Stress, psychiatric disorders, molecular targets, and more

被引:19
作者
Atrooz, Fatin [1 ]
Liu, Hesong [2 ]
Salim, Samina [1 ]
机构
[1] Univ Houston, Coll Pharm, Dept Pharmacol & Pharmaceut Sci, Houston, TX 77030 USA
[2] Baylor Coll Med, Houston, TX 77030 USA
来源
MOLECULAR BASIS OF NEUROPSYCHIATRIC DISORDERS: FROM BENCH TO BEDSIDE | 2019年 / 167卷
关键词
EARLY-LIFE STRESS; MAJOR DEPRESSIVE DISORDER; BDNF VAL66MET POLYMORPHISM; ANTENATAL MATERNAL ANXIETY; MEDIAL PREFRONTAL CORTEX; OXIDATIVE DNA-DAMAGE; FACTOR MESSENGER-RNA; NEUROTROPHIC FACTOR; BRAIN-DEVELOPMENT; PSYCHOSOCIAL STRESS;
D O I
10.1016/bs.pmbts.2019.06.006
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Mental health is central to normal health outcomes. A widely accepted theory is that chronic persistent stress during adulthood as well as during early life triggers onset of neuropsychiatric ailments. However, questions related to how that occurs, and why are some individuals resistant to stress while others are not, remain unanswered. An integrated, multisystemic stress response involving neuroinflammatory, neuroendocrine, epigenetic and metabolic cascades have been suggested to have causative links. Several theories have been proposed over the years to conceptualize this link including the cytokine hypothesis, the endocrine hypothesis, the oxidative stress hypothesis and the oxido-neuroinflammation hypothesis. The data discussed in this review describes potential biochemical basis of the link between stress, and stress-induced neuronal, behavioral and emotional deficits, providing insights into potentially novel drug targets.
引用
收藏
页码:77 / 105
页数:29
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