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For example, epigenetic modifications to the gene BDNF (brain derived neurotrophic factor), as well as Drosophila ATF-2 (dATF-2), as a result of stress can be passed on to offspring. Chronic variable stress induces offspring hypothalamic gene expression modifications, including elevated methylation levels of the BDNF promoter in the hippocampus ...
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.
Anxiety is the Big Bad Wolf of the modern wellness conversation: How to get rid of it, how to get to sleep with it, how to meditate it away. But what if there’s another way of interpreting anxiety?
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 ...
The ANS responds reflexively to both physical stressors (for example baroreception), and to higher level inputs from the brain. [ 38 ] The ANS is composed of the parasympathetic nervous system and sympathetic nervous system , two branches that are both tonically active with opposing activities.
Based on the monoamine hypothesis of depression, which asserts that decreased concentrations of monoamine neurotransmitters leads to depressive symptoms, the following relations were determined: "Norepinephrine may be related to alertness and energy as well as anxiety, attention, and interest in life; [lack of] serotonin to anxiety, obsessions ...
A repeat length polymorphism in the promoter of this gene has been shown to affect the rate of serotonin uptake and may play a role in sudden infant death syndrome, aggressive behavior in Alzheimer disease patients, post-traumatic stress disorder and depression-susceptibility in people experiencing emotional trauma.
This conversion can significantly impact estrogen levels in brain areas. These OCD-linked effects have been demonstrated by aromatase knockout mice (ArKO), who lack a functional enzyme to convert androgens to estrogen. This ArKO knockout strategy has provided a model to examine the physiological impact of lower than normal amounts of estrogen. [25]