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group_4_presentation_3_-_alzheimer_s_disease [2016/04/01 20:59] venkaa2 |
group_4_presentation_3_-_alzheimer_s_disease [2018/01/25 15:18] (current) |
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| {{:stages-of-alzheimers.jpg|}} | {{:stages-of-alzheimers.jpg|}} | ||
| - | **Figure 1: The stages of Alzheimer's disease starting from mild cognitive impairment leading up to more severe stages.** | + | **Figure 1:** The stages of Alzheimer's disease starting from mild cognitive impairment leading up to more severe stages. |
| ==== Prognosis ==== | ==== Prognosis ==== | ||
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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|}} | ||
| + | |||
| + | **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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| ==== Tau Hypothesis ==== | ==== Tau Hypothesis ==== | ||
| - | 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.** | + | **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 ==== | ||
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| ======References====== | ======References====== | ||
| - | ("Healthy Brain Versus Alzheimer's Brain | Alzheimer's Association," 2011) | + | (“Healthy Brain Versus Alzheimer's Brain | Alzheimer's Association,” 2011) |
| - | (Hardy & Allsop, "Amyloid deposition as the central event in the aetiology of Alzheimer's disease," 1991, pp. 383-388) | + | A next-generation approach to Alzheimer's treatment. (n.d.). Retrieved April 01, 2016, from http://www.cobas.com/home/innovation/next-gen-alzheimers-treatment.html |
| - | (Bouras, Hof, Giannakopoulos, Michel, & Morrison, "Regional Distribution of Neurofibrillary Tangles and Senile Plaques in the Cerebral Cortex of Elderly Patients: A Quantitative Evaluation of a One-Year Autopsy Population from a Geriatric Hospital," 1994, pp. 138-150) | + | (Bouras, Hof, Giannakopoulos, Michel, & Morrison, “Regional Distribution of Neurofibrillary Tangles and Senile Plaques in the Cerebral Cortex of Elderly Patients: A Quantitative Evaluation of a One-Year Autopsy Population from a Geriatric Hospital,” 1994, pp. 138-150) |
| - | Gauthier, S., Cummings, J., Ballard, C., Brodaty, H., Grossberg, G., Robert, P., & Lyketsos, C. (2010). Management of behavioral problems in Alzheimer's disease. //International Psychogeriatrics//, 22(03), 346-372. | + | (Hardy & Allsop, “Amyloid deposition as the central event in the aetiology of Alzheimer's disease,” 1991, pp. 383-388) |
| - | Grossberg, G. T., & Desai, A. K. (2003). Management of Alzheimer's disease. //The Journals of Gerontology Series A: Biological Sciences and Medical Sciences//, 58(4), M331-M353. | + | Gauthier, S., Cummings, J., Ballard, C., Brodaty, H., Grossberg, G., Robert, P., & Lyketsos, C. (2010). Management of behavioral problems in Alzheimer's disease. International Psychogeriatrics, 22(03), 346-372. |
| - | Management | + | |
| - | Hernández, F., & Avila, J. (2007). Tauopathies. Cell. Mol. Life Sci. //Cellular and Molecular Life Sciences//,64(17), 2219-2233. | + | Grossberg, G. T., & Desai, A. K. (2003). Management of Alzheimer's disease. The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, 58(4), M331-M353. Management |
| + | |||
| + | Hernández, F., & Avila, J. (2007). Tauopathies. Cell. Mol. Life Sci. Cellular and Molecular Life Sciences,64(17), 2219-2233. | ||
| Ibbotson, T., & Goa, K. L. (2002). Management of Alzheimer’s Disease. Disease management and health outcomes, 10(1), 41-54. | Ibbotson, T., & Goa, K. L. (2002). Management of Alzheimer’s Disease. Disease management and health outcomes, 10(1), 41-54. | ||
| - | Yankner, B., Duffy, L., & Kirschner, D. (1990). Neurotrophic and neurotoxic effects of amyloid beta protein: Reversal by tachykinin neuropeptides. //Science//, 250(4978), 279-282. | + | Iijima, K., Liu, H., Chiang, A., Hearn, S. A., Konsolaki, M., & Zhong, Y. (2004). Dissecting the pathological effects of human A 40 and A 42 in Drosophila: A potential model for Alzheimer's disease. Proceedings of the National Academy of Sciences, 101(17), 6623-6628. |
| - | Karran, E., Mercken, M., & Strooper, B. D. (2011). The amyloid cascade hypothesis for Alzheimer's disease: An appraisal for the development of therapeutics. //Nature Reviews Drug Discovery Nat Rev Drug Discov//,10(9), 698-712. | + | Imbimbo, B.P., Solfrizzi, V., & Panza, F. (2010). Are NSAIDs Useful to Treat Alzheimer's Disease or Mild Cognitive Impairment?Frontiers in Aging Neuroscience, (2), 19 |
| - | Iijima, K., Liu, H., Chiang, A., Hearn, S. A., Konsolaki, M., & Zhong, Y. (2004). Dissecting the pathological effects of human A 40 and A 42 in Drosophila: A potential model for Alzheimer's disease. //Proceedings of the National Academy of Sciences//, 101(17), 6623-6628. | + | Karran, E., Mercken, M., & Strooper, B. D. (2011). The amyloid cascade hypothesis for Alzheimer's disease: An appraisal for the development of therapeutics. Nature Reviews Drug Discovery Nat Rev Drug Discov,10(9), 698-712. |
| - | Nistor, M., Don, M., Parekh, M., Sarsoza, F., Goodus, M., Lopez, G., . . . Head, E. (2007). Alpha- and beta-secretase activity as a function of age and beta-amyloid in Down syndrome and normal brain. //Neurobiology of Aging//, 28(10), 1493-1506. | + | Kumar, A., & Singh, A. (2015). A review on Alzheimer's disease pathophysiology and its management: an update. Pharmacological Reports, 67(2), 195-203. |
| - | Shen, Z. (2004). Brain cholinesterases: II. The molecular and cellular basis of Alzheimer's disease. //Medical Hypotheses//, 63(2), 308-321. | + | Ledesma, M.D., & Dotti, G.C. (2005). The conflicting role of brain cholesterol in Alzheimer's disease: lessons from the brain plasminogen system. PubMed, (72), 129-138 |
| - | Schenk, D. (2002). Amyloid-β immunotherapy for Alzheimer's disease: the end of the beginning. //Nature Reviews Neuroscience//, 3(10), 824-828. | + | Maccioni, R. B., Farías, G., Morales, I., & Navarrete, L. (2010). The revitalized tau hypothesis on Alzheimer's disease. Archives of medical research, 41(3), 226-231. |
| - | Patterson, C., Feightner, J.W., Garcia, A., Hsiung, R., MacKnight, C., & Sadovnick, A.D. (2008). Diagnosis and treatment of dementia: 1. Risk assessment and primary prevention of Alzheimer disease. //Practice//, 178(5), 548-556. | + | Mayeux, R., & Sano, M. (1999). Treatment of Alzheimer’s disease. N Engl J Med, 341(22), 1670-9. |
| - | Ledesma, M.D., & Dotti, G.C. (2005). The conflicting role of brain cholesterol in Alzheimer's disease: lessons from the brain plasminogen system. //PubMed//, (72), 129-138 | + | Nistor, M., Don, M., Parekh, M., Sarsoza, F., Goodus, M., Lopez, G., . . . Head, E. (2007). Alpha- and beta-secretase activity as a function of age and beta-amyloid in Down syndrome and normal brain. Neurobiology of Aging, 28(10), 1493-1506. |
| - | Imbimbo, B.P., Solfrizzi, V., & Panza, F. (2010). Are NSAIDs Useful to Treat Alzheimer's Disease or Mild Cognitive Impairment?//Frontiers in Aging Neuroscience//, (2), 19 | + | Patterson, C., Feightner, J.W., Garcia, A., Hsiung, R., MacKnight, C., & Sadovnick, A.D. (2008). Diagnosis and treatment of dementia: 1. Risk assessment and primary prevention of Alzheimer disease. Practice, 178(5), 548-556. |
| - | Yiannopoulou, K.G., & Papageorgiou, S.G. (2013). Current and future treatments for Alzheimer's disease. //Therapeutic Advances in Neurological Disorders//, 6(1), 19-33 | + | Reitz, C., Brayne, C., & Mayeux, R. (2011). Epidemiology of Alzheimer disease. Nature Reviews Neurology, 7(3), 137-152. |
| - | Sperling, R. A., Aisen, P. S., Beckett, L. A., Bennett, D. A., Craft, S., Fagan, A. M., ... & Park, D. C. (2011). Toward defining the preclinical stages of Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimer's & Dementia, 7(3), 280-292. | + | Schenk, D. (2002). Amyloid-β immunotherapy for Alzheimer's disease: the end of the beginning. Nature Reviews Neuroscience, 3(10), 824-828. |
| - | Reitz, C., Brayne, C., & Mayeux, R. (2011). Epidemiology of Alzheimer disease. Nature Reviews Neurology, 7(3), 137-152. | + | Shen, Z. (2004). Brain cholinesterases: II. The molecular and cellular basis of Alzheimer's disease. Medical Hypotheses, 63(2), 308-321. |
| - | Mayeux, R., & Sano, M. (1999). Treatment of Alzheimer’s disease. N Engl J Med, 341(22), 1670-9. | + | Sperling, R. A., Aisen, P. S., Beckett, L. A., Bennett, D. A., Craft, S., Fagan, A. M., … & Park, D. C. (2011). Toward defining the preclinical stages of Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimer's & Dementia, 7(3), 280-292. |
| - | Kumar, A., & Singh, A. (2015). A review on Alzheimer's disease pathophysiology and its management: an update. Pharmacological Reports, 67(2), 195-203. | + | Yankner, B., Duffy, L., & Kirschner, D. (1990). Neurotrophic and neurotoxic effects of amyloid beta protein: Reversal by tachykinin neuropeptides. Science, 250(4978), 279-282. |
| - | Maccioni, R. B., Farías, G., Morales, I., & Navarrete, L. (2010). The revitalized tau hypothesis on Alzheimer's disease. Archives of medical research, 41(3), 226-231. | + | Yiannopoulou, K.G., & Papageorgiou, S.G. (2013). Current and future treatments for Alzheimer's disease. Therapeutic Advances in Neurological Disorders, 6(1), 19-33 |
