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group_2_presentation_3_-_bipolar_disorder [2017/04/07 10:13] ramachg |
group_2_presentation_3_-_bipolar_disorder [2018/01/25 15:18] (current) |
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| {{:cyclothymia_graph.png}} | {{:cyclothymia_graph.png}} | ||
| - | Fig 1: This image is used to outline and explain the major classifications for bipolar disorder. | + | **Figure 1**: This image is used to outline and explain the major classifications for bipolar disorder. |
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| {{:2011-06-bipolar-chart_tcm7-116499.jpg}} | {{:2011-06-bipolar-chart_tcm7-116499.jpg}} | ||
| - | Fig 2: This image outlines the main results from the study done by Merikangas et al. | + | **Figure 2**: This image outlines the main results from the study done by Merikangas et al. |
| ===== Societal Impact ===== | ===== Societal Impact ===== | ||
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| Over the past 40 years, neurobiological studies of mood disorders have primarily focused on abnormalities of the monoaminergic neurotransmitter systems, on characterizing alterations of individual neurotransmitters in disease states, and on assessing response to mood stabilizer and antidepressant medications. The monoaminergic system consists of a network of limbic, striatal and prefrontal cortical neuronal circuits thought to support the behavioral and visceral manifestations of mood disorders (Drevets, 2000). It is hypothesized that BD arises from the complex interaction of multiple susceptibility and protective genes and environmental factors. The phenotypic expression of the disease includes mood disturbance, as well as cognitive, motor, autonomic, endocrine and sleep or wake abnormalities (Schloesser et al., 2008). | Over the past 40 years, neurobiological studies of mood disorders have primarily focused on abnormalities of the monoaminergic neurotransmitter systems, on characterizing alterations of individual neurotransmitters in disease states, and on assessing response to mood stabilizer and antidepressant medications. The monoaminergic system consists of a network of limbic, striatal and prefrontal cortical neuronal circuits thought to support the behavioral and visceral manifestations of mood disorders (Drevets, 2000). It is hypothesized that BD arises from the complex interaction of multiple susceptibility and protective genes and environmental factors. The phenotypic expression of the disease includes mood disturbance, as well as cognitive, motor, autonomic, endocrine and sleep or wake abnormalities (Schloesser et al., 2008). | ||
| - | Figure X shows the pathophysiology of BD from different perspectives, and how these different systems are interlinked. For instance, there are different physiological levels at which the disease manifests: molecular, cellular, and behavioral. In addition, there are environmental factors which also contribute to the onset of BD (Schloesser et al., 2008). Once there is a dysfunction in one physiological level, it has been observed in the literature that there is a cascade of downstream events which are ultimately responsible for primary abnormalities in signaling pathways. | + | Figure 3 shows the pathophysiology of BD from different perspectives, and how these different systems are interlinked. For instance, there are different physiological levels at which the disease manifests: molecular, cellular, and behavioral. In addition, there are environmental factors which also contribute to the onset of BD (Schloesser et al., 2008). Once there is a dysfunction in one physiological level, it has been observed in the literature that there is a cascade of downstream events which are ultimately responsible for primary abnormalities in signaling pathways. |
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| Many signaling pathways play critical roles not only in synaptic plasticity, the cellular process that results in lasting changes in the efficacy of neurotransmission, but also in the long-term atrophic processes. Therefore, plasticity plays a role in the cascading effect for the pathophysiology of the disease (Schloesser et al., 2008). | Many signaling pathways play critical roles not only in synaptic plasticity, the cellular process that results in lasting changes in the efficacy of neurotransmission, but also in the long-term atrophic processes. Therefore, plasticity plays a role in the cascading effect for the pathophysiology of the disease (Schloesser et al., 2008). | ||
| - | In healthy humans, there are numerous biological mechanisms which underlie neuroplasticity, a broader term that encapsulates changes in intracellular signaling cascades and gene regulation, modifications of synaptic number and strength, variations in neurotransmitter release, modeling of axonal and dendritic architecture, and in some areas of the CNS, the generation of new neurons. The remarkable plasticity of neuronal circuits is achieved through different biological means, including alterations in gene transcription and intracellular signaling cascades. These changes thereby modify diverse neuronal properties such as neurotransmitter release, synaptic function and even morphological characteristics of neurons. However, it has been shown that people with BD have abnormalities in cellular signaling cascades that regulate diverse physiologic functions, thereby causing tremendous medical comorbidity associated with BD (Figure Y) (Schloesser et al., 2008). | + | In healthy humans, there are numerous biological mechanisms which underlie neuroplasticity, a broader term that encapsulates changes in intracellular signaling cascades and gene regulation, modifications of synaptic number and strength, variations in neurotransmitter release, modeling of axonal and dendritic architecture, and in some areas of the CNS, the generation of new neurons. The remarkable plasticity of neuronal circuits is achieved through different biological means, including alterations in gene transcription and intracellular signaling cascades. These changes thereby modify diverse neuronal properties such as neurotransmitter release, synaptic function and even morphological characteristics of neurons. However, it has been shown that people with BD have abnormalities in cellular signaling cascades that regulate diverse physiologic functions, thereby causing tremendous medical comorbidity associated with BD (Figure 4) (Schloesser et al., 2008). |
| **Figure 4**: Cellular signaling cascades that regulate diverse physiologic functions have shown to be disrupted in patients with BD. Retrieved from Schloesser et al., 2008. | **Figure 4**: Cellular signaling cascades that regulate diverse physiologic functions have shown to be disrupted in patients with BD. Retrieved from Schloesser et al., 2008. | ||
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| === Structural Neuroimaging Findings === | === Structural Neuroimaging Findings === | ||
| - | Many forms of neural plasticity involve structural changes in the brain. Since neuroplasticity and cellular cascade changes play a role in BD, many studies to date have used neuroimaging and postmortem human brains to investigate the potential alterations in structural plasticity in mood disorders. Studies on people with BD using the aforementioned pathological techniques have revealed several functional and structural abnormalities in brain regions involved in the perception and control of mood states and emotions. These include the prefrontal cortex (PFC), amygdala, insula, hippocampus, anterior cingulate cortex, and ventral striatum (Figure Z). In addition, post-mortem morphometric brain studies in mood disorders have demonstrated that patients with mood disorders undergo cellular atrophy and/or loss (Table A) (Schloesser et al., 2008). | + | Many forms of neural plasticity involve structural changes in the brain. Since neuroplasticity and cellular cascade changes play a role in BD, many studies to date have used neuroimaging and postmortem human brains to investigate the potential alterations in structural plasticity in mood disorders. Studies on people with BD using the aforementioned pathological techniques have revealed several functional and structural abnormalities in brain regions involved in the perception and control of mood states and emotions. These include the prefrontal cortex (PFC), amygdala, insula, hippocampus, anterior cingulate cortex, and ventral striatum (Figure 5). In addition, post-mortem morphometric brain studies in mood disorders have demonstrated that patients with mood disorders undergo cellular atrophy and/or loss (Table 1) (Schloesser et al., 2008). |
| {{:screen_shot_2017-04-04_at_6.42.57_pm.png|}} | {{:screen_shot_2017-04-04_at_6.42.57_pm.png|}} | ||
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| The prefrontal cortex (PFC) is a key brain region involved in the regulation of emotional behaviour, executive function and fear extinction. This area is sensitive to the remodeling effects of stress. Several studies have shown structural and functional frontal lobe abnormalities (reduction in size) in BD, including the anterior cingulate and subnegual PFC. These are consistent with the cognitive deficits found in BD (Kapczinski et al., 2008). | The prefrontal cortex (PFC) is a key brain region involved in the regulation of emotional behaviour, executive function and fear extinction. This area is sensitive to the remodeling effects of stress. Several studies have shown structural and functional frontal lobe abnormalities (reduction in size) in BD, including the anterior cingulate and subnegual PFC. These are consistent with the cognitive deficits found in BD (Kapczinski et al., 2008). | ||
| - | Figure (?) encapsulates the brain rewiring that happens after recurrent stress and mood episodes in BD patients. Neural substrate reactivity is altered in BD patients, leading to cell endangerment, pro-apoptotic cascades, thereby leading to altered size of brain parts involved in emotional processing and coping. Such brain rewiring is related to increased emotionality and poor coping which render subjects more vulnerable to life stress (Kapczinski et al., 2008). | + | Figure 6 encapsulates the brain rewiring that happens after recurrent stress and mood episodes in BD patients. Neural substrate reactivity is altered in BD patients, leading to cell endangerment, pro-apoptotic cascades, thereby leading to altered size of brain parts involved in emotional processing and coping. Such brain rewiring is related to increased emotionality and poor coping which render subjects more vulnerable to life stress (Kapczinski et al., 2008). |
