Pathophysiology Of Depression

Depression is a serious illness that can worsen or last for years if it is left untreated. Depression can occur in a number of ways for different reasons. It is common to feel depressed as a reaction to loss, life's struggles, or an injured self-esteem. When these feelings become too much to handle they can prevent you from living a normal, healthy life. If you or a family member think you are experiencing depression signs to look out for include difficulty concentrating, fatigue, guilt, worthlessness, Insomnia, Irritability, restlessness, and thoughts of suicide. These are only some of the signs associated with depression, and if symptoms worsen over time a trip to the doctor is necessary. Unfortunately, a lot of the people who experience symptoms never do get diagnosed or treated for their illness because they are too afraid to speak out.

Xekardaki, A., Santos, M., Hof, P., Kövari, E., Bouras, C., & Giannakopoulos, P. (2012). Neuropathological substrates and structural changes in late-life depression: The impact of vascular burden. Acta Neuropathologica, 124(4), 453-64. doi:http://dx.doi.org.southuniversity.libproxy.edmc.edu/10.1007/s00401-012-1021-5

The cerebral cortex directs functions like speech, behavior, reactions, movement, thinking, and learning. In fact, some research suggests that bipolar disorder originates with problems with the thalamus, which links sensory input to good and bad feelings. The hippocampus also affects depression. It, like the amygdala, is part of the limbic system. It is vital in processing long-term memory. This section of the brain registers recurring fear. In people with clinical depression, the hippocampus is much smaller. Research suggests, even, that ongoing exposure to stress impairs the growth of nerve cells in this part of the brain. One of the most important jobs of the brain is to process senses, through neurons. Neurotransmitters are specific substances that help relay information to the brain. Scientists have identified many neurotransmitters that affect depression. A lack or excess of the neurotransmitters acetylcholine, serotonin, norepinephrine, dopamine, glutamate, lithium carbonate and gamma-aminobutyric acid are thought to contribute to depression. Acetylcholine is involved in learning and enhances memory. Serotonin helps regulate sleep, appetite, and mood, and inhibits pain. Research shows the idea that many depressed people have reduced levels of serotonin. Low levels of a byproduct of serotonin have been linked to a high risk for suicide. Norepinephrine is a neurotransmitter which constricts blood vessels and raises blood pressure. An excess in

Clinical Depression is a serious common neurological disorder that can affect anyone from the adolescents to the elderly. Clinical Depression affects the mood, thoughts, feelings, and behaviors, and symptoms could become severe if left untreated. Clinical Depression is widespread and common, but also misunderstood and we should be well informed on the causes, effects, and treatments of depression.

Another interesting finding in research, is that of reduced hippocampal volume in depressed patients (Roy & Campbell, 2013).. There are various models accounting for this such as the neurotoxicity hypothesis which states that the reduction in volume occurs because of prolonged stress and hormone levels. The vulnerability hypothesis states that individuals with a familial risk of depression have a significantly smaller hippocampus than controls (Chan et al., 2016). The Chan et al. (2016) study examined individuals with depression and healthy controls. The participants with depression had reduced hippocampal volume when compared to the control group. The researchers posit reduced hippocampal volume as a possible neural marker of depression and the potential for this to be viewed as a vulnerability marker for future depressive episodes (Assareh et al., 2015). It can be theorized that Toni and her family may have reduced volume of the

The pathophysiology of depression is multifaceted and difficult to pinpoint. Depression can arise from a multitude of precipitating factors, both external and internal to the patient. There are varying theories about the cause of depression, each of which “are based on studies investigating psychosocial stress and stress hormones, neurotransmitters such as serotonin, norepinephrine, dopamine, glutamate and gamma-aminobutyric acid (GABA), neurocircuitry, neurotrophic factors, and circadian rhythms” (Hasler, 2010). Due to the vast immensity of theories available, Woo, & Robinson (2016) recommends that treatment for depression should be tailored to each patient and their disease state individually. In Mary Smith’s case her depression appears

Although many studies have shown that impaired neurotransmission of serotonergic and dopaminergic pathways are related to depression [2], the pathophysiology of depression is yet to be fully elucidated [3]. Several studies are being conducted to unravel the underlying mechanism in evaluating the therapeutic efficacy of antidepressants [4,5]. More so, chronic stress exposure has been found to cause atrophy of neurons in rodent hippocampus. [6,7] As such, decreased hippocampal plasticity might be closely connected to depression. Recent studies have found that administration of antidepressant agents to either stress-induced models or patients could heighten developed neurons in the hippocampus, which in turn attenuates the depression symptoms [8,9]. Researches have demonstrated that the expression of SYP is reduced in brain of depressed patients, suggesting a correlation to the pathophysiology of depression [10,11]. Brain magnetic resonance imaging shows that hippocampal volume is significantly smaller in patients with depression compared with normal control [12]. In vitro experiments have also established that depression ensues along with high levels of cell apoptosis as well as increased protein level of Beclin 1 and LC3 [13, 14]. Thus, apoptosis and autophagy

Impaired serotonin function has clearly demonstrated to be linked to clinical depression, because low levels of serotonin may negatively affect mechanisms involved in maintaining recovery from depression. However, there is evidence the serotonin pathways may not directly influence mood but may be important mechanisms in depression due to an indirect consequence of shifts in autonomic emotional responses, i.e., the impaired function may simply cause emotional responses to become unstable contributing to depression. Therefore, Prozac, which acts as an inhibitor of the mechanism that reduces serotonin, can help to reduce this emotional imbalance. However, serotonin alone is often not sufficient in treating depression, as there are many mechanisms involved that are associated with depression.

Everyone will have a sad moment in their life, whether it is a death, a friend betraying he or she, or not getting accepted to the college of his or her choice. Depression can be described with many different words, but it will come down to sadness. People who live with depression will see lack of joy, energy, and happiness. They will not enjoy life, or living. They see it as pointless and useless. Many people will have a depressing moment at some point in their lifetime. The people who develop depression do not have to be poor or unsuccessful. They can be making millions a year and still be depressed, showing that money and success does not guarantee happiness. To be able to fully understand what depression is, one will need to know the

In multiple other studies, depression vulnerabilities have been examined independently. However, this study proposes to look at the interrelatedness of cognitive, behavioral and interpersonal depression vulnerabilities at varying levels of depressive symptoms in patients with acute coronary syndrome (ACS) (Rieckmann, Burg, Gerin, Chaplin, Clemow & Davidson, 2006).

Research has determined that depression is identified by an individual's failure to concentrate, biases seem to be implying that this comes from a negative set of memories and experiences that make up a persons’ beliefs. This mind set results in a deeply thoughtful style described by a lack of logical thinking which leads to depressed emotions and behaviours. The neurobiology behind depression shows that changes in the brain system are commonly linked to this theoretical way of thinking. This similarity proves the cognitive process behind the theory of depression and it also shows the noticeable features of a depressed brain described by neurobiologists

Doctors are not sure what causes depression, but studies have shown that there is a change in brain activity and brain shape with the rapid change in a person’s mood. The brain is reported to shrink, or at least certain parts do, such as the hippocampus, which function is to store and create a human’s memories and the frontal lobes which are involved in motor function, problem solving, spontaneity, memory, language, initiation, judgment, impulse control, and social and sexual behavior. This destruction of the brain is linked to Alzheimer’s and other forms of dementia.

Depression effects different aspects of the anatomy of the brain. A common hypothesis is that depression stems from the limbic system (Carroll et al.; 1976). The limbic system is the part of the brain that regulates emotions, sexual drive, and responses to stimuli like stress; it is the part of the brain that senses “how you feel about stimuli”. The limbic system lies within the temporal lobe and includes the cingulate gyrus, the amygdala, the hypothalamus, the insular cortex, and the hippocampus. The prefrontal cortex (PFC) is related to the expression of personality, and is broadly divided into three sections: the dorsolateral portion, the orbitofrontal or paralimbic portion, and the anterior cingulate cortex. The dorsolateral portion of

In addition, the word hippocampal pertains to the hippocampus, which remains accountable for short-term and long-term memory. Thus, to determine if both specific aims are true or false, the study was established on “12 in-patients with depression receiving antidepressant pharmacological treatment referred for ECT” (Nordanskog et al., 2014, p. 303). And to ensure that the researchers selected the proper patients for the study, they tested the patients with the Montgomery-Asberg Depression Rating Scale (MADRS) and a neurological test battery, before and after ECT. The assessments were repeated for 6 and 12 months with a baseline of 10, and hippocampal volumes were measured by the usage of a Tesla MRI. As a result, the left hippocampal would significantly increase for the first couple of months; however, the hippocampal would return to the starting point when patients would meet for the 6 month. Also, depression levels would decrease among patients after a couple of ECT sessions, which reinforced that ECT remains as an effective method to reduce

: According to mechanisms of inflammation- associated depression which cytokines plays a major role in progression of these disorders open new possibilities for developing anti-inflammatory drugs or new anti-depressant compounds targeting neuroinflammation or its pathways. Also an effective strategy for detecting depression in the early stage can prevent neuroinflammation subsequently neuroinflammatory