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group_4_presentation_3_-_alzheimer_s_disease [2016/04/01 21:08] venkaa2 |
group_4_presentation_3_-_alzheimer_s_disease [2018/01/25 15:18] (current) |
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| Risk factors such as family history and genetic factors can play a huge role in developing Alzheimer’s disease. Individuals with Parents, brothers or sisters with the disease are more likely to develop the disorder. There is an increase in the risk of attaining the illness if more than one family member has the disease. Furthermore scientist have discovered risk genes that increase the likelihood of someone developing the disease. The gene with the strongest risk factor is called the apolipoprotein E-e4 (APOE-e4) which is a factor that increases the chances of Alzheimer’s by 20-25 % (Reitz et al., 2011). If you inherit one APOE-e4 gene from a parent you will have an increased risk, but if you inherit from both parents have an even higher risk (Reitz et al., 2011). By inheriting the gene from both parents the signs and symptoms of Alzheimer’s is going to show up at a younger age than usual (Reitz et al., 2011). Moreover genes that guarantee the disorder are called deterministic genes (Reitz et al., 2011). By coding three proteins, scientists have discovered the genes the variations that directly cause Alzheimer’s disease (Reitz et al., 2011). The three proteins are amyloid precursor protein (APP), presenilin-1 (PS-1) and presenilin-2(PS-2) (Reitz et al., 2011). When these genes cause the Alzheimer’s disorder, it is called “autosomal dominant Alzheimer’s disease (ADAD) or Familial Alzheimer’s disease (Reitz et al., 2011). When effected by this autosomal disease the symptoms usually appear well before the age of 60. It may occur as early as a person’s 30s or 40s. This form of Alzheimer’s have been found in only a few hundred families worldwide (Reitz et al., 2011). This rare form of Alzheimer’s accounts for less than 5% of cases worldwide (Reitz et al., 2011). | Risk factors such as family history and genetic factors can play a huge role in developing Alzheimer’s disease. Individuals with Parents, brothers or sisters with the disease are more likely to develop the disorder. There is an increase in the risk of attaining the illness if more than one family member has the disease. Furthermore scientist have discovered risk genes that increase the likelihood of someone developing the disease. The gene with the strongest risk factor is called the apolipoprotein E-e4 (APOE-e4) which is a factor that increases the chances of Alzheimer’s by 20-25 % (Reitz et al., 2011). If you inherit one APOE-e4 gene from a parent you will have an increased risk, but if you inherit from both parents have an even higher risk (Reitz et al., 2011). By inheriting the gene from both parents the signs and symptoms of Alzheimer’s is going to show up at a younger age than usual (Reitz et al., 2011). Moreover genes that guarantee the disorder are called deterministic genes (Reitz et al., 2011). By coding three proteins, scientists have discovered the genes the variations that directly cause Alzheimer’s disease (Reitz et al., 2011). The three proteins are amyloid precursor protein (APP), presenilin-1 (PS-1) and presenilin-2(PS-2) (Reitz et al., 2011). When these genes cause the Alzheimer’s disorder, it is called “autosomal dominant Alzheimer’s disease (ADAD) or Familial Alzheimer’s disease (Reitz et al., 2011). When effected by this autosomal disease the symptoms usually appear well before the age of 60. It may occur as early as a person’s 30s or 40s. This form of Alzheimer’s have been found in only a few hundred families worldwide (Reitz et al., 2011). This rare form of Alzheimer’s accounts for less than 5% of cases worldwide (Reitz et al., 2011). | ||
| + | {{:ad_epidimeology.jpeg|}} | ||
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| + | **Figure 2:** This graph depicts the prevalence of the disease as being most abundant in Brazil, Europe, USA and China. | ||
| ======Pathophysiology====== | ======Pathophysiology====== | ||
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| {{ :alzheimer_brain.jpg }} | {{ :alzheimer_brain.jpg }} | ||
| - | **Figure 2:**This figure shows a comparison of a normal brain and one with Alzheimer's disease. The atrophy and degeneration of brain tissue in the brain on the right is visible. (Alz, 2011). | + | **Figure 3:**This figure shows a comparison of a normal brain and one with Alzheimer's disease. The atrophy and degeneration of brain tissue in the brain on the right is visible. (Alz, 2011). |
| ====== Disease Mechanism ====== | ====== Disease Mechanism ====== | ||
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| {{ :screen_shot_2016-03-25_at_6.36.45_pm.png }} | {{ :screen_shot_2016-03-25_at_6.36.45_pm.png }} | ||
| - | **Figure 3:**This figure shows a simplification of the cascade of events that occur in Alzheimer's disease as predicted by the Amyloid Hypothesis. (Karran, 2011). | + | **Figure 4:**This figure shows a simplification of the cascade of events that occur in Alzheimer's disease as predicted by the Amyloid Hypothesis. (Karran, 2011). |
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| The Tau Hypothesis suggests that the formation of Neurofibrillary tangles (NFTs) --that is characteristic of Alzheimer’s Disease-- is due to the hyperphosphorylation of Tau proteins. Tau proteins normally play a role of structural support as they are responsible for microtubule stabilization. However, Tau Hyphosphorylation results in clumping of other Tau proteins which eventually develop into NFTs in Alzheimer’s Disease. Research has shown that Tau Hyperphosphorylation has led to neuronal cell death through microtubule dysfunction which disrupts the structural integrity of the cell. As a result, this has been associated with the cognitive decline that is seen in Alzheimer’s Disease (Maccioni et al., 2010). | The Tau Hypothesis suggests that the formation of Neurofibrillary tangles (NFTs) --that is characteristic of Alzheimer’s Disease-- is due to the hyperphosphorylation of Tau proteins. Tau proteins normally play a role of structural support as they are responsible for microtubule stabilization. However, Tau Hyphosphorylation results in clumping of other Tau proteins which eventually develop into NFTs in Alzheimer’s Disease. Research has shown that Tau Hyperphosphorylation has led to neuronal cell death through microtubule dysfunction which disrupts the structural integrity of the cell. As a result, this has been associated with the cognitive decline that is seen in Alzheimer’s Disease (Maccioni et al., 2010). | ||
| - | ====== Management ====== | + | ====== Intervention Strategies ====== |
| ==== Treatment ==== | ==== Treatment ==== | ||
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| {{ :snip20160327_1.png }} | {{ :snip20160327_1.png }} | ||
| - | **Figure 4: This figure shows two promising approaches of utilizing anti-Aβ plaque antibodies to limit the progression of Alzheimer's Disease (Schenk, 2002).** | + | **Figure 5**: This figure shows two promising approaches of utilizing anti-Aβ plaque antibodies to limit the progression of Alzheimer's Disease (Schenk, 2002). |
| ==== Management ==== | ==== Management ==== | ||
