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![Alzheimer Society of Canada (2016). Stages of Alzheimer's Disease (Web Page).
Toronto: Alzheimer Society Canada. www.alzheimer.ca/en/About-dementia/Alzheimer-
s-disease/Stages-of-Alzheimer-s-disease [Accessed: 11/07/17]
Alzheimer Society of Canada (2016). Alzheimer's disease (Web Page). Toronto:
Alzheimer Society Canada. http://www.alzheimer.ca/en/About-dementia/Alzheimer-s-
disease [Accessed: 11/07/17]
Mayo Clinic (2015). Alzheimer’s disease (Web Page). Rochester, NY: Mayo
Foundation for Medical Education and Research. http://www.mayoclinic.org/diseases-
conditions/alzheimers-disease/home/ovc-20167098 [Accessed: 11/07/17]
Lakhan, S.E. (2017). Alzheimer disease (Web page). Medscape Drugs and Diseases.
New York, NY: WebMD LLC. http://emedicine.medscape.com/article/1134817-overview
[Accessed: 11/07/17]
Tobias, M, Yeh, L.C., Johnson, E. (2008). Burden of Alzheimer's disease: population-
based estimates and projections for New Zealand, 2006-2031. Aust NZ J Psychiatry;
42(9):828-36.](https://image.slidesharecdn.com/alzheimerrajatppt-190813061737/75/Alzheimer-s-Disease-and-its-pathophysiology-19-2048.jpg)
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Alzheimer's Disease and its pathophysiology
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- 2. Welcome, in upcomingslides we will find out following things about Alzheimer's disease: Introduction Causes Pathophysiology Sign and symptoms Diagnosis Medications Treatment Risk factors So, let’s begin……….
- 3. Introduction Alzheimer disease (AD)is the most common cause of dementia in the elderly population. The disease usually manifests with the insidious onset of impaired higher intellectual function and altered mood and behavior. Later, this progresses to disorientation, memory loss, and aphasia, findings indicative of severe cortical dysfunction, and over another 5 to 10 years, the patient becomes profoundly disabled, mute, and immobile. AD is characterized by a progressive decline in cognitive function. AD is substantially increased among people aged 65 years or more, with a progressive decline in memory, thinking, language and learning capacity. AD should be differentiated from normal age-related decline in cognitive function, which is more gradual and associated with less disability. Disease often starts with mild symptoms and ends with severe brain damage. People with dementia lose their abilities at different rates
- 4. Alzheimer's disease iscaused by a combination of genetic, lifestyle and environmental factors that affect the brain over time. Less than 1 percent of the time, Alzheimer's is caused by specific genetic changes that virtually guarantee a person will develop the disease. These rare occurrences usually result in disease onset in middle age. The exact causes of Alzheimer's disease aren't fully understood, but at its core are problems with brain proteins that fail to function normally, disrupt the work of brain cells (neurons) and unleash a series of toxic events. Neurons are damaged, lose connections to each other and eventually die. The damage most often starts in the region of the brain that controls memory, but the process begins years before the first symptoms. The loss of neurons spreads in a somewhat predictable pattern to other regions of the brains. By the late stage of the disease, the brain has shrunk significantly. https://www.mayoclinic.org/diseases-conditions/alzheimers-disease/symptoms-causes/syc-20350447 CAUSES:
- 5. The pathophysiology ofAD is related to the injury and death of neurons, initiating in the hippocampus brain region that is involved with memory and learning, then atrophy affects the entire brain. 7 Amyloid beta, also written Aβ, is a short peptide that is an abnormal proteolytic byproduct of the transmembrane protein amyloid precursor protein (APP), whose function is unclear but thought to be involved in neuronal development. Amyloid beta monomers are soluble and contain short regions of beta sheet at sufficiently high concentration, they undergo a dramatic conformational change to form a beta sheet-rich tertiary structure that aggregates to form amyloid fibrils. These fibrils deposit outside neurons in dense formations known as senile plaques or neuritic plaques, in less dense aggregates as diffuse plaques, and sometimes in the walls of small blood vessels in the brain in a process called amyloid angiopathy or congophilic angiopathie. . https://www.who.int/medicines/areas/priority_medicines/BP6_11Alzheimer.pdf PATHOPHYSIOLOGY
- 6. In Alzheimer diseaseabnormal aggregation of the tau protein, a microtubule- associated protein expressed in neurons is also observed. Tau protein acts to stabilize microtubules in the cell cytoskeleton. Like most microtubule-associated proteins, tau is normally regulated by phosphorylation. In AD patients, hyper phosphorylated tau P-tau accumulates as paired helical filaments that in turn aggregate into masses inside nerve cell bodies known as neurofibrillary tangles and as dystrophic neurites associated with amyloid plaques
- 7. Researchers are focusedon the role of two proteins: •Plaques. Beta-amyloid is a leftover fragment of a larger protein. When these fragments cluster together, they appear to have a toxic effect on neurons and to disrupt cell-to-cell communication. These clusters form larger deposits called amyloid plaques, which also include other cellular debris. •Tangles. Tau proteins play a part in a neuron's internal support and transport system to carry nutrients and other essential materials. In Alzheimer's disease, tau proteins change shape and organize themselves into structures called neurofibrillary tangles. The tangles disrupt the transport system and are toxic to cells. Image source- https://i2.wp.com/discoveryeye.org/wp-content/uploads/2017/11/alzheimer-brain.png?ssl=1
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- 9. Neurobiological mechanisms involvedin the pathogenesis of Alzheimers disease
- 10. The formation ofplaques and tangles also prevents the production of some important brain chemicals, called neurotransmitters (eg: acetylcholine, which is important in memory function). Over time the loss of brain cells causes the brain to shrink. While there is no known cause for Alzheimer's disease, some research studies have indicated that the following factors may play an important role in the development of the condition: •Genetic factors, such as the presence of, or changes to, certain genes •Environmental factors, such as long-term exposure to some environmental solvents (eg: pesticides, glues and paints) or infection with certain viruses or bacteria •Lifestyle factors, such as a lack of exercise, poor-quality sleep and a diet lacking fruit and vegetables. www.southerncross.co.nz/group/medical-library/alzheimers-disease-causes- symptoms-prevention
- 11. Signs and symptoms Thedegenerative changes that occur with Alzheimer's disease affect the areas of the brain that control thought, memory and language resulting in gradual signs and symptoms related to a person’s behaviour and mental function. Often, physical functions such as bowel and bladder control are also affected. With Alzheimer’s disease there is great individual variability as to the nature of symptoms experienced and the speed at which deterioration occurs. The types of behaviour change and the length of time symptoms are present are different for each person. The symptoms of Alzheimer's disease typically develop quite slowly. The time between the onset of the disease and death can range from five to 20 years.
- 12. Symptoms commonly experiencedduring the early stages of Alzheimer's disease include: •Mild forgetfulness – especially short-term memory loss •Mood changes, including irritability and anxiety •Difficulty processing new information and learning new things •Loss of spontaneity and initiative •Confusion about time and place •Communication difficulties •Decline in ability to perform routine tasks. As Alzheimer’s disease progresses the following symptoms may develop: •Increasing short-term memory loss and confusion •Difficulty recognising family and friends •Shorter attention span and feelings of restlessness •Difficulty with reading, writing and numbers •Possibly neglectful of hygiene •Loss of appetite •Personality changes (eg: aggression, significant mood swings) •Requires increasing assistance with daily tasks.
- 13. Towards the laterstages of the disease the following symptoms may be experienced: •Inability to understand or use speech •Incontinence of urine / faeces •Inability to recognise self or family •Severe disorientation •Increasing immobility and sleep time. The changes brought about by Alzheimer's disease can be increasingly difficult for family members and friends as the person’s condition deteriorates and they become unable to recognise loved ones. Although a person loses many abilities as the disease progresses, it is often helpful to focus on the abilities that do remain, such as the senses of touch and hearing and the ability to respond to emotion.
- 14. Diagnosis There is ano single test to diagnose Alzheimer’s disease. Diagnosis involves a full assessment of medical and psychiatric history to rule out other possible causes. Therefore, a variety of tests are required to obtain a conclusive diagnosis, which may include: •A neurological and physical examination •Blood and urine tests •Brain scans •Mental status assessment to determine the level of mental deterioration •Caregiver interview to determine the level of dependency. Scans to check brain structure and function may be recommended. The different types of scans used may include CT scanning (computerised tomography), MRI (magnetic resonance imaging) and PET (positron emission tomography).
- 15. Medications Medications such assleeping tablets and tranquillisers may help to control symptoms such as sleeplessness and agitation. However, they often cause increased confusion, so their use should be limited. A group of medications called cholinesterase inhibitors have shown some effectiveness in slowing the progression of the condition in some people. These medications help prevent the breakdown of acetylcholine, a neurotransmitter responsible for memory. Cholinesterase inhibitor medications that are available in New Zealand include donepezil, rivastigmine and galantamine. More recently, another drug - memantine - has become available in New Zealand. Memantine works in a different way to the cholinesterase inhibitors, aiming to prevent the entry of an excess amount of calcium into brain cells. Higher than normal levels of calcium in the brain cells causes damage to them and also prevents them from receiving signals from other brain cells. Research continues into the development of other medications for the treatment of Alzheimer's disease. Medications being investigated include those that prevent the build- up of amyloid deposits in the brain, as well as looking at the use of some anti- inflammatory and hormone medications. Research also continues into the use of alternative therapies such as anti-oxidants like Vitamin E, curcumin, selenium and some herbal extracts (ginko balboas in particular).
- 16. Treatment As there isno known cure for Alzheimer’s disease, treatment focuses on managing symptoms and supporting the person and their family. This may include: •Treating medical conditions that may contribute to confusion or physical decline eg: lung disease or anaemia •Encouraging stimulating activities in order to encourage the person to continue their normal activities as much as possible •Providing memory aids and memory triggers such as calendars and written reminders •Encouraging social interaction to help prevent feelings of loneliness and depression •Contacting support groups that may be able to offer family/caregivers assistance •Encouraging regular routine to reduce confusion •No Smoking
- 17. Prevention / riskreduction There are no proven ways to prevent the development of Alzheimer's disease. However, there is epidemiological evidence to suggest that leading a healthy lifestyle can reduce the risk of Alzheimer's disease. Regular physical activity and exercise may have a general protective effect on brain health and may slow progression of Alzheimer's disease. Although there are no specific dietary specifications for Alzheimer's, a Mediterranean-style diet (ie: plant foods such as vegetables, fruits, beans, whole grains, nuts, olives and olive oil, along with some cheeses, yoghurt, fish, poultry and eggs) may reduce the risk of Alzheimer's disease, and has the added benefit of lowering cardiovascular disease and type2 diabetes risk. For more diet information, refer to our healthy heart diet.
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- 19. Alzheimer Society ofCanada (2016). Stages of Alzheimer's Disease (Web Page). Toronto: Alzheimer Society Canada. www.alzheimer.ca/en/About-dementia/Alzheimer- s-disease/Stages-of-Alzheimer-s-disease [Accessed: 11/07/17] Alzheimer Society of Canada (2016). Alzheimer's disease (Web Page). Toronto: Alzheimer Society Canada. http://www.alzheimer.ca/en/About-dementia/Alzheimer-s- disease [Accessed: 11/07/17] Mayo Clinic (2015). Alzheimer’s disease (Web Page). Rochester, NY: Mayo Foundation for Medical Education and Research. http://www.mayoclinic.org/diseases- conditions/alzheimers-disease/home/ovc-20167098 [Accessed: 11/07/17] Lakhan, S.E. (2017). Alzheimer disease (Web page). Medscape Drugs and Diseases. New York, NY: WebMD LLC. http://emedicine.medscape.com/article/1134817-overview [Accessed: 11/07/17] Tobias, M, Yeh, L.C., Johnson, E. (2008). Burden of Alzheimer's disease: population- based estimates and projections for New Zealand, 2006-2031. Aust NZ J Psychiatry; 42(9):828-36.