Journal of Child and Adolescent Psychiatry

Topics of interests include

• The occurrence of PTSD in adolescents
• Neurobiological disorders of PTSD, notably at neurotrophic and inflammation levels
• The underlying mechanism of PTSD and the changes in neuroglia, neuroinflammation, apoptosis and epigenetic modulation
• After PTSD, the pharmacological mechanism of psychotherapeutic drugs
• Molecular mechanisms in both neuroinflammation and adolescent posttraumatic stress disorder

Reviews which include the comparative view, Original research papers as well as short communications and letters on new developments and applications are welcome and are to be written in Standard English. Formatting of the manuscript with headings and Sub headings is necessary and views are to be presented clearly. New approaches are mainly in interest.

To cover the costs of publication, an Article Processing Charge is essential and the charge levied for each article of any type upon acceptance is $900 USD.

Metrics:

Welcomes submissions to the thematic concept on "Neuroinflammation Associated Adolescent PTSD"

The study area:
Posttraumatic stress disorder (PTSD) is a pathological response to a traumatic event. Adolescent PTSD is of particular concern, as PTSD is more chronic and highly prevalent at this crucial developmental stage, coupled with the increased risk for later psychological disorders in life. In recent year, growing evidence have supported that neuroinflammation can play an important role in PTSD. Neuroinflammation may be the key important pathological factor in PTSD, as “neuro-imaging” is associated with significantly decreased numbers of neurons. In PTSD, both macrophages and microglia display impaired and prolonged activation. The main marker of brain inflammation is the activation of microglia. Microglia mediated chronic inflammatory response and plays an important role in the occurrence and development of PTSD. Microglia activated by various causes, release pro-inflammatory cytokines (e. g. IL-6, TNF, IL-1β), free radicals, which are key players in neuronal injury. In turn, neuronal impairment can activate microglia, which can activate neuroinflammation response and trigger neurotoxicity. However, the potential pathological and pharmacological mechanism in the adolescent PTSD still remain further researches.