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Epigenetics of anxiety and stress–related disorders is the field studying the relationship between epigenetic modifications of genes and anxiety and stress-related disorders, including mental health disorders such as generalized anxiety disorder (GAD), post-traumatic stress disorder, obsessive-compulsive disorder (OCD), and more.
Key symptoms include excessive anxiety about multiple events and issues, and difficulty controlling worrisome thoughts, that persists for at least 6 months. Antidepressants provide a modest-to-moderate reduction in anxiety in GAD, [25] and are superior to placebo in treating GAD. The efficacy of different antidepressants is similar.
The locus coeruleus is the major source of noradrenergic innervation in the brain and sends widespread connections to rostral (cerebral cortex, hippocampus, hypothalamus) and caudal (cerebellum, brainstem nuclei) brain areas [24] and. [25] Indeed, an alteration of this structure could contribute to several symptoms observed in MECP2-deficient mice.
“Estrogen, particularly estradiol, the strongest form, plays a critical role in the brain’s health and functionality, earning it the title of the ‘master regulator’ of women’s brain health.
A hypothesized gene–environment interaction between the short/short allele of the 5-HTTLPR and life stress as predictor for major depression has suffered a similar fate: after an influential [34] initial report in 2003 [35] there were mixed results in replication in 2008, [36] and a 2009 meta-analysis was negative. [37] See 5-HTTLPR for more ...
Amygdala (in red) brain structures linked to anxiety disorders. The pathophysiology of GAD is an active and ongoing area of research often involving the intersection of genetics and neurological structures. [8] Generalized anxiety disorder has been linked to changes in functional connectivity of the amygdala and its processing of fear and ...
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