SlideShare verwendet Cookies, um die Funktionalität und Leistungsfähigkeit der Webseite zu verbessern und Ihnen relevante Werbung bereitzustellen. Wenn Sie diese Webseite weiter besuchen, erklären Sie sich mit der Verwendung von Cookies auf dieser Seite einverstanden. Lesen Sie bitte unsere Nutzervereinbarung und die Datenschutzrichtlinie.
SlideShare verwendet Cookies, um die Funktionalität und Leistungsfähigkeit der Webseite zu verbessern und Ihnen relevante Werbung bereitzustellen. Wenn Sie diese Webseite weiter besuchen, erklären Sie sich mit der Verwendung von Cookies auf dieser Seite einverstanden. Lesen Sie bitte unsere unsere Datenschutzrichtlinie und die Nutzervereinbarung.
ALZHEIMER’S DISEASE<br />Presentation by Hulya Diels<br />Shenzhou Open University<br />June 18, 2011<br />
Contents :<br />Motivation for the study<br />Definition of the disease<br />Mechanism of the disease<br />Causes of the disease<br />Symptoms of the disease<br />Detection & Diagnosis of the disease<br />Potential Treatments<br />Conclusion<br />Motivation for the study is to create awareness due to<br />Expected & alarming growth rate of number of people living with Alzheimer’s disease (AD) in all over the world.<br />Increase in death rate - It’s the 5th leading cause of death and while other causes of death continue to decline, AD increased by 66 % in 2010.<br />Unavailability of proven treatment to slow or stop the deterioration of brain cells in AD.<br />
Definition of the disease<br />AD is a neurodegenerative disease associated with the loss of nerve cells in areas of the brain that are vital to memory and other mental abilities.<br />Progressive cognitive, behavioral and physical impairmentsare the main characteristics.<br />AD was first identified in 1906 by German psychiatrist and neuropathologist, Alois Alzheimer and but research into this disease has only gained momentum in last 30 years.<br /> It is the most common form of dementia among elderly, with 50 to 70% of clinical cases confirmed as AD after death.(post-mortem)The others are vascular dementia, dementia with Lewy bodies, fronto-temporal dementia. The boundries among these subtypes are indistinct and in mixed forms. <br />Although it mainly affects older people, there is a growing awareness that it could start before the age of 65 but likelihood of developing dementia doubles every 5 years after age 65.<br /> <br /> <br />
<ul><li>It affects more than 35.6 millions of patients worldwide as of 2010; this number is expected to reach 115.4 million by 2050 as population age.
The fastest growth in the elderly population is taking place in China, India, South Asian and Western Pacific countries.
Source: World Alzheimer’s Report 2010, Alzheimer’s Disease International</li></li></ul><li>Mechanismof the disease<br />Brain is our most powerful organ, yet weighs only about 1.4 kilograms. It has a texture similar to firm jelly.<br /> It has three main parts:<br />The cerebrum fills up most of skull. It is involved in remembering, problem solving, thinking, and feeling. It also controls movement. <br />The cerebellum sits at the back of the head, under the cerebrum. It controls coordination and balance. <br />The brain stem sits beneath the cerebrum in front of the cerebellum. It connects the brain to the spinal cord and controls automatic functions such as breathing, digestion, heart rate and blood pressure.<br />
Neuron Forest<br />• The real work of the brain goes on in individual cells. An adult brain contains about 100 billion nerve cells, or neurons, with branches that connect at more than 100 trillion points. Scientists call this dense, branching network a "neuron forest."<br />• Signals traveling through the neuron forest form the basis of memories, thoughts, and feelings.<br />• Neurons are the chief type of cell destroyed by Alzheimer's disease.<br />
Cell signaling<br />• Signals that form memories and thoughts move through an individual nerve cell as a tiny electrical charge.<br />• Nerve cells connect to one another at synapses. When a charge reaches a synapse, it may trigger release of tiny bursts of chemicals called neurotransmitters that travel across the synapse, carrying signals to other cells.<br />• Alzheimer's disease disrupts both the way electrical charges travel within cells and the activity of neurotransmitters.<br />
Under the microscope<br />• Alzheimer tissue has many fewer nerve cells and synapses than a healthy brain. <br />• Plaques, abnormal clusters of protein fragments, build up between nerve cells. <br />• Dead and dying nerve cells contain tangles, which are made up of twisted strands of another protein. <br />• Scientists are not absolutely sure what causes cell death and tissue loss in the Alzheimer’s brain, but plaques and tangles are prime suspects.<br />
Plaques<br /><ul><li>Plaques form when protein pieces called</li></ul>beta-amyloid clump together. It comes from a larger protein found in the fatty membrane surrounding nerve cells. <br /><ul><li> Amyloid is a general term for protein fragments that the body produces normally. Beta amyloid is chemically sticky protein fragment snipped from an amyloid precursor protein (APP).
In a healthy brain, these protein fragments are broken down and eliminated. In Alzheimer's disease, the fragments accumulate to form hard, insoluble plaques.</li></ul>• The most damaging form of beta-amyloid may be groups of a few pieces rather than the plaques themselves. The small clumps may block cell-to-cell signaling at synapses. They may also activate immune system cells that trigger inflammation and devour disabled cells.<br />
APP is best known and most commonly studied as the precursor molecule whose proteolysis (digestion of proteins by cellular enzymes called proteases )<br /> generates <br />beta amyloid (Aβ), a 39- to 42-amino acid peptide whose amyloid fibrillar form is the primary component of amyloid plaques found in the brains of Alzheimer's disease patients.<br />
Tangles<br /><ul><li>Tangles destroy a vital cell transport system made of proteins. This electron microscope picture shows a cell with some healthy areas and other areas where tangles are forming. </li></ul> In healthy areas: <br />• The transport system is organized in orderly parallel strands somewhat like railroad tracks. Food molecules, cell parts and other key materials travel along the “tracks.” <br /><ul><li>A protein called tau helps the tracks stay straight .</li></ul>In areas where tangles are forming:<br />• Tau collapses into twisted strands called tangles. The tracks can no longer stay straight. They fall apart and disintegrate. Nutrients and other essential supplies can no longer move through the cells, which eventually die.<br />
Alzheimer’s changes the whole brain<br />These images show:<br /><ul><li>A brain without the disease
How the two brains compare</li></ul>Alzheimer’s disease leads to a loss of neurons and the tissue that connects them throughout the brain. Over time, the brain shrinks dramatically, affecting nearly all its functions. It’s called brain atrophy.<br />
Advanced changes in the brain<br />Here is another view of how massive cell loss changes the whole brain in advanced Alzheimer's disease. This slide shows a crosswise "slice" through the middle of the brain between the ears.<br />In the Alzheimer’s brain:<br />• The cortex shrivels up, damaging areas involved in thinking, planning and remembering. <br />• Atrophy is especially severe in the hippocampus, an area of the cortex that plays a key role in formation of new memories. <br />• Ventricles (fluid-filled spaces within the brain) grow larger.<br />
Stages of AD and Progressionthrough the brain<br />•Plaques and tangles (shown in the blue-shaded areas) tend to spread through the cortex in a predictable pattern as Alzheimer’s disease progresses.<br />• The rate of progression varies greatly. People with Alzheimer’s live an average of eight years, but some people may survive up to 20 years. The course of the disease depends in part on age at diagnosis and whether a person has other health conditions.<br />• Earliest Alzheimer's – changes may begin 20 years or more before diagnosis. <br />• Mild to moderate Alzheimer stages – generally last from 2 - 10 years. <br />• Severe Alzheimer’s – may last from 1 - 5 years.<br />
CAUSES OF THE DISEASE<br /><ul><li>Cholinergic (acetylcholine-producing ) Hypothesis, which proposes that AD is caused by reduced synthesis of the neurotransmitter acetylcholine.
In the peripheral nervous system acetylcholine plays a role in skeletal muscle movement, as well as in the regulation of smooth muscle and cardiac muscle. In the central nervous system acetylcholine is believed to be involved in learning, memory, and mood.
Acetylcholine is synthesized from choline and acetyl coenzyme A through the action of the enzyme choline acetyltransferaseand becomes packaged into membrane-bound vesicles . After the arrival of a nerve signal at the termination of an axon, the vesicles fuse with the cell membrane, causing the release of acetylcholine into the synaptic cleft . For the nerve signal to continue, acetylcholine must diffuse to another nearby neuron or muscle cell, where it will bind and activate a receptor protein.
This hypothesis has not maintained widespread support, largely because medications intended to treat acetylcholine deficiency have not been very effective. Despite this information , some believe, drugs that inhibit acetylcholinesterase in a reversible manner have been shown to improve memory in some people with Alzheimer's disease. </li></li></ul><li><ul><li>The Amyloid Hypothesis (1991) postulated that amyloid beta (Aβ) deposits are the fundamental cause of the disease. Support for this postulate comes from the location of the gene for the amyloid beta precursor protein (APP).
To date, only four of the genes in the human genetic map (the “genome”) have been conclusively shown to affect AD development. Mutations in three genes—the APP gene found on chromosome 21, the PS1 gene on chromosome 14, and the PS2 gene on chromosome 1—are linked to the rare, early-onset form of AD. The APP gene is responsible for making APP, PS1 and PS2 are responsible for making the presenilin protein. The fourth gene, APOE, affects the course of late-onset AD, depending on which allele, or variation, of the gene is inherited. (APOE-e2 may provide some protection against AD, APOE-e3 may play a neutral role in AD, and APOE-e4 increases the risk of developing AD.)
In 2009, this theory was updated, suggesting that a close relative of the beta-amyloid protein, and not necessarily the beta-amyloid itself, may be a major culprit in the disease. The theory holds that an amyloid-related mechanism that prunes neuronal connections in the brain in the fast-growth phase of early life may be triggered by aging-related processes in later life to cause the neuronal withering of Alzheimer's disease. Various inflammatory processes and cytokines may also have a role in the Pathology of Alzheimer's disease.</li></li></ul><li>Risk Factors<br />Despite the exact causes of Alzheimer’s being almost impossible to pinpoint, there are a number of different Alzheimer’s risk factors that have been noted to be a good indication that a person may develop Alzheimer’s. The risk factors for Alzheimer’s include:<br />Age- Alzheimer’s is much more likely to develop in people over the age of 65. People over 85 have an even higher risk. <br />Family History – Most Alzheimer’s disease cannot be inherited, however, early on-set Alzheimer’s is thought to be passed on through genes. <br />Gender – Women are more likely to develop Alzheimer’s than men. <br />Head Injury – A blow to the head or other forms of head injury are thought to play a role in causing Alzheimer’s. <br />Toxin Exposure – Exposure to certain toxins, like aluminum, has shown to cause an increase in the risk of Alzheimer’s. <br />Other Indicators – Developing Alzheimer’s has also been linked to high blood pressure and high cholesterol<br />
SYMPTOMS OF THE DISEASE<br />Alzheimer’s disease affect people in different ways but the most common symptom pattern begins with short term memory loss since disruption of brain cell function usually begins in regions involved in new memories.<br />There are 10 generally accepted symptoms of disease<br /> Memory loss that disrupts daily life<br /> Challenges in planning or solving problems<br /> Difficulty in completing familiar tasks at home, at work and at leisure<br /> Confusion with time or place<br /> Trouble understanding visual images and spatial relationships<br /> New problems with words in speaking or writing<br /> Misplacing things and losing the ability to retrace steps<br /> Decreased or poor judgment<br /> Withdrawal from work or social activities<br /> Changes in mood and personality<br />
DETECTION & DIAGNOSIS OF THE DISEASE<br />The early stages of Alzheimer's disease are difficult to diagnose.<br />First diagnosis is most commonly made by patient's primary care physician by obtaining a medical and family history .Ideally, a family member or person close to patient is available to provide input.<br />Secondly physician conducts cognitive tests, physical and neurologic examinations. When a neuropsychologist or other professional in the field of psychology or psychiatry sees a person exhibiting symptoms of Alzheimer's, a set of criteria is often used to help make an accurate diagnosis. The Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition), also known as the DSM-IV, outlines a detailed set of criteria for the diagnosis of Alzheimer’s.<br />Thirdly , the patient undergo computed tomography (CT), magnetic resonance imaging (MRI) scans to identify the changes in brain functions to rule out other possible causes of cognitive decline.<br />
Diagnostic Criteria for Dementia of the Alzheimer's Type (DSM-IV)<br />The development of multiple cognitive deficits manifested by both<br />memory impairment (impaired ability to learn new information or to recall previously learned information)<br />(2) one (or more) of the following cognitive disturbances:<br />aphasia (language disturbance<br />(b) apraxia (impaired ability to carry out motor activities despite intact motor function)<br />(c) agnosia (failure to recognize or identify objects despite sensory function)<br />(d) disturbance in executive functioning (i.e., planning, organizing, sequencing, abstracting)<br />B. The cognitive deficits in Criteria Al and A2 each cause significant impairment in social or occupational functioning and represent a significant decline from a previous level of functioning<br />C. The course is characterized by gradual onset and continuing cognitive decline.<br />D. The cognitive deficits in Criteria Al and A2 are not due to any of following:<br />(1) other central nervous system conditions that cause progressive deficits in memory and cognition (e.g., cerebrovascular disease, Parkinson's disease, Huntington's disease, subdural hematoma, normal-pressure hydrocephalus, brain tumor)<br />(2) systemic conditions that are known to cause dementia (e.g., hypothyroidism, vitamin B12 or folic acid deficiency, niacin deficiency, hypercalcemia, neurosyphilis, HIV infection)<br />(3) substance-induced conditions<br />E. The deficits do not occur exclusively during the course of a delirium<br />F. The disturbance is not better accounted for by another Axis I disorder (e.g., Major Depressive Disorder, Schizophrenia).<br />
POTENTIAL TREATMENTS<br />Despite all the research and investment, currently there is no cure for AD, available treatments offer relatively small symptomatic benefit but remain palliative in nature.<br />Patients who are diagnosed today have a number of treatments available, including medication, therapy, hormone replacement, alternative medicines.<br />None of these treatment options have proven to be 100 %effective, and not all of them will provide results for every patient.<br />AD Medication<br />Three types of drugs are currently used to treat symptoms: <br />blockers of the formation of amyloid deposits, like alzhemed,<br /> inhibitors of acetylcholine esterase, like tacrine, galantamine and rivastigmine<br />N-methyl-D-aspartate glutamate receptor antagonists, like memantine<br />These drugs produce improvements in cognitive and behavioural symptoms of AD. Other treatments<br />that are considered involve secretase inhibitors, drugs for<br />lowering cholesterol levels, chelators of metals, anti-inflammatory drugs and protein beta-amyloid vaccination, to stimulate the immune system to clean up the amyloid.<br />
TCM APPROACH – IMPLANT ACUPUNCTURE<br /><ul><li>Due to the fact, that the neurotransmitter "acetylcholine" is decreased in these patients, there is evidence, that Implant-Acupuncture is able to increase it. One should also consider the excess acetylcholine causes neuromuscular paralysis (i.e. interminable muscle contractions) throughout the entire body, leading to death by asphyxiation.
In contrast to conventional acupuncture, Implant-Acupuncture ensures a permanent stimulation on the acupuncture points. This enables the body to harmonize malfunctions continuously and enhances the bodies self-healing potential in a way,.
In the past, resolvable catgut filaments were implanted into the skin of the external ear in order to trigger a permanent curing .
Now, titanium needles and bio-resolvable needles are used for implantation. The implant-needle made from medical titanium has only the size of the tip of a pin. It can be implanted directly under the skin with the help of an especially designed device.</li></li></ul><li>CONCLUSION<br />Let’s support ALZHEIMER’S DISEASE Awareness since ;<br />Lack of awareness is a global problem and millions of people with AD, their families and friends are affected on personal, emotional, financial and social levels. Proper understanding of the societal costs of AD and its impact on families, health and social care services as well as goverments may help to address the problem.<br />The total estimated worldwide costs of AD are Usd 604 billion in 2010.These costs account for 1 % of the world’s gross domestic product. It’s higher in high income countries since lower income countries relies more on unpaid support of caregivers rather than nursing homes.<br />