F43.1, F62.0; DSM-IV-TR code: 309.81) [1, 2] is a complex severe and chronic psychiatric illness influenced by environmental and genetic factors [3-10]. PTSD is an anxiety disorder developed in a person experiencing, wit‐ nessing, or learning about an extreme physically or psychologically distressing event, asso‐ ciated with unprecedented violence [11, 12]. Traumatic events that can trigger PTSD include massacres, mass murder scenes, international, civil, political, ethnic and religious wars, gen‐ ocides, natural and man-made disasters, criminal assaults, serious accidents, terrorist at‐ tacks, incarceration, trafficking, rape and other types of sexual assaults [12-17], life threatening illness and the sudden death of a loved one, serious medical illness, injury, sur‐ gery, hostage, kidnapping, difficult labors, etc [18-20]. Individuals who experience a trauma of this nature may develop symptoms that fall into three distinct clusters: re-experiencing phenomenon; avoidance and numbing; and autonomic hyperarousal. Symptoms usually be‐ gin within the first 3 months after the traumatic event and last for many years, although there may be a delay of months, or even years, before symptoms appear. PTSD patients are characterized by severe emotional state, sharp reduction in adaptive and information receiv‐ ing abilities. They usually remain out of society, become drug addicted, alcoholic and often commit suicide [21-24]. Degrees of risk to develop PTSD from different traumatic events are presented in table 1.