Research papers on bipolar disorder
When the genetics of bipolar disorder were first being studied, less precise tools were available, but they still yielded interesting information. For example, studies comparing specific regions of postmortem brain tissue from persons with bipolar disorder with tissue from control subjects have consistently shown that levels of expression of oligodendrocyte-myelin–related genes appear to be decreased in brain tissue from persons with bipolar disorder. For example, investigators have demonstrated that 2 chemically unrelated drugs (lithium and valproate) used to treat bipolar disorder both upregulate the expression of the cytoprotective protein Bcl-2 in the frontal cortex and the hippocampus of rat brains. In 2008, Mathew et al published a review of novel drugs and therapeutic targets for severe mood disorders that focus on increasing neuroplasticity and cellular resiliency. Melanie Klein was one of the major proponents of this formulation. This led to the catecholamine hypothesis, which holds that an increase in epinephrine and norepinephrine causes mania and a decrease in epinephrine and norepinephrine causes depression. Three of the other associated genes in this study also interact with the Wnt signaling pathway upstream and downstream of glycogen synthase kinase 3-beta (GSK3β). These loci are grouped as major affective disorder (MAFD) loci and numbered in the order of their discovery. E. Therefore, the best way to write an essay mania serves as a defense against the feelings of depression. The age of onset of bipolar disorder varies greatly. Another approach to delineating the pathophysiology of bipolar disorder involves studying changes in gene expression induced in rodent brains after administration of pharmacologic agents used to treat bipolar disorder. In 7% of these patients, symptoms do not recur, 45% of patients experience more episodes, and 40% go on to have a persistent disorder. However, twin, family, and adoption studies all indicate that bipolar disorder has a significant genetic component. They see the depression as the manifestation of losses (i. Most cases of bipolar disorder commence when individuals are aged 15–19 years. Thus, another suggested cause of bipolar disorder is damage to cells in the critical brain circuitry that regulates emotion. Many loci are now known to be associated with the development of bipolar disorder. L-type calcium channel blockers have been used to treat research papers on bipolar disorder bipolar disorder, and there has been speculation that at least some mood stabilizers may mediate their effects via modulating calcium channel high quality article writing service signaling in bipolar illness. 4% for subthreshold bipolar disorder, and 2. Only 50-60% of patients with BPI who are on lithium gain research papers on bipolar disorder control of their symptoms. The blood pressure drug reserpine, which depletes catecholamines from nerve terminals, was noted incidentally to cause depression. 5%. For example, pregnancy is a particular stress for women with a manic-depressive illness history and increases the possibility of postpartum psychosis. In cross-sectional, face-to-face household research papers on bipolar disorder surveys of more than 61,000 adults across 11 countries, Merikangas et al, using the World Mental Health version of the World Health helper to do dissertation research Organization Composite International Diagnostic Interview, version 3. CACNA1C, on chromosome 12, encodes the alpha subunit of the L-type voltage-gated calcium ion channel found in the brain. Neuroimaging studies of individuals with bipolar disorder or other mood disorders also suggest evidence of cell loss or atrophy in these same brain regions. 73. According to this hypothesis, mood stabilizers and research papers on bipolar disorder antidepressants are thought to alter mood by stimulating cell survival pathways and increasing levels of neurotrophic factors to improve cellular resiliency. Calcium channel blockers have been used to treat mania, which may also result from a disruption of intracellular calcium regulation in neurons as suggested by experimental and genetic data. 4% for bipolar spectrum. Within the first 2 years after the initial episode, 40-50% of these patients experience another manic attack. Lithium-mediated inhibition of GSK3β is thought to result in downregulation of molecules involved in cell death and upregulation of neuroprotective factors. 0, determined that the aggregate lifetime prevalences were 0. The loss of self-esteem and the sense how to write a high school application 50th of worthlessness). The proposed disruption of calcium regulation may be caused by various neurologic insults, such as excessive glutaminergic transmission or ischemia. The second most frequent age range of onset is 20–24 years. Globally, the lifelong prevalence rate of bipolar disorder is 0. Genetic markers in 4 regions were associated with all 5 disorders, including variants in the CACNA1C gene, research papers on bipolar disorder another gene for an L-type voltage-gated calcium channel research papers on bipolar disorder subunit, CACNB2, and markers on chromosomes 3p21 and 10q24. Many practitioners see the dynamics of manic-depressive illness as being linked through a single common pathway. Patients with BPI fare worse than patients with a major depression. 3–1. writing up a phd thesis Often, the cycling between depression and mania accelerates with age. Gene expression studies are one way of measuring the relative activity doctoral dissertation of karl marx or inactivity of genes, and they have already been proven useful for illuminating the pathophysiology of psychiatric disorders, including bipolar disorder. The research papers on bipolar disorder pathophysiology of bipolar affective disorder, or manic-depressive illness (MDI), has not been determined, and no objective biologic markers correspond definitively with the disease state. In some instances, the cycle may be directly linked to external stresses or the external pressures may serve to exacerbate some underlying genetic or biochemical predisposition. For both BPI and BPII, the age range is from childhood to 50 years, with a mean age of approximately 21 years. In fact, first-degree relatives of a person with bipolar disorder are approximately 7 times more likely to develop bipolar disorder than the rest of the population, and the heritability of bipolar I disorder (BPI) has recently been estimated at 0. 6% for BPI, 0. Specific expression of common genetic variants at different times during development, or in different regions of the brain, and in concert with other genetic variants could help to explain differences in disease phenotypes. 4% for BPII, 1. Interestingly, valproate specifically upregulates expression of a calcium chaperone protein, GRP 78, which may be one of its chief mechanisms of cellular protection.