Stress can affect cognitive function in many ways. Stress can cause short-term, acute changes in certain areas of the brain as well as chronic stress leading to changes in the brain which can cause long-term damage to certain brain areas.
The role of ubiquitination in cells is being looked at as a possible cause in neurological loss of function. Repeated stress may contribute to a loss of neurological function by a suppression of glutamatergic transmission by facilitating glutamate receptor turnover, which in turn causes a detrimental effect on the Prefrontal Cortex ( PFC) - dependent cognitive processes. There is a loss of glutamatergic transmission – resulting in reduced synaptic transmission.
The adrenal corticosterone, the major stress hormone plays a role through the activation of the glucocorticoid receptor (GR) and mineralocorticoid receptor (MR) which can induce long-lasting influences particularly on both cognitive and emotional processes.
It is not necessarily stress, but the inappropriate response to stress which seems to be the bigger culprit. The growing evidence is pointing toward inappropriate response to stress as a trigger for much of the mental illnesses.
For example:
Post Traumatic Stress Disorder (PTSD) is associated with hypocortisolaemia (insufficient cortisol)
Depression is associated with hypercortisolaemia (excessive cortisol)
Therefore, corticosteroid hormones are thought to be a key in controlling homeostasis.
Homeostasis refers to stability, balance, or equilibrium within a cell or the body itself. Homeostasis is the ability to maintain a constant internal environment in response to external environmental changes. What is responsible for homeostasis? The nervous system and endocrine system control homeostasis in the body through feedback mechanisms which involve organs and organ systems.
The Prefrontal Cortex (PFC) is a primary target of many of the stress hormones. The Prefrontal Cortex (PFC) is the executive part of the brain making important decisions, responsible for inhibition of distraction, novelty seeking, and includes working memory format.
At this point it, dysfunction of glutamatergic transmission is considered the core feature and fundamental pathology of mental disorders. Even in vitro long-term exposure to corticosterone suppresses glutamate receptors and synaptic transmission.
Chronic stress affects electrophysiological results and biochemical results in the human body.
To understand the potential mechanism underlying the region specificity of the effects of repeated stress on glutamate receptor expression and function of special interest is the PFC, striatum and hippocampus. Regarding specific regions of the brain such as the PFC, striatum and hippocampus – research shows that out of these the PFC seems to be more affected by chronic stress.
The loss of glutamate receptors after repeated stress may involve the increased ubiquitin/proteasome-mediated degradation. The ubiquitin pathway is a key mechanism regarding long-term chronic stress and the neural pathways regarding synaptic activity. As degradation occurs by the ubiquitin-proteasome pathway in PFC neurons, this causes the loss of glutamate receptor expression and function, which leads to the deficit of PFC-mediated cognitive processes. Prefrontal Cortex dysfunction is implicated in various stress-related mental disorders.
Cognitive Symptoms Checklist
Constant worrying
Racing thoughts
Forgetfulness and disorganization
Inability to focus
Poor judgment
Being pessimistic or seeing only the negative side