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group_1_presentation_1_-_alzheimer_s_disease [2016/09/26 00:19] cunanajk |
group_1_presentation_1_-_alzheimer_s_disease [2018/01/25 15:18] (current) |
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| - | ==========**Alzheimer's Disease**========= | + | ==========Alzheimer's Disease========= |
| ======Origin and Background====== | ======Origin and Background====== | ||
| - | In 1906, a German psychiatrist and neuropathologist by the name of Alois Alzheimer was drawn to the case of a woman showing unusual symptoms. Post mortem analysis of the brain tissue of the woman, started the journey of Dr. Alzheimer’s description of the neurodegenerative disease (Hippius, 2013). Alzheimer disease is an incurable disorder of cognitive and behavioural impairment with a long and progressive timeline. 75% of patients with dementia are thought to have genetically based Alzheimer’s, however the incidence can also be sporadic (Chapman et al, 2006). In Alzheimer’s, misfolded amino acid aggregates known as plaques develop in brain areas and impact and impede neuronal communication causing brain cell atrophy. This neurodegeneration begins in the hippocampus, then spreads to the rest of the brain over time and increasing severity of the disease. The affected region of the brain is the reduction of the memory encoding hippocampus, along with associated regions of the cerebral cortex involved in thinking, decision making, and planning (Purohit et al, 1998) | + | In 1906, a German psychiatrist and neuropathologist by the name of Alois Alzheimer was drawn to the case of a woman showing unusual symptoms. Post mortem analysis of the brain tissue of the woman started the journey of Dr. Alzheimer’s description of the neurodegenerative disease (Hippius, 2013). Alzheimer disease is an incurable disorder of cognitive and behavioural impairment with a long and progressive timeline. 75% of patients with dementia are thought to have genetically based Alzheimer’s, however the incidence can also be sporadic (Chapman et al, 2006). In Alzheimer’s, misfolded amino acid aggregates known as plaques develop in brain areas and impact and impede neuronal communication causing brain cell atrophy. This neurodegeneration begins in the hippocampus, then spreads to the rest of the brain over time and increasing severity of the disease. The affected region of the brain is the reduction of the memory encoding hippocampus, along with associated regions of the cerebral cortex involved in thinking, decision making, and planning (Purohit et al, 1998) |
| ======Epidemiology====== | ======Epidemiology====== | ||
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| {{:alzchart.jpg|}} | {{:alzchart.jpg|}} | ||
| - | **Figure 1:**This figure shows that dementia has the largest economic burden in the UK, but receives the lowest funding. (Abott, 2011). | + | **Figure 1:**This figure shows that dementia has the largest economic burden in the UK, but receives the lowest funding. (Abbott, 2011). |
| {{:alzdeathcause.jpg|}} | {{:alzdeathcause.jpg|}} | ||
| - | **Figure 2:**This figure shows the leading causes of death by sex (2015).ince Alzheimer's disease is not one of the leading causes of death due to its long course, not as much funding is allocated to it. | + | **Figure 2:**This figure shows the leading causes of death by sex (2015). Since Alzheimer's disease is not one of the leading causes of death due to its long course, not as much funding is allocated to it (Statistics Canada Leading causes of death, by sex (Both sexes) 2015). |
| ===== Symptoms ===== | ===== Symptoms ===== | ||
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| {{:alzbrain.jpg|}} | {{:alzbrain.jpg|}} | ||
| - | **Figure 3:**This figure illustrates the comparison between a pre-clinical and severe Alzheimer's brain. | + | **Figure 3:**This figure illustrates the comparison between a pre-clinical and severe Alzheimer's brain (Neergaard, 2016). |
| ======Disease Progression====== | ======Disease Progression====== | ||
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| {{:alzdiseaserisk.jpg|}} | {{:alzdiseaserisk.jpg|}} | ||
| - | **Figure 5:**This graph shows that the ApoE4 allele is a risk factor for sporadic Alzheimer's disease. It appears that ApoE2 and ApoE3 lower the risk for Alzheimer's disease. | + | **Figure 5:**This graph shows that the ApoE4 allele is a risk factor for sporadic Alzheimer's disease. It appears that ApoE2 and ApoE3 lower the risk for Alzheimer's disease (Kandel et al, 2013). |
| **Familial Cases** | **Familial Cases** | ||
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| - | **Figure 9:** Plaques, neurofibrillary tangles, synaptic and neuronal loss appear in the brain prior to significant cognitive decline. | + | **Figure 9:** Plaques, neurofibrillary tangles, synaptic and neuronal loss appear in the brain prior to significant cognitive decline (Abbott, 2011). |
| ===Technique 1: Physical, neurological and neuropsychological examination=== | ===Technique 1: Physical, neurological and neuropsychological examination=== | ||
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| ===Technique 3- PET=== | ===Technique 3- PET=== | ||
| - | Amyloid plaques can be visualized using Positron Emission Tomography (PET) using a new radioactive compound called Pittsburgh compound B (PIB) that binds with high affinity to amyloid beta or tau (Kandel et al, 2013). PIB is injected into the bloodstream. In Alzheimer’s, PIB is retained specifically in areas with amyloid deposition (Kandel et al, 2013). Other PET labelling agents have been developed to image inflammation as reflected by activated microglia and reactive astrocytes that surround plaques (Kandel, 2013). | + | Amyloid plaques can be visualized using Positron Emission Tomography (PET) using a new radioactive compound called Pittsburgh compound B (PIB) that binds with high affinity to amyloid beta or tau (Kandel et al, 2013). PIB is injected into the bloodstream. In Alzheimer’s, PIB is retained specifically in areas with amyloid deposition (Kandel et al, 2013). Other PET labelling agents have been developed to image inflammation as reflected by activated microglia and reactive astrocytes that surround plaques (Kandel et al, 2013). |
| {{:alzpetpib.jpg|}} | {{:alzpetpib.jpg|}} | ||
| - | **Figure 10:**This image clearly shows PIB retained in brain areas associated with amyloid deposition. There is a lot more PIB in the brain on the right, the Alzheimer's brain, compared with the healthy brain on the left. | + | **Figure 10:**This image clearly shows PIB retained in brain areas associated with amyloid deposition. There is a lot more PIB in the brain on the right, the Alzheimer's brain, compared with the healthy brain on the left (Kandel et al, 2013). |
| ===Technique 4- Fluid Biomarkers=== | ===Technique 4- Fluid Biomarkers=== | ||
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| {{:alzexperimentplot.jpg|}} | {{:alzexperimentplot.jpg|}} | ||
| - | **Figure 11:** Using fluid biomarkers as a method to detect Alzheimer's. On the left, there are lower concentrations of amyloid beta 42 in cerebrospinal fluid compared to the control due to the aggregation of amyloid beta 42. On the right, there are higher concentrations of tau in the cerebrospinal fluid compared to the control, due to the cell death releasing tau. | + | **Figure 11:** Using fluid biomarkers as a method to detect Alzheimer's. On the left, there are lower concentrations of amyloid beta 42 in cerebrospinal fluid compared to the control due to the aggregation of amyloid beta 42. On the right, there are higher concentrations of tau in the cerebrospinal fluid compared to the control, due to the cell death releasing tau (Kandel et al, 2013). |
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| {{:alztreatments.jpg|}} | {{:alztreatments.jpg|}} | ||
| - | **Figure 12:** Table showing treatments according to severity. Image frome Alzheimer's Association, 2016. | + | **Figure 12:** Table showing treatments according to severity. Image from Alzheimer's Association, 2016. |
| ====Drug Treatment==== | ====Drug Treatment==== | ||
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| - | **The A4 Study (Anti-Amyloid Treatment in Asymptomatic Alzheimer’s)** | + | ===The A4 Study (Anti-Amyloid Treatment in Asymptomatic Alzheimer’s)=== |
| {{:alzpetscan.jpg|}} | {{:alzpetscan.jpg|}} | ||
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| Mayo Clinic Staff. (2015). Alzheimer's disease. Retrieved September 25, 2016, from http://www.mayoclinic.org/diseases-... | Mayo Clinic Staff. (2015). Alzheimer's disease. Retrieved September 25, 2016, from http://www.mayoclinic.org/diseases-... | ||
| - | Neergaard, L. (2016). Testing brain pacemakers to zap Alzheimer's damage (Update). Medicalxpress.com. Retrieved 21 September 2016, from http://medicalxpress.com/news/2013-01-brain-pacemakers-zap-alzheimer.html (only used an image from here) | + | Neergaard, L. (2016). Testing brain pacemakers to zap Alzheimer's damage (Update). Medicalxpress.com. Retrieved 21 September 2016, from http://medicalxpress.com/news/2013-01-brain-pacemakers-zap-alzheimer.html |
| Patterson, C., Feightner, J., Garcia, A., Hsiung, G., MacKnight, C., & Sadovnick, A. (2008). Diagnosis and treatment of dementia: 1. Risk assessment and primary prevention of Alzheimer disease. Canadian Medical Association Journal, 178(5), 548-556. http://dx.doi.org/10.1503/cmaj.0707 | Patterson, C., Feightner, J., Garcia, A., Hsiung, G., MacKnight, C., & Sadovnick, A. (2008). Diagnosis and treatment of dementia: 1. Risk assessment and primary prevention of Alzheimer disease. Canadian Medical Association Journal, 178(5), 548-556. http://dx.doi.org/10.1503/cmaj.0707 | ||
