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Alzheimer’s Disease Putting the pieces together
Catherine Nelson, RN
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Click on the topic that interests you!
Where are we going? Click on the topic that interests you! Alzheimer’s Facts – What do we know? Brain Anatomy & Physiology. Alzheimer’s Brain Anatomy & Physiology. New Research What’s the future look like? References
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What We Know 4.5 million people have Alzheimer’s Disease (AD).
It is responsible for 50% of all nursing home placements. It can last 20 years. It can be inherited. It can have an early onset—before 65 years of age-often by 30’s or 40’s. It can have a late onset—after 65 years of age.
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What We Know (continued)
Late onset AD affects almost half of all people over the age of 85. Given the aging of the baby boomers and the growing number of very old people (80 and above) 11 to 13.1 million Americans will have AD by 2050. Faces of AD
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Faces and Facts
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Check your knowledge What percentage of nursing home placements are due to AD? A. 50% B. 10% C. 30% D. 90% Click on the answer
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Right! Friends and family members
can care for people with different diseases but when AD is added, care becomes unmanageable in the home setting.
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Wrong! 10% & 30% is too low. 90% is too high.
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Brain Anatomy & Physiology
Normal Brain Tissue Neuron Function Lobe Function The Hippocampus Anatomy & Physiology Used with permission.
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Used with permission of Dr. Karen Myhr, Wayne State University
Neurons: Messengers of the brain The orange neuron sends information to the yellow neuron at synapses the where neurons touch. The yellow neuron combines the signal from many cells. If the combined signal is large enough, the yellow neuron signals the red neuron through their synapses. Used with permission of Dr. Karen Myhr, Wayne State University
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Lobe Function and AD Different areas of the brain are responsible for different functions. AD attacks neurons in the regions of the brain that control: thought memory speech The areas most affected: frontal lobes temporal lobes Parietal Lobe Frontal Lobe Occipital Lobe Temporal Lobe Cerebellum Used with permission
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Hippocampus The Computer Center
Responsible for: Information processing. Acquiring new memory and retrieval of old memory. Neurofibrillary tangles interfere with and isolate the hippocampus and make it useless. Picture
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Used with permission. text/health/alzheim/brain.gif
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Check your knowledge Neuron Function
True or False The neurons collect information and transmit it through the brain. TRUE FALSE
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Check your knowledge Neuron Function
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Check your knowledge Neuron Function
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Check your knowledge Hippocampus Function
True or False The hippocampus houses memory. TRUE FALSE
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Check your knowledge Hippocampus Function
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Check your knowledge Hippocampus Function
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Check your knowledge Lobe Function
True or False The lobes that are most affected by AD are the frontal and temporal lobes. TRUE FALSE
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Alzheimer’s A & P 3 Cardinal Signs Brain shrinkage. Found on neurons
Neurolitic Plaques. Filled with Amyloid-beta protein. Neurofibrillary tangles.
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Check your knowledge Alzheimer’s A & P
True or False Alzheimer’s Disease is responsible for brain shrinkage, neurolitic plaques and neurofibrillary tangles. TRUE FALSE
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Check your knowledge Alzheimer’s A & P
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Brain Shrinkage As the disease develops, the brain shrinks causing damage to the cortex and hippocampus, and enlarging the ventricles. Used with permission
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Check your knowledge Disease Development
True or False Brain shrinkage causes damage to the cortex, hippocampus and enlarges the ventricles. TRUE FALSE
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Check your knowledge Disease Development
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Check your knowledge Disease Development
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Plaques Also known as Senile Plaques.
They look like flat clusters of deteriorated nerve terminals which surround an amyloid peptide. Found in areas of cerebral cortex that are linked to intellectual function.
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Check your knowledge Plaque
True or False Plaque lies across cell membranes. TRUE FALSE
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Check your knowledge Plaque
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Check your knowledge Plaque
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Amyloid beta (A4) Amyloid beta precursor protein (APP)
Characteristics: Lie across cell membrane so part is inside the cell and part of it is outside. Proteins cut APP into pieces and amyloid beta peptides seep outside the cell.
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Check your knowledge Amyloid beta (A4)
True or False When cleaved A4 seeps outside the cell. TRUE FALSE
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Check your knowledge Amyloid beta (A4)
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Check your knowledge Amyloid beta (A4)
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Neurofibrillary Tangles
Composed of Tau protein and amyloid deposits. Cause senile plaques & accumulate in the cerebral-vascular systems. Resistant to chemical breakdown and absorption. Cause neuron death.
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Check your knowledge Neurofibrillary Tangles
True or False Neurofibrillary tangles cause neuron death. TRUE FALSE
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Check your knowledge Neurofibrillary Tangles
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Check your knowledge Neurofibrillary Tangles
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Tau and Neurons Tau is a protein found in the axon of healthy neurons where it binds to the structure of the neuron “microtubules”. It acts as a crosspiece and stabilizes the neuron structure. Together, Tau and microtubules act as railway tracks over which information is transported from one part of the neuron to another. In AD brain cells, microtubules may unravel and develop into neurofibrillary tangles. More >
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Used with permission http://www.ahaf.org/alzdis/about/AD_2003.jpg
Tau In AD, the sticky Tau proteins get tangled up with each other. Neurofibrillary tangles (NFT) develop and the neuron dies. Used with permission
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Check your knowledge Tau and Neurons
True or False Tau and plaque work together to prevent the development of neurofibrillary tangles. TRUE FALSE
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The New Research Chromosome 21 Chromosome 19 Lipids Inflammation
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Genetics The APP Gene Located on chromosome 21.
Mutations in the APP gene are thought to be responsible for Type I, Early On-Set AD. Also known as Familial Alzheimer’s Disease. A small but significant portion of Alzheimer’s Disease which has the characteristic of early on-set. Makes the Amyloid Precursor Protein that lies across the cell membrane. Located on chromosome 21. Used with permission.
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APP Gene Mutation Mutations in the APP gene lead to increased levels of the amyloid beta peptide protein fragments. These protein products are sticky and tend to “clump”. The clumps are called amyloid plaques and can cross the brain-blood barrier to increase the vasoconstriction in arteries.
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APP Gene Mutation These plaques are found only in Alzheimer disease. The accumulation of amyloid plaques lead to the signs and symptoms of this disease. Interestingly, these plaques appear to be closely related to structures found in Down's Syndrome.
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Check your knowledge Genetics
True or False Early onset AD is caused by mutation to the APP gene on chromosome 21. TRUE FALSE
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The role of Lipids Lipids transport cholesterol which is an essential ingredient of all cell membranes. Cholesterol helps membrane fluidity. High levels of cholesterol are associated with increased risk of AD. Cholesterol affects amyloid-beta production by binding to it and contributing to amyloid plaques.
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Check your knowledge Lipids
True or False Lipids bind to Tau and contribute to the development of AD. TRUE FALSE
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Check your knowledge Lipids
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Genetics Apolipoprotein E (ApoE)
APOE is a protein + a fat. Responsible for metabolism of Very Low Density Cholesterol. A mutation of APOE – APOE-e4 is thought to be responsible for Type 2 – Late on-Set AD. Located on chromosome 19. Used with permission.
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Apolipoprotein E Theories about how ApoE may work:
ApoE may promote the accumulation of amyloid plaques. ApoE may prevent the removal of amyloid plaques. ApoE may contribute to the development of neurofibrillary tangles. ApoE does not bind to Tau – allowing Amyloid beta precursor protein to form the neurofibrillary tangles.
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ApoE 4 and Women A mutant form of APOE thought to be responsible for late onset AD especially in women. A woman with one APOE4 allele has 4 times the AD risk of a woman with no allele. A woman with two APOE4 allele has 16 times the AD risk & results in a smaller hippocampus. APOE4 genotype is three times as likely to develop deposits of amyloid-beta on cerebral vessel walls which can lead to ischemia.
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Check your knowledge Genetics ApoE
True or False Late onset AD is caused by mutation to the ApoE gene on chromosome 19. TRUE FALSE
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Inflammation Upon examination, one type of brain cell, the microglia cell, is associated with the plaques in AD. Researchers are suspicious of this cell because it also participates in classic inflammatory processes. The good news is that non-steroidal anti-inflammatory drugs reduce the inflammatory response of these cells. Hope! Halliday G, Robinson SR, Shepherd C, Kril J. 2006
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Check your knowledge Inflammation
True or False The inflammatory response and AD have microglia cells in common. TRUE FALSE
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Hope for Alzheimer's Disease
Non-Steroidal Anti-Inflammatory Drugs Researchers are investigating the use of NSAIDs: Clinical trials are being conducted on Ibuprofen & Naproxen. inhibit platelet activation. decrease the formation of beta - amyloid which compromises the brain-blood barrier and vaso-activity. reduce the inflammatory response of brain cells. Halliday G, Robinson SR, Shepherd C, Kril J.2006
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Non-Steroidal Anti-Inflammatory Drugs
Some studies show: NSAIDS may delay the onset of AD. NSAIDS may slow the progression of the disease. NSAIDS may reduce the risk of developing the disease. Researchers caution: All NSAIDS can cause stomach irritation, gastrointestinal bleeding, heart attack, and stroke.
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Check your knowledge NSAIDs
True or False NSAIDs reduce inflammatory response, inhibit platelet activation and decreases the formation of beta-amyloid. TRUE FALSE
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Alzheimer’s disease (AD)
Overview of Alzheimer’s disease (AD) Alzheimer’s disease begins to damage the brain long before symptoms appear. The cells that process information have already begun to deteriorate and die. The hallmarks of AD are two abnormal microscopic structures called "plaques" and "tangles" . The amyloid plaques are clumps of protein that accumulate outside the brain’s nerve cells. The tangles are twisted strands of another protein that form inside cells. Brain atrophy and shrinkage results. New drugs targeting amyloid protein are being developed.
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References http://www.ahaf.org/alzdis/about/AD_2003.jpg
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References http://www.clevelandclinicmeded.com/diseasemanagement/
neurology/alzheimers/alzheimer Holliday G, Robinson SR, Shepherd C, Kril J. 2006 december2004/pg1.html
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References http://www.portfolio.mvm.ed.ac.uk/studentwebs/
session3/7/Genetics.htm text/health/alzheim/brain.gif
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