Neural Plasticity Theory Of Depression Research Paper

Major depressive disorder is one of the most common mental disorders, with a 12-month prevalence of 6.7% of adults in the United States (NIMH). There is no definite etiology of depression, but several risk factors have been identified. Functional and structural changes in the brain have also been explored. The most common treatment for depression is the use of drugs that act on monoamine transmitters, including norepinephrine, dopamine, and serotonin. Decreases in these transmitters, especially serotonin, were hypothesized to play an important role in the cause of depression (Breedlove & Watson, 2013). The serotonin hypothesis led to the development of selective-serotonin reuptake inhibitors (SSRIs), which increase the amount of serotonin in the brain. Further research suggests that the serotonin hypothesis is not entirely accurate and the neurobiology of depression is much more complex. The “chemical imbalance” explanation of depression may not reflect the full range of causes and may be given greater credibility by patients and doctors than is supported by evidence based research.

The depression diseasing our society today is mostly caused by stress related activities. Because our society demands so much out of us we struggle to handle all the stress it throws out us. STanford researchers found people who had depression had smaller hippocampuses; the part of the brain that controls long term memory and emotions. The researchers also found that this smaller hippocampus was caused by a deterioration of it over time, not in one sudden moment. THe deterioration is caused by, you guessed it, stress. However, it’s a double edged sword, because as stress causes the deterioration, it also prevents the healing process by preventing neurons from growing around the

Depression can be defined as a mental disorder that affect the way people think, feel, and act. According to researchers, this mental disorder affects two parts of the brain such as the prefrontal cortex and the hippocampus. This areas of the brain have different role. The prefrontal cortex is the part of the brain that controls attention and focus whereas the hippocampus responsible for learning

There has been a myriad of research investigating the symbiotic relationship between hippocampal volume and major mood disorders (MDD) like depression. Despite being one of the most prevalent illnesses, the underlying pathogenesis and neurobiology of MDD remain unclear. It has been widely documented that patients with a MDD tend to have smaller hippocampal volumes (Sheline et al., 1996, Nordanskog et al., 2014). The hippocampus is known to be closely affiliated with the hypothalamic-pituitary-adrenal axis, which is required to produce glucocorticoids that are involved in stress mechanisms (Chen et al., 2010). Moreover, stressful life events are considered a critical risk factor in the development of depression (Zannas et al., 2013). This, coupled with findings which suggest that depressed patients have difficulty with hippocampal-dependent learning and memory tasks (Gould et al., 1998, Gould et al., 2007), accentuates the relationship between the hippocampus and MDD being mediated through stress. There are various hypotheses regarding what may cause hippocampal volume diminution as a consequence of stress. Major propositions involve hippocampal neurogenesis in the dentate gyrus (Becker and Wojtowicz, 2007), glial numbers, apoptosis (Czeh and Lucassen, 2007) and granule neuron numbers (Boldrini et al., 2013). Other mechanisms that may affect hippocampal volume like neuropil reduction, shifts in fluid balance between the ventricles and brain tissue and changes in

This affects the the brain-derived neurotrophic factor (BDNF)- a crucial factor in the neurobiology of depression. The hippocampus is rich in BDNF, which is related in neuronal growth, survival and maturation, as well as arborization and synaptic plasticity in the adult brain. Stress suppresses BDNF synthesis in the hippocampus showing low concentrations in depressed patients, correlating with the severity of the depression. The use of antidepressant drugs increase its synthesis and signalling in the hippocampus and PFC. In a post-mortem study of depressed patients at the time of death, there were significant differences between the BDNF concentrations in treated and untreated patients. Antidepressants work by balancing neurotransmitters that affect mood and emotion. The use of antidepressants and going to therapy are the most effective ways to treating depression. Weight gain and the feeling of mental numbness is a side effect of antidepressants. Depression can be prevented. Daily exercise, having strong relationships,and watching alcohol intake are ways to prevent depression. Depression is a long term,recurrent condition often taking a chronic course. It is associated with significant morbidity, comorbidity and mortality (suicide and physical illness). In order to achieve and maintain optimum brain function and reduce the risk of recurrence, antidepressant drug treatment full remission is

Depression is a debilitating mental disorder, which can be detrimental to a person’s way of living. For example, depression can cause an individual to have negative thoughts, experience chronic distress, and hopelessness (Pourbabaee, n.d.). Researchers focus on two causes of depression. Those who support the cognitive-behavioral perspective believe depression results from faulty thinking associated with low self-esteem or learned helplessness, as well as environmental influences such as the loss of a loved one or a job. Whereas, those who support the biological perspective believe depression results from the genes a person inherits, chemical imbalances that change the functions of the brain, as well as damage to the anatomy of the brain.

(Ernst, Olson, Pinel, Lam, & Christie, 2006), investigated, antidepressant effects of exercise: Adult neurogenesis refers to the growth of new neurons in the adult brain, initially reports of adult neurogenesis were viewed with a great deal of skepticism, because neurogenic activity had been assumed to be limited to the developmental period; however, the legitimacy of adult neurogenesis in some brain areas has since gained wide acceptance. It is now clear that some regions of the adult mammalian brain contain populations of active progenitor cells that can give rise to new neurons and glia cells. It has been hypothesized that a decrease in the synthesis of new neurons in the adult hippocampus might be linked to major depressive disorder (MDD).

Depression being an affective mood disorder is a serious global public health issue with over 350 million sufferers worldwide8,10,11. Although it is described with feelings of low mood, inadequacy, guilt, low self-worth, loss of motivation, interest, pleasure and concentration; it is also associated with a functional deficit of the monoamine transmitters (serotonin and noradrenaline) in certain brain regions such as amygdala, hippocampus and prefrontal cortex6,10. It can also induce biological symptoms like retardation of thought and action as well as sleep disturbances, loss of appetite and libido and if left untreated, it can eventually lead to disability8,11. Therefore, the pharmacotherapy plays a crucial role in the treatment of depression.

A deficiency in both serotonin and norepinephrine neurotransmitters specifically in the locus coeruleus, and the dorsal raphe nucleus, which both are important in relations to serotonin receptors can cause depression in AD. Individuals who had both AD and depression showed fewer neurons in the two locations when compared to non-demented individuals (Modrego, 2010 as cited by Zubenk, Moossy & Knopp, 1990). The use of animal shows the links of depressive behavior and AD. Ledo et al. (2016) used a mouse model to show an association of amyloid beta oligomers (AβOs) and depressive like behavior. It was hypothesized that AβOs induced depressive behavior in AD by causing an inflammatory response, which was triggered by activation of microglial cells. Ledo et al. (2016) found that AβOs decreased serotonin levels in the mice. This suggest that the decrease levels in the brains are leading to abnormalities in the AβOs, which then causes cognitive impairments.

Depression has dramatically increased over the years. It is becoming a chronic disease for people. According to Wimett and Laustsen (2005), “Depression is a psychiatric disorder that affects an estimated 18 million U.S citizens and is expected to be the second leading cause of death or injury by 2020”. Depression is the change in brain chemistry that comes with a feeling of severe despondency and dejection. Although there are more than several types, the most familiar type is called Major Depressive Disorder. In 2003, Kessler, Berglurd, Demler, … & Wang noted that “Major Depressive Disorder is a common disorder, widely distributed in the population, and usually associated with substantial symptom severity and role impairment”. There are many types of treatment for Major Depressive Disorder, which include various types of therapies, electric shock therapy, and medication. The most common form of treatment is Cymbalta alongside some various types of therapy. Cymbalta is a medicine prescribed by doctors or therapists to reduce the symptoms of depression.

Disruption of hippocampal function, including the capacity for neuroplasticity, could contribute to a range of aspects of major depression. In addition to the role in declarative memory, the hippocampus is the primary regulator of prefrontal cortical function; hippocampus and DLPFC function together to regulate explicit memory. Disruption of hippocampal function in major depression may therefore add to observed deficits in concentration. Hippocampal afferents are important regulators of both the nucleus accumbens and the ventral tegmental area (VTA). It has been suggested that an indirect excitatory projection from hippocampus to VTA is critical for coordinating the firing of VTA cells in response to novelty; impairment of this hippocampal

Two structural proteins, synaptophysin (hereafter: SYP) and microtubule-associated protein 2 (hereafter: MAP-2), which are implicated in neuronal plasticity, were chosen as molecular targets. The underlying reason was to ascertain whether or not gestational stress modifies the expression of the proteins, SYP and MAP-2, in the rat’s hippocampus. If it indeed does, then subsequent monitoring of the recovery process of the stress-induced changes in control and treatment groups would be of prime importance so as to discern and comprehend the roles of these two proteins pertaining the actions of gestational stress administration of

The linkage of serotonin to depression has been known for the past five years. From numerous studies, the most concrete evidence of this connection is the decreased concentration of serotonin metabolites like 5-HIAA (5-hydroxyindole acetic acid) in the cerebrospinal fluid and brain tissues of depressed people. If depression, as suggested, is a result of decreased levels of serotonin in the brain, pharmaceutical agents that can reverse this effect should be helpful in treating depressed patients. Therefore, the primary targets of various antidepressant medications are serotonin transports of the brain. Since serotonin is activated when released by neurons into the synapse, antidepressants function at the synapse to enhance serotonin activity. Normally, serotonin's actions in the synapse are terminated by its being taken back into the neuron then releases it at which point "it is either recycled for reuse as a transmitter or broken down into its metabolic by products and transported out of the brain." As a result, antidepressants work to increase serotonin levels at the synapse by blocking serotonin reuptake (2).

(3) While successful drug therapies which act on neurotransmitters in the brain imply that depression is a neurobiological condition (4), the fact that such medications do not help about 20 percent of depression-sufferers seems to show that not all depression is due to such imbalances. Rather, depression is not caused by one single factor; it is most often caused by many different things. Genetics, biochemical factors, medicines and alcohol, developmental and other external factors, and relationships, marriage and children all have effect on the development of clinical depression. (5) The strongest hypotheses on the pathways to depression are in decreases in the activity of specific neurotransmitters, or the overactivity of certain hormonal systems. (3)

The severity of depression has been supported through scientific evidence that indicates that depression has a biological basis in the brain of a depressed person along with psychological and social implications. Whilst there are many catalysts in a person’s life that can be identified as a possible root cause of depression, such as stressful life events or the death of a loved one, the issue is far more complex, as the biological triggers of depression are not as easily expressed, such as faulty mood regulation in the brain, vulnerable genetics in the DNA, and other medical problems. Many things are altered in the brain of the depressed person. Firstly, what most understand to be an imbalance in the levels of chemicals that regulate emotions, is in reality far more elaborate. The true issue surrounding the many chemicals involved inside and outside of the nerve cells that undergo numerous chemical reaction which make up the dynamic system that is responsible for mood, perceptions, and the way one experiences life you experiences life can be altered in different ways that affect how one lives. Along with the brains chemicals, the connections between nerve cells called neurons decrease and deteriorate, meaning the