Alzheimers Disease: Symptoms and Treatment - Term Paper Example

Running head: Alzheimer’s disease Alzheimer’s disease Andrew Cosentino 2 June 2009 OCM BOCES Liverpool Instructor: Mrs. Vigliotti Abstract Alzheimers disease with its etiological heterogeneity is a disease associated with the brain and its functions, usually affecting the elderly people. This paper outlines the severity and progress of this disease and explains the various symptomatic manifestations along with clinical and pathological findings. Its treatment and management based upon the type of symptoms have been explained along with certain guidelines for the caregivers of patients affected with this distressing disease as proposed by the American Psychiatric Association. Current research in various related fields and approaches to the treatment and management of this disease have been highlighted. Table of Contents Content Page No. 1. Introduction 4 1.1 History 4 2. Associated with the disease 5 2.1 Causes and triggers of Alzheimer’s disease 5 2.2. Clinical and pathological indications 7 2.3 Symptoms and manifestations 9 2.4 Diagnosis 10 2.5 Treatment 11 3. Conclusion 13 1. Introduction Alzheimers disease is a neurological disorder leading to dementia, and most commonly described as loss of mental abilities such as memory and reasoning. With its progressive nature, it manifests as slight memory and language problems in the beginning and further leading to confusion, personality and behavioral changes. Thus, this disease manifests in the form of cognitive and behavioral symptoms. This disease affects the brain cells, nerves, and the neurotransmitters in the brain. This disease commonly affects people aged above 65 years; the chance of getting affected is about one in 20, and after the age of 80, chances further increase to one in five. In Europe, studies of 2000 have shown that about 15% of population aged over 65 years and 3% aged over 80 years were affected by this disease (Barnes, J, Archer, H, and Fox, N.C; 2007). Till date, no ultimate cure has been found for this disease. This disease requires a symptomatic treatment through periodic clinical, pathological tests, and disease modifying therapies coupled with a thorough monitoring of disease progression, all of which can provide maximum benefit. Treatment plans for Alzheimers disease include cognitive and behavioral symptoms management separately. 1.1 History The first description of Alzheimer’s disease dates back to 1906, named after Alzheimer, and was first granted by his mentor, Kraepelin in 1910 (Bellanger, J F; 2006). In his eighth edition of Handbook of psychiatry, Kraepelin explained the autopsy study corresponding with Alzheimer’s description and similar to the changes that represented the most serious form of senile dementia. Despite the connection of Alzheimer’s disease discovery to Alios Alzheimer’s, there has been lot of debate over the issue as these symptoms were already noticed by other scientists and reported. Nevertheless, there is not much evidence that Alzheimer claimed for the discovery. In his study of a woman’s brain who died at the age of 51 following a progressive memory damage and brain injury, Alzheimer found small lesions called amyloid plaques and neurofibrillary tangles in her gray matter. About half century later, scientists linked this unusual disease of middle-aged people to common condition of old-aged people. Even today, extensive research is being carried out to prove the point that Alzheimer’s findings are actually the cause of this disease. Hereditary and age factors are linked to the disease. Scientists are now linking abnormalities in chromosome 19 to be associated with Alzheimer’s disease. Other conditions related to the disease are high risk for people aged between 30-50 with a family history, relating to chromosome 1, chromosome 14, and chromosome 21 (Agronin, M.E; 2007). 2. Associated with Alzheimers disease 2.1 Causes and triggers of Alzheimer’s disease Alzheimers disease, like most other chronic diseases, is likely to be caused by a complex interaction of genetic and environmental risk factors. A few definite risk factors associated with Alzheimer’s disease, identified by Kuhn and Bennett (2003), are advanced age, family history in firs-degree blood relation, genetics, Down’s syndrome, history of head trauma, and low educational and occupational status. Other potential risk factors include female sex, history of strokes or cerebrovascular disease, Parkinson’s disease, race and ethnicity (African-Americans are high-potential risks), environmental toxins, diet, lack of exercise, stress, and depression (Turner,F.J; 2005). People with high cholesterol levels also carry high risk of Alzheimers disease. Environmental toxins as causative agents of Alzheimer’s disease have been debated intensely. As ingestion of toxic metals such as lead can cause brain damage, there has been extensive research to find out toxic substances in environment that can trigger Alzheimers disease. Kuhn and Bennett (2003) have quoted that a study in the U.S. showed an increased risk of Alzheimers disease among people exposed to organic solvents such as benzene and toluene. Another study linked high risk of Alzheimers disease in people exposed to glues, pesticides, and fertilizers. Exposure to electromagnetic fields may also pose risk of this disease. Other toxic substances such as tobacco consumed through smoking are also considered to be a risk factor based upon a statistical study; however, this fact is yet to be confirmed. The data also proved that smoking is linked to memory loss. Diet rich in fat and calories increases risk of Alzheimers disease. Lack of exercise between ages 20 to 59 had high risk for developing the disease than for those who exercised. Intense psychological stress is often linked with Alzheimers disease. Familial Alzheimer’s disease (FAD) is often reported with early onset and progresses faster than the more common form of Alzheimer’s disease. Almost fifty percent of FAD is related to the defects in genes of the above mentioned three chromosomes. In the late-onset Alzheimers disease, a gene on the chromosome 19 has been identified affect the production of protein, apolipoprotein (ApoE) that is responsible for transporting cholesterol in the blood. One of the three types of this gene is inherited from each parent. One of the three types is ApoE4 which carries high risk of causing the disease. The disease has also been reported in the absence of any family history. In the absence of any family history, age is an important trigger for development of Alzheimers disease. 2.2. Clinical and pathological indications Alzheimers disease is the most common form of dementia in the elderly people aged above 65. The most common clinical findings in this disease include loss of recent memory, problems in calculation and execution of activities. These difficulties eventually progress to dementia in a span of eight to nine years. Motor functions may get impaired in the terminal stages of the disease causing inability to walk or move. The pathological precursors of this disease begin several decades before the clinical symptoms are manifested. The most important characteristic features of this disease, as described by Alois Alzheimer in 1907, are neuronal loss, profuse extracellular deposition of amyloid B peptide (AB), and widespread formation of intraneuronal neurofibrillary tangles, usually found in the higher order cortical regions including frontal, parietal, and temporal cortex and the limbic system, and are relatively rare in primary motor or sensory areas except for olfaction. For this reason, Alzheimers disease is looked at more like a cognitive disorder than motor one (Rogers, J.; 2001). However, the reasons for neurodegeneration are still unknown. The peripheral inflammation is linked to cell death and deposition of highly inert and insoluble deposits, aggregated amyloid B and neurofibrillary tangles. This inflammation is likely to cause further damage to the surrounding healthy cells. Abnormalities have been reported in different cells of the nervous system and brain. For instance, astrocytes which are essential for normal function of neurons typically show a hypertrophied reactive morphology characterized by enhanced expression of glial fibrillary acidic protein (GFAP). They may also divide extensively, exhibiting a peri-plaque localization around amyloid B deposits. Astrocytes are reported to have an inhibiting action on microgilal clearance of amyloid B cells by depositing peptidoglycans on the plaque. These cells can also be found surrounding the neurofibrillary tangles. Reaction of astrocytes in Alzheimers disease condition include expression of early response genes, adhesion proteins, cytokines, proteases, eicosanoids, and other cytotoxic products. Ectoenzymes that result in breaking down the amyloid B cells in plaques or the paired helical filaments in neurofibrillary tangles may also be secreted. Microglia may present with profuse phagocytic function, especially in the cortical gray matter. This results in production of wide range of inflammatory mediators including complement, cytokines, chemokines, reactive oxygen intermediates, secreted proteases, excitatory amino acids, and nitric oxide. Again the profuse secretion of these cells is believed to be caused by amyloid B cells. Neurons are also capable of producing inflammatory mediators, including complement, cyclooxygenase, pro-inflammatory cytokines which the body’s immune system perceives as invasive and inflammatory cells of the body’s immune system start to dissolve the neurons. The neurofibrillary tangles block the flow of nutrients from the cell body to the nerve endings, interrupting the communication inside the cell and eventually dissolving it. In some cases, neurons degenerated without any evidence of tangles or plaques. In such cases, lack of acetylcholine, a chemical messenger for communication between neurons, was evidenced in those neurons (Fotuhi, M; 2004). 2.3 Symptoms and manifestations Alzheimers disease manifestations can be seen in the brain with disruption of three key processes, i.e., nerve cell communication, metabolism, and repair. This disruption ultimately causes nerve cells to stop functioning, lose connections with other nerve cells, and die. The disease progresses in stages; firstly, in the form of early mild forgetfulness, and then to severe loss of mental function, referred to as dementia. The cognitive symptoms include problems with thought processes like memory, language, and judgment. Behavioral symptoms include agitation, suspicion, and depression. Symptoms of depression include irritability, crying spells, apathy, difficulty concentrating or remembering, sleep disturbance, fatigue, problems with eating (weight gain or loss), diminished interest in pleasurable activities, and feelings of worthlessness and hopelessness. For people with Alzheimers disease, loss of intellectual abilities occurs gradually. A growing dependency on others because of limitations imposed by the disease may diminish their self-esteem. With the frontal lobes getting affected, the patient may become disorganized or exhibit inappropriate behavior. When the parietal lobes are affected, the patient may lose his orientation skills. Eventually, when all lobes get affected, the patient may lose the ability to perform routine and daily tasks. 2.4 Diagnosis People having difficulties with memory and other mental functions are examined by a healthcare provider to diagnose Alzheimers disease. This examination includes person’s history, complete physical exam, laboratory tests, brain scans, and a series of other tests to measure cognitive skills such as memory, language skills and other abilities related to brain functioning. Here, it is important to rule dementia caused due to other illnesses and medications. Consequent to the pathological processes associated with this disease, biological changes in the brain can be observed at a microscopic level. These changes include neurotransmittal loss, dendritic pruning of neurons, and neuronal cell death. Complex imaging techniques are used to assess these changes. Various functional imaging techniques used include single photon emission computerized tomography (SPECT), positron emission tomography (PET), proton magnetic resonance spectroscopy (MRS), diffusion tensor imaging, and functional magnetic resonance imaging (fMRI). Structural imaging of the brain is studied through magnetic resonance imaging (MRI) and computerized tomography (CT) (Barnes, J, Archer, H, and Fox, N.C; 2007) 2.5 Treatment The established fact that there is no cure for Alzheimers disease has resulted in extensive research and advances in its treatment, including medications and non-medication approaches through symptom management, aimed to improve daily functioning and maximize quality of life. Management of Alzheimers disease is done separately for cognitive and behavioral symptoms. A comprehensive care plan for this disease includes appropriate treatment options and a continuous monitoring of the options for their effectiveness; changing of treatment course and exploring alternatives as necessary; consider individual and family goals for treatment and tolerance for risk; appropriate counseling for caretakers of the patients. According to The American Psychiatric Association (2006), the Food and Drug Association (FDA) has two types of approved medication for cognitive symptoms that act by temporarily delaying the memory loss process. First type is the cholinesterase inhibitors that inhibit the break down of acetylcholine, and thereby, support communication among nerve cells i.e., artificially mimicking the natural process to some extent. These medications include Donepezil, Rivastigmine, and Galantamine. The benefits of these drugs include slight improvement for a period of many months in memory, language skills, and the ability to handle tasks like personal grooming. Though high doses of these drugs have reported evident benefits, their side effects like diarrhea, vomiting and nausea cannot be ruled out. The second type of drugs work by regulating the activity of glutamate, another chemical neurotransmitter; the drug approved is Memantine. Vitamin E is also prescribed for cognitive symptoms, and it delays loss of ability to carry out daily activities. Behavioral symptoms treatment is classified as non-drug treatments and prescription medications. The non-drug treatment includes identifying the symptom and cause followed by changing the environment to remove challenges or obstacles; often change in patient’s environment causes the symptom. Medications approved in treatment of behavioral symptoms are anti-anxiety medications, anti-depressants and anti-psychotic drugs. Two interrelated causes of depression have been identified, psychological disturbances and biological changes. Anti-depressants known as Selective Serotonin Reuptake Inhibitors or SSRIs are prescribed to relieve symptoms of depression. These are known to have fewer side effects than the traditional drugs. Drugs like Zoloft, Paxil, Prozac, Luvox, and Celexa form a part of this prescription (Kuhn, D & Bennett, A; 2003). These medications can cause side effects and hence should be given to the patients only under appropriate prescription and close supervision. Because responses to drugs vary from person to person, different types of drugs and different dosages may have to be tried before improvement is seen. The Alzheimers Association’s guidelines (Basics of Alzheimers disease; 2005) for caregivers in management of behavioral symptoms can be very helpful in managing the behavioral and cognitive symptoms to a large extent. Caregivers need to ensure a calm, safe setting is created by eliminating clutter, noise, and glare. They should develop soothing rituals with regular easy daily routines with comforting objects. Gentle music and a frequent reassuring touch can help. They can provide opportunities for exercise and satisfying activities suitable to the person’s abilities. Caregivers need to constantly check the patient’s reactions, any pain, hunger, thirst, constipation, full bladder, fatigue, infection and skin irritation. They need to have lot of patience while dealing with the patient’s frustration and avoid any situation that may be distressing on the patient’s mental status. Caregivers need to simplify tasks for the patients and do not indulge them in extended discussions or talks. Periodic rest should be given to the patients. Usage of labels to prompt or remind them will help. Safety of the patients and appropriate supervision should be taken care of. With these current drugs being used to treat Alzheimers disease, numerous researches are being carried out all over the world to develop further approaches to treating, slowing, or even preventing this disease. A few approaches described by Kuhn and Bennett include treatment with anti-inflammatory drugs, statin drugs to reduce cholesterol levels, and estrogen-replacement therapy for women. Other approaches include trials of antioxidants to counter the free radicals in brain, for which vitamin E is being tested in various ways. Further studies involving supplemental folate, selenium, B6 and B12 are being carried out. Many other contemporary and alternative medicinal approaches are receiving high resurgence from all over the world. Practices such as acupuncture, acupressure, massage, aromatherapy, and herbal medicine are a few options being considered. Production of vaccine has also been tried which was quite useful when tried in mice; however, due to its side effects, had to be stopped from being used in humans. Nevertheless, research still continues in this field. 3. Conclusion In conclusion, Alzheimers disease is a disorder identified with many etiologies and is connected with brain and its functions. The dementia associated with this disease is more serious as it progresses. It is associated with deterioration of cognitive functions followed by behavioral functions. No specific cause can be attributed to this distressing disease which affects elderly persons. It impairs the person mentally and physically to some extent. The amyloid B cells play a central role in the pathogenesis of this disease. From an incurable stage, it has reached a stage where most of the symptoms can now be addressed with appropriate care and frequent monitoring. A myriad of treatment methodologies are being developed to manage this disease through prevention, slowing and treating its symptoms. As this disease requires wide-ranging, rigorous, and serious management, its treatment can prove very expensive. The family members and community play a vital role in bringing about improvement in the patient’s condition. References Agronin, M.E. (2007) Alzheimer’s disease and Other Dementias: A Practical Guide. Edition 2. Published by Lippincott Williams & Wilkins. http://books.google.co.in/books?id=IlY13n4mlmYC&pg=PA92&dq=Chromosome+1,+14,+21+Alzheimers American Psychiatric Association (2006). American Psychiatric Association practice guidelines for the treatment of psychiatric disorders. Published by American Psychiatric Pub. http://books.google.co.in/books?id=zql0AqtRSrYC&pg=PA169&dq=American+Psychiatric+Association+(2006).++American+Psychiatric+Association+practice+guidelines+for+the+treatment+of+psychiatric+disorders.+Published+by+American+Psychiatric+Pub#PPA102,M1 Bellanger, J F. (2006) Progress in the history of Alzheimer’s disease: the importance of context. In Perry, G’s (Ed.) Alzheimers disease: a century of scientific and clinical research. Journal of Alzheimer’s disease, 2006. Published by IOS Press. pp 5-13 http://books.google.co.in/books?id=QPqCvP0wFjUC&printsec=frontcover&dq=alzheimer%27s+disease&lr= Fotuhi, M. (2004) The Memory Cure: How to Protect Your Brain Against Memory Loss and Alzheimers Disease. Published by McGraw-Hill Professional. http://books.google.co.in/books?id=eFruMLHTupoC&pg=PA51&dq=inflammation+neurons+Alzheimer%27s+disease&lr=#PPA55,M1 Kuhn, D and Bennett, D.A. (2003). Alzheimers early stages: first steps for families, friends, and caregivers. Edition 2. Published by Hunter House. http://books.google.co.in/books?id=iDsIb50oSa8C&pg=PA47&dq=risk+factors+of+alzhemier%27s+disease#PPA48,M1 Rogers, J. (2001) Neuroinflammatory mechanisms in Alzheimers disease: basic and clinical research. Published by Birkhäuser. http://books.google.co.in/books?id=x5y3wRrRquAC&pg=PA3&dq=alzhemier%27s+disease&lr=#PPA3,M1 Barnes, J, Archer, H, and Fox, N.C. (2007) Imaging cerebral atrophy in Alzheimers disease. In Sun, M.K’s (Ed) Research progress in Alzheimers disease and dementia. Published by Nova Publishers Inc. pp. 403-435. http://books.google.co.in/books?id=o2kw6t8oRFAC&pg=PA403&dq=alzheimer%27s+disease+above+65+years+and+above+80+years Turner, F. J. (2005). Social work diagnosis in contemporary practice. Published by Oxford University Press US, 2005. http://books.google.co.in/books?id=2IW0b4TjKmUC&pg=PA419&dq=history+of+alzheimer%27s+disease#PPA420,M1 Website Basics of Alzheimer’s disease: What it is and what you can do. (2005) Alzheimers Association. http://clk.about.com/?zi=1/XJ&sdn=alzheimers&cdn=health&tm=4124&gps=200_1400_1003_622&f=00&su=p284.9.336.ip_p736.5.336.ip_&tt=2&bt=0&bts=0&zu=http%3A//www.alz.org/national/documents/brochure_basicsofalz_low.pdf Read More