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ALZHEIMER’S WHAT IS IT – WHAT TO DO ABOUT IT. VIDEO

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Presentation on theme: "ALZHEIMER’S WHAT IS IT – WHAT TO DO ABOUT IT. VIDEO"— Presentation transcript:

1 ALZHEIMER’S WHAT IS IT – WHAT TO DO ABOUT IT

2 VIDEO http://www.nia.nih.gov/alzheimers/alzheimers-disease-video http://www.nia.nih.gov/alzheimers/alzheimers-disease-video http://www.nia.nih.gov/alzheimers/alzheimers-disease-video

3 HISTORY OF ALZHEIMER In 1901, Dr. Alois Alzheimer encountered a 51-year-old patient named Mrs. Auguste Deter who was living in the Frankfurt Asylum in Germany. Mrs. Deter exhibited strange behavioral and cognitive symptoms, including a loss of short-term memory and agitation. Alzheimer followed her case from 1901 until her death in April of 1906. - See more at: http://www.healthcentral.com/alzheimers/cf/slideshows/the- history-of-alzheimer-s-disease#slide=3http://www.healthcentral.com/alzheimers/cf/slideshows/the- history-of-alzheimer-s-disease#slide=3 http://www.healthline.com/health- slideshow/alzheimers-history#promoSlide Psychiatrist Emil Kraepelin, Dr. Alzheimer’s colleague, coined the term “Alzheimer’s disease” in a 1910 medical book. http://www.healthline.com/health- slideshow/alzheimers-history#promoSlide http://www.healthline.com/health- slideshow/alzheimers-history#promoSlidehttp://www.healthline.com/health- slideshow/alzheimers-history#promoSlide

4 HISTORY CONTINUED http://www.healthcentral.com/alzheimers/cf/slideshows/the-history-of- alzheimer-s-disease#slide=4 In 1976, the neurologist Dr. Robert Katzman declared AD the most common form of dementia and a substantial public health challenge in an editorial. This brought awareness to the disease and helped launch many brain-related research projects through the NIH.

5 PROTEINS IDENTIFIED The main markers of Alzheimer’s disease in the brain are high amounts of two proteins: beta-amyloid and tau. Beta-amyloid was discovered in 1984. Two years later, tangles of tau were discovered in AD patients. Both proteins may cause brain cell damage. Researchers don’t know yet if high levels of tau and beta-amyloid cause AD, or if they’re just symptoms of it. http://www.healthline.com/health-slideshow/alzheimers-history#promoSlide http://www.healthline.com/health-slideshow/alzheimers-history#promoSlide http://www.healthline.com/health-slideshow/alzheimers-history#promoSlide

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7 Damage to Brain Structure and Function Alzheimer’s disease affects five million people in the U.S., according to the Alzheimer’s Association. The progressive disease disrupts memory and thinking, impairing and eventually killing brain cells. This impairment can lead to symptoms like forgetfulness, having difficulty with time, language problems, or an inability to recognize loved ones.five million http://www.healthline.com/health-slideshow/alzheimers-and-brain http://www.healthline.com/health-slideshow/alzheimers-and-brain http://www.healthline.com/health-slideshow/alzheimers-and-brain

8 PLAQUE FORMS In Alzheimer’s disease, a protein called beta-amyloid shows up in irregular clumps or clusters in the brain. This protein comes from a precursor protein found in a fatty membrane that covers nerve cells. The clumps of beta-amyloid fragments stick together to form plaque. These sticky clusters interrupt signals between synapses. Synapses are the spaces between nerve cells where information passes from one cell to another.

9 CAUSE OR EFFECT? Scientists are still not certain whether beta-amyloid plaque causes Alzheimer’s disease, or whether the irregular clusters in the brain result from the disease process. Investigators are also still sorting out whether clumped or unclumped versions of beta-amyloid cause Alzheimer’s. Researchers do know that mutations in APP, the precursor protein that forms beta-amyloid plaque, causes early-onset Alzheimer’s, which is rare.

10 TANGLES AND CELL DEATH In normal brain tissue, a protein called tau stabilizes microtubules. Microtubules are key parts of cell structure. In a diseased brain, these protein strands, or threads, become tangled. As a result, the orderly brain system of transporting cell nutrients along parallel structures—sometimes compared to railroad tracks—falls apart. Without critical nutrients, the brain cells die.

11 CONNECTIONS LOST Memory and thinking depend on transmission of signals among 100 billion neurons in the brain. Alzheimer’s interferes with cell signal transmission, as well as the activity of brain chemicals called neurotransmitters. The scrambled chemistry produces flawed signaling, so the brain’s messages are lost. This impacts the ability to learn, remember, and communicate

12 BRAIN INFLAMMATION / SHRINKS Microglia are a type of cell that initiates immune response in the brain and spinal cord. When Alzheimer’s disease is present, microglia interpret the beta-amyloid plaque as cell injury. The microglia go into overdrive, stimulating excess inflammation that further damages brain cells. Some Alzheimer’s research currently focuses on how this inflammatory response can be reduced or controlled. In advanced Alzheimer’s, the surface layer that covers the cerebrum, the largest part of the brain, withers and shrinks. This damage to the cortex plays havoc with the normal ability to plan ahead, recall, and concentrate. Alzheimer’s disease also affects the hippocampus. This part of the brain plays an important role in memory. Alzheimer’s disease causes the hippocampus to shrivel, which harms the brain’s ability to create new memories.

13 LESSEN SYMPTOMS Unfortunately, there is currently no cure for Alzheimer’s disease, and its brain damaging progress can’t be stopped. However, certain treatments, such as behavioral therapy and medication, can help ease the symptoms of the disease. Some medications may help to ease symptoms of confusion and memory loss. These include cholinesterase inhibitors and memantine, which are sometimes used together


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