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1.
Psychiatry Investigation ; : 4-15, 2019.
Artigo em Inglês | WPRIM | ID: wpr-741923

RESUMO

To conceptualize a novel bio-psychosocial-behavioral treatment model of panic disorder (PD), it is necessary to completely integrate behavioral, psychophysiological, neurobiological, and genetic data. Molecular genetic research on PD is specifically focused on neurotransmitters, including serotonin, neuropeptides, glucocorticoids, and neurotrophins. Although pharmacological interventions for PD are currently available, the need for more effective, faster-acting, and more tolerable pharmacological interventions is unmet. Thus, glutamatergic receptor modulators, orexin receptor antagonists, corticotrophin-releasing factor 1 receptor antagonists, and other novel mechanism-based anti-panic therapeutics have been proposed. Research on the neural correlates of PD is focused on the dysfunctional “cross-talk” between emotional drive (limbic structure) and cognitive inhibition (prefrontal cortex) and the fear circuit, which includes the amygdala-hippocampus-prefrontal axis. The neural perspective regarding PD supports the idea that cognitive-behavioral therapy normalizes alterations in top-down cognitive processing, including increased threat expectancy and attention to threat. Consistent with the concept of “personalized medicine,” it is speculated that Research Domain Criteria can enlighten further treatments targeting dysfunctions underlying PD more precisely and provide us with better definitions of moderators used to identify subgroups according to different responses to treatment. Structuring of the “negative valence systems” domain, which includes fear/anxiety, is required to define PD. Therefore, targeting glutamate- and orexin-related molecular mechanisms associated with the fear circuit, which includes the amygdala-hippocampus-prefrontal cortex axis, is required to define a novel bio-psychosocial-behavioral treatment model of PD.


Assuntos
Glucocorticoides , Biologia Molecular , Fatores de Crescimento Neural , Neuropeptídeos , Neurotransmissores , Antagonistas dos Receptores de Orexina , Transtorno de Pânico , Pânico , Serotonina
2.
Chinese Journal of Pharmacology and Toxicology ; (6): 1185-1193, 2017.
Artigo em Chinês | WPRIM | ID: wpr-705236

RESUMO

Post-traumatic stress disorder (PTSD) is a mental disorder that develops after individual exposure to one or more traumatic events.Natural disasters and war are the major primers of PTSD.Tt is affracting more attention due to the high prevalence in war veterans and natural disasters.The risk factors range from gender,environment to physiology.Hypothalamic-pituitary-adrenal (HPA) axis plays an important role in stress reaction and dysfunction of HPA axis leads to disorder of neuroendocrine.In addition,chronic inflammation,including adaptive and innate immune response disorder,has been reported in many PTSD studies.Neural imaging studies have found that there are significant changes in the brain structure and neural circuits of PTSD patients.However,the biological mechanism underlying PTSD is largely unknown.Currently,based on the clinic symptoms of PTSD patients,anti-depression and anxiety drugs are the first choice for treatment,but the outcomes are diverse.Some potential therapeutic drugs or avenues that are derived from the identified targets are still under investigation.In this review,we overview and summarize the biological changes of PTSD,focusing on disorder of neuroendocrine,chronic inflammation,brain structure and circuits changes and therapeutic strategies in clinical and preclinical trials.This review aims to will provide new ideas for revelation of PTSD mechanisms and develop novel therapies.

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