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group_4_presentation_2_-_cte [2018/11/02 20:07] baruaa1 [References] |
group_4_presentation_2_-_cte [2018/11/04 01:21] (current) kimr1 |
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| ===== Risk Factors ===== | ===== Risk Factors ===== | ||
| - | The major risk for developing CTE is trauma to the central nervous system, therefore individuals who experience more head trauma are at a higher risk (DeKosky, Blennow, Ikonomovic & Gandy, 2013). Other factors such as the age at first head trauma and the length of the exposure to the head trauma also need to be taken into account and can increase risk to developing the disorder. Studies show that individuals who experience their first head trauma before the age of 12 are at a higher risk for developing CTE and have worse outcomes (Stamm et al., 2015). Furthermore, individuals who have a career with longer exposures to head trauma have a higher risk for CTE than those with a shorter career (Lakhan & Kirchgessner, 2012). Further research needs to be done on the genetic risk factors of CTE, as several have been proposed but remain to be established (DeKosky, Blennow, Ikonomovic & Gandy, 2013). | + | The major risk for developing CTE is trauma to the central nervous system, therefore individuals who experience more head trauma are at a higher risk (DeKosky, Blennow, Ikonomovic & Gandy, 2013). Other factors such as the age at first head trauma and the length of the exposure to the head trauma also need to be taken into account and can increase risk to developing the disorder. Studies show that individuals who experience their first head trauma before the age of 12 are at a higher risk for developing CTE and have worse outcomes (Stamm et al., 2015). Furthermore, individuals who have a career with longer exposures to head trauma have a higher risk for CTE than those with a shorter career (Lakhan & Kirchgessner, 2012). Further research needs to be done on the genetic risk factors of CTE, as some have been proposed but not yet confirmed (DeKosky, Blennow, Ikonomovic & Gandy, 2013). |
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| ===== Pathophysiology and Mechanisms ===== | ===== Pathophysiology and Mechanisms ===== | ||
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| Currently, the neurological effects of chronic traumatic encephalopathy (CTE) can only be studied post-mortem. The pathophysiology of the disease is unclear as there is a lack of clinical evidence and the symptoms can also be attributed to other factors such as aging, medications, and other diseases (Petraglia et al., 2014). | Currently, the neurological effects of chronic traumatic encephalopathy (CTE) can only be studied post-mortem. The pathophysiology of the disease is unclear as there is a lack of clinical evidence and the symptoms can also be attributed to other factors such as aging, medications, and other diseases (Petraglia et al., 2014). | ||
| - | To be diagnosed with CTE as opposed to other neurological diseases such as Alzheimer’s disease, the following four criteria need to be present in the brain tissue: the presence of perivascular foci of phospho-tau (p-tau) immunoreactive astrocytic tangles and neurofibrillary tangles, presence of irregular cortical distribution of p-tau immunoreactive neurofibrillary tangles and astrocytic tangles (with a predilection for the depth of cerebral sulci), groups of subpial and periventricular astrocytic tangles in the cerebral cortex, diencephalon, basal ganglia and brainstem, and finally the presence of neurofibrillary tangles in the cerebral cortex located preferentially in the superficial layers (McKee et al., 2013). Other pathological findings from individuals diagnosed with CTE are general atrophy (with greatest concentration in the frontal and temporal lobes, somewhat in parietal lobe, and nearly none in occipital lobe), scarring of cerebellar tonsils, a fenestrated cavum septum pellucidum, and enlargement of the ventral and third ventricles (Yi, Padalino, Chin, Montenegro, and Cantu, 2013). | + | To be diagnosed with CTE as opposed to other neurological diseases such as Alzheimer’s disease, the following four criteria need to be present in the brain tissue: the presence of phospho-tau (p-tau) around the brain's blood vessels, irregular cortical distribution of p-tau immunoreactive neurofibrillary tangles and astrocytic tangles (with a preference for the cerebral sulci), groups of subpial and periventricular astrocytic tangles in the cerebral cortex, diencephalon, basal ganglia and brain stem, and finally the presence of neurofibrillary tangles located preferentially in the superficial layers of the cerebral cortex (McKee et al., 2013). Other pathological findings from individuals diagnosed with CTE are general atrophy (with greatest concentration in the frontal and temporal lobes, somewhat in parietal lobe, and nearly none in occipital lobe), scarring of cerebellar tonsils, a fenestrated cavum septum pellucidum, and enlargement of the ventral and third ventricles (Yi, Padalino, Chin, Montenegro, and Cantu, 2013). |
| {{:cte_1.jpg?300|}} {{:cte_2.jpg?300|}} | {{:cte_1.jpg?300|}} {{:cte_2.jpg?300|}} | ||
| - | **Figure 5: ** (Left to right) Degeneration of brain tissue associated with each stage of CTE | + | **Figure 5: ** (Left to right) Degeneration of brain tissue associated with each stage of CTE (McKee et al., 2013) |
| In one study, researchers evaluated the development of CTE by exposing unanesthetized mice to closed head impacts. There were three groups in this study: control, single-hit, and repetitive. The study found increased p-tau immunoreactivity in the single-hit mice group and the repetitive-hit group after one month. Both groups also had elevated inflammatory cytokine levels, mediated by microglial and astroglial cells. However, after six months, the single-hit group recovered substantially while the repetitive-hit group’s p-tau immunoreactivity increased significantly. The repetitive-hit group also had substantial and widespread microglial and astroglial activation, indicating a major neuroinflammatory response (Petraglia et al., 2014). | In one study, researchers evaluated the development of CTE by exposing unanesthetized mice to closed head impacts. There were three groups in this study: control, single-hit, and repetitive. The study found increased p-tau immunoreactivity in the single-hit mice group and the repetitive-hit group after one month. Both groups also had elevated inflammatory cytokine levels, mediated by microglial and astroglial cells. However, after six months, the single-hit group recovered substantially while the repetitive-hit group’s p-tau immunoreactivity increased significantly. The repetitive-hit group also had substantial and widespread microglial and astroglial activation, indicating a major neuroinflammatory response (Petraglia et al., 2014). | ||
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| - | **Figure 6: ** Comparison of brains taken from a control mouse and a repetitive-hit mouse | + | **Figure 6: ** Comparison of brains taken from a control mouse and a repetitive-hit mouse (Petraglia et al., 2014) |
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| - | **Figure 7: ** Illustration of the neurotoxic effects of proinflammatory cytokines and chemokines acting together with amino acids (mainly glutamate). | + | **Figure 7: ** Illustration of the neurotoxic effects of proinflammatory cytokines and chemokines acting together with amino acids (mainly glutamate) (Blaylock and Maroon, 2011) |
