Pathophysiology of Depression: Analysis
Depression is one of the most distinctive diseases that affect society in the 21st century due to the blurring of work-life balance and excessive emotional fulfillment. In fact, depression is a severe neuropsychiatric disorder that affects over 264 million individuals worldwide. According to current estimates, about one-fifth of the general population will suffer from depression at some point in their lives. Currently, less than 50 % of patients with distinctive symptoms of depression receive adequate therapy, owing in part to a lack of understanding of the biology of depression (Huang et al., 2021). It is critical to involve pathophysiology in studying depression since it is a disorder with a complicated etiology that appears to include numerous brain areas. In particular, these areas include hippocampus, prefrontal cortex, and cerebellum, according to neuroanatomical and imaging investigations in patients.
One of the benefits of depression analysis might be for scientists to approach the studies from different perspectives owing to the diversity of its influence on personal life. From a traditional standpoint, stress and depression are linked to cell shrinkage and decreased synaptic connection in brain areas such as the hippocampus and prefrontal cortex, which contribute to depressive symptoms, and antidepressant therapy can repair these deficiencies. The significance of neurotrophic factors, notably brain-derived neurotrophic factors, has received special attention because these factors significantly affect the activity-dependent control of synaptic plasticity (Wang et al., 2022). At the same time, scientists evidenced that in the case of negative exposure to stress and depression, the human organism diminishes BDNF expression in the hippocampus. Consequently, antidepressants treatment can up-regulate BDNF in the adult brain and reverse the effects of stress by appropriately evaluating BDN factor.
From the other time-adjusted perspective, the depression might be explained through mitochondria dysfunctional activity. More specifically, mitochondria are crucial for giving energy to an organism’s cells while controlling oxidative stress and apoptosis. Scientists substantially evidence that mitochondria-related abnormalities are common during depression or chronic stress (Allen et al., 2021). Similar researches enforce the concept that extreme psychosocial stress causes mitochondrial malfunction, increasing the risk of developing depressive symptoms. By implementing high-quality approaches to evaluate mitochondrial dysfunction, scientists might significantly advance in the domain of effective depression treatment.
Pathophysiology of Depression: Comparison and Discussion
In this case study, two possible drugs are prescribed for depression treatment. On the one hand, the new antidepressant agomelatine, which combines the features of a 5-HT2C antagonist and a melatonergic MT1/MT2 receptor agonist, has been shown to be highly successful in resetting the disrupted sleep/wake cycle (Stein, 2021). In fact, agomelatine is being used to treat depressive individuals who have changes in the amplitude and shape of their melatonin secretion cycle. Agomelatine has also been proven to be beneficial in the treatment of sleep disorders and the clinical condition of people suffering from the seasonal affective disorder. Because agomelatine is the first antidepressant to directly stimulate melatonin activity, it may be administered instead of another medication (Stein, 2021). Agomelatine directly boosts noradrenaline and dopamine activity by acting like melatonin at the melatonin’s target areas (Wang et al., 2022). Finally, there are no challenges in incorporating agomelatine into everyday use because it interacts organically with all other dietary components except milk-based goods.
Ketamine, on the other hand, is a medication that causes fast synaptic and antidepressant behavioral effects that are dependent on the activity-dependent release of BDNF. This quick BDNF release varies from usual monoaminergic drugs, which require chronic administration to achieve a gradual increase of BDNF expression, commensurate with the time lag for therapeutic efficacy (Riggs & Gould, 2021). The sole disadvantage of using ketamine is that it can cause severe blood pressure swings, which may be considerably worse if the substance is consumed. The most notable feature of ketamine is its efficacy in a short period with a low intensity of drug use. In terms of the drug’s effect on glutamate receptors, regrowing and reactivating synapses improves the brain’s ability to adapt, which may help it move out of depression. In terms of the drug’s impact on glutamate receptors, regrowing and reactivating synapses improves the brain’s ability to adapt, which may aid in the brain’s transition out of depression (Riggs & Gould, 2021). That might also explain why antidepressants or psychotherapy that didn’t work before ketamine may now work afterward. Last but not least, the medicine may interact with all other supporting drugs and even enhance its efficacy when used in conjunction with other medications.
When it comes to pathophysiology role in adolescent depression treatment, it is critical to understand that specific drugs consummation might play an important role in physical exposure to young adults. However, the main approach for scientists and doctors should be focused on individual work with the patients. In the case of a simple medical prescription type of treatment, an adolescent might experience a significant but inconsistent and short-term increase of general emotional background. In fact, the role of professional medicine is to consolidate the effect of the treatment course so that young adults will know how to practically fight depression in the future.
References
Allen, J., Caruncho, H. J., & Kalynchuk, L. E. (2021). Severe life stress, mitochondrial dysfunction, and depressive behavior: A pathophysiological and therapeutic perspective.Mitochondrion, 56, 111–117. Web.
Huang, M., de Koning, T. J., Tijssen, M. A., & Verbeek, D. S. (2021). Cross-disease analysis of depression, ataxia and dystonia highlights a role for synaptic plasticity and the cerebellum in the pathophysiology of these comorbid diseases.Biochimica et Biophysica Acta (BBA) – Molecular Basis of Disease, 1867(1), 165976. Web.
Riggs, L. M., & Gould, T. D. (2021). Ketamine and the future of rapid-acting antidepressants.Annual Review of Clinical Psychology, 17(1), 207–231. Web.
Stein, D. J. (2021). Evidence-based pharmacotherapy of generalized anxiety disorder: Focus on agomelatine. Advances in Therapy, 38(S2), 52–60. Web.
Wang, Y. Q., Jiang, Y. J., Zou, M. S., Liu, J., Zhao, H. Q., & Wang, Y. H. (2022). Antidepressant actions of melatonin and melatonin receptor agonist: Focus on pathophysiology and treatment. Behavioural Brain Research, 420. Web.