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group_5_presentation_2_-_alzheimers [2018/11/02 22:47] jiangh14 [Conclusion] |
group_5_presentation_2_-_alzheimers [2018/11/04 18:27] (current) chuj19 [Alzheimer's Disease] |
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| ======= Alzheimer's Disease ======= | ======= Alzheimer's Disease ======= | ||
| + | {{ :alzheimer-disease.jpg?direct&600 |}} | ||
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| {{ :amyloid_process.jpg?600 |}} | {{ :amyloid_process.jpg?600 |}} | ||
| - | Figure 1: The APP process in healthy individual (left) verses in late-onset Alzheimer's patient | + | Figure 1: The APP process in healthy individual (left) verses in late-onset Alzheimer's patient (right) |
| **Tau Protein and Neurofibrillary Tangle:** | **Tau Protein and Neurofibrillary Tangle:** | ||
| - | Another hallmark of Alzheimer's disease is characterized by the abnormality in the Tau protein. In healthy person the Tau protein act as a regulator for of tubulin which controls the stabilization of microtubules (Wang et al., 2013). This allows for many cellular dynamic activities such structuring, transporting materials and DNA replication. However, Tau protein is hyperphosphorylated by the overexpression of Tau kinase in Alzheimer's patients. This causes these proteins to misfold and aggregate to form neurofibrillary tangles that leads to the loss of neurons in the patient's brain, however the specific mechanism behind this is still unknown. | + | Another hallmark of Alzheimer's disease is characterized by the abnormality in the Tau protein. In healthy person the Tau protein act as a regulator for of tubulin which controls the stabilization of microtubules (Wang et al., 2013). This allows for many cellular dynamic activities such structuring, transporting materials and DNA replication. However, Tau protein is hyperphosphorylated by the overexpression of Tau kinase in Alzheimer's patients (Jouanne & Voisin-Chiret, 2017). This causes these proteins to misfold and aggregate to form neurofibrillary tangles that leads to the loss of neurons in the patient's brain, however the specific mechanism behind this is still unknown. |
| {{ :tau.jpg?500 |}} | {{ :tau.jpg?500 |}} | ||
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| ==== Aducanumab Targeting Beta-amyloid Protein ==== | ==== Aducanumab Targeting Beta-amyloid Protein ==== | ||
| - | According to the alzheimer’s association, there are currently many targets and studies being conducted to prevent AD. Beta-amyloid is present in those who have Alzheimer’s by the two enzymes beta-secretase and gamma-secretase which ultimately forms the beta-amyloid protein (Alzheimer’s Association, 2018). Aducanumab, also known as BIIB037, tries to target the aggregated forms of beta-amyloid that can eventually develop into the amyloid plaque. This antibody was derived by a biotech company in Switzerland and has passed its phase 1, 2, and is currently in phase 3 (Alzforum, 2018). A one-year data for the 6 mg/kg dose of aducanumab showed significant reduction in brain amyloid levels and therefore a study consisting of the phase 3 trials objective is to evaluate how effective doses of aducanumab is in individuals with AD (Alzforum, 2018). This is currently conducted within around 1605 participants with a dosages of monthly intravenous infusions. Furthermore, this drug is still in the research and is not released to the public. This study has started in September 30, 2015, and is expected to be completed by April 30, 2022 (National Library of Medicine, 2018). | + | According to the Alzheimer’s Association, there are currently many targets and studies being conducted to prevent AD. Beta-amyloid is present in those who have Alzheimer’s by the two enzymes beta-secretase and gamma-secretase which ultimately forms the beta-amyloid protein (Alzheimer’s Association, 2018). Aducanumab, also known as BIIB037, tries to target the aggregated forms of beta-amyloid that can eventually develop into the amyloid plaque. This antibody was derived by a biotech company in Switzerland and has passed its phase 1, 2, and is currently in phase 3 (Alzforum, 2018). A one-year data for the 6 mg/kg dose of aducanumab showed significant reduction in brain amyloid levels and therefore a study consisting of the phase 3 trials objective is to evaluate how effective doses of aducanumab is in individuals with AD (Alzforum, 2018). This is currently conducted within around 1605 participants with a dosages of monthly intravenous infusions. Furthermore, this drug is still in the research and is not released to the public. This study has started in September 30, 2015, and is expected to be completed by April 30, 2022 (National Library of Medicine, 2018). |
| ==== AADvac1 Targeting Tau Protein ==== | ==== AADvac1 Targeting Tau Protein ==== | ||
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| {{ :375px-pdb_1i8h_ebi.jpg?direct&300 |}} Figure 6: Picture of the tau protein structure. | {{ :375px-pdb_1i8h_ebi.jpg?direct&300 |}} Figure 6: Picture of the tau protein structure. | ||
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| ====== Conclusion ====== | ====== Conclusion ====== | ||
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| + | Although there currently is not a definite cure for Alzheimer's disease, current research such as Aducanumab and AADvac1 shows promising progression with research. Furthermore, other research focusing on the inflammation of the brain with the disease is also being researched and will hopefully pass the trials so patients are able to use the drug. There are also many preventive ways described within the 4 pillars of Alzheimer's Prevention and the management of the patient is just as important. | ||
| + | ====== References ====== | ||
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| Alzheimer's Disease. (n.d.). Retrieved from https://www.saintlukeskc.org/condition/alzheimers-disease | Alzheimer's Disease. (n.d.). Retrieved from https://www.saintlukeskc.org/condition/alzheimers-disease | ||
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| + | Alzheimer's Disease: Symptoms and Care | Emed Multi Specialty Group. (2018, May 07). Retrieved from https://emedmultispecialtygroup.com/2018/03/20/alzheimers-disease-symptoms-care/ | ||
| Alzheimer's Prevention. (2018). Alzheimer's Prevention through Diet and Supplements, Stress Management, Exercise, and Spiritual Fitness. [online] Available at: http://alzheimersprevention.org/4-pillars-of-prevention/ [Accessed 30 Oct. 2018]. | Alzheimer's Prevention. (2018). Alzheimer's Prevention through Diet and Supplements, Stress Management, Exercise, and Spiritual Fitness. [online] Available at: http://alzheimersprevention.org/4-pillars-of-prevention/ [Accessed 30 Oct. 2018]. | ||
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| Wang, J. Z., Xia, Y. Y., Grundke-Iqbal, I., & Iqbal, K. (2013). Abnormal hyperphosphorylation of tau: sites, regulation, and molecular mechanism of neurofibrillary degeneration. Journal of Alzheimer's Disease, 33(s1), S123-S139. | Wang, J. Z., Xia, Y. Y., Grundke-Iqbal, I., & Iqbal, K. (2013). Abnormal hyperphosphorylation of tau: sites, regulation, and molecular mechanism of neurofibrillary degeneration. Journal of Alzheimer's Disease, 33(s1), S123-S139. | ||
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| + | Wisniewski, T., Castano, E. M., Golabek, A., Vogel, T., & Frangione, B. (1994). Acceleration of Alzheimer's fibril formation by apolipoprotein E in vitro. The American journal of pathology, 145(5), 1030. | ||
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