Alzheimer's disease is the most common form of the dementia among old people. Dementia is a brain disease that affects a person’s memory and cognition. Alzheimer’s disease is a form of brain disorder that affects the cerebral system in a progressive and irreversible manner. Onset of the disease occurs after 60 years of age although it may appear earlier (in some rare cases). The span between onset of the disease and death span 8-10 years. Symptoms of the disease include cognitive deterioration, increasing requirements for care, loss of functional dependence and changes in behavior. Individual with the disease may also exhibit such behaviors like wandering, motor disturbances and catastrophic reactions to minor stressors. This paper will discuss the best possible ways of treating AD.
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Alzheimer’s disease is characterized by degeneration of cortical neurons in addition to the formation of senile plaques and neurofibrillary changes. It is the most common cause of dementia in people over the age of 65 in the developed world. According to Jorm (2001), Alzheimer’s is a type of dementia where the nerve cells change in an irreversible way to cause progressive brain disorder leading to death of the brain cells. Dr. Alois Alzheimer discovered the disease in 1906. He described the disease to have hallmarks known as plaques and tangles, which stimulate damage of the nerve cells in the brain. Due to the degenerating process, there occurs a resultant deficiency in cholinergic function. Severity of dementia correlates to the loss of central cholinergic activity. The incidence of Alzheimer’s disease has increased in the recent past as a result of the extended lengthy of life. This paper seeks to discuss the causes, diagnosis and treatment of Alzheimer’s disease. Early clinical signs that are believed to be as a consequence of Alzheimer’s disease are a decline in memory and executive functions.
This disease begins from disruption of brain cells damaging the synapses gradually. The synapses comprise of nerve cells, which transfer information for memories, skills, and thoughts. Gaminiratne (1996) adds that damage of synapses leads to individual experience of loss of remembering, reasoning, and thinking. This disease affects aging group with 65 years and above. It estimates that one out of every 85 people in the old age suffers this disease (Jorm 2001; Gaminiratne 1996).
Discovery and Incidence of Alzheimer’s
Alzheimer’s disease was first described in 1907 as a disease of the cerebral cortex whose characteristics were ‘senile’ plaques and neurofibrillary tangles. Neocortical cerebral amyloid deposits have been positively identified in about 50% of brains from people that are over the age of 75. However, the presence of Alzheimer’s disease dementia does not reach 50% the person is over the age of 85. The patholological process of Alzheimer’s disease in this day and age, is noticeable during life only when the disease manifests clinically.
Alzheimer’s Relation to Dementia
Dementia is an acquired syndrome whereby there is a decline in memory and thinking which is sufficient to one’s day to day activities and performance. Some people may demonstrate deficits either in memory and other cognitive domains or deficits in alone that are indicative of an abnormality but are not quite severe enough to be termed dementia. A large number of people who go on to develop dementia often go through a transitional stage that may be termed as very mild dementia while others term it mild cognitive impairment or ‘cognitively impaired no dementia’. Cognitive impairment and dementia can be caused by a variety of things such as a range of neurodegenerative disorders, infections, tumors, vascular damage and other causes (Perrin, & Holtzman, 2009).
Causes/risk factors of Alzheimer’s:
Age is the greatest risk factor for Alzheimer’s disease. The risk of developing Alzheimer’s disease significantly increases with advancement in age. After the age of 65, the risk of developing this disease doubles every five years and by the age of 85, the risk is 50%. In a family without any history of this disease, the risk of developing Alzheimer’s is estimated at 15%.
Women seem to be at a higher risk of developing Alzheimer’s disease; however, scientists are not sure whether being female in itself is a risk factor or is it because women live longer or perhaps because of the drop in estrogen levels which may be protective against memory loss as a result of menopause, thus they may be predisposed to this disease (Medifocus.com).
There exists a considerable retrospective epidemiological literature indicating that a traumatic injury to the head is associated with an increase in the risk of developing Alzheimer’s. However, not all studies have confirmed this association. A meta-analysis of 7 case control studies calculated the relative risk of developing Alzheimer’s disease of 1.82 for head injury that results in loss of consciousness but it only reaches statistical significance for men, who form the majority of the people that have suffered head injuries. (Silver, 2011).
The MIRAGE study from Boston University run by Dr. Lindsay Farrer examines genetic risk factors that influence the development of Alzheimer’s has documented a cumulative risk of developing Alzheimer’s disease aong first degree relatives at about twice the risk in non relatives. Unaffected siblings of patients that suffer from Alzheimer’s disease have a higher risk of developing dementia, about two- to fourfold risk of developing dementia, above that of the general population that are of the same age. Other researchers in New York and Washington D.C., have shown that the manifestation of Alzheimer’s disease in a first degree relative increases that individuals lifetime risk of Alzheimer’s threefold (Sabbagh, 2009).
There is a high prevalence of Alzheimer’s disease among older adults with Down syndrome. Autopsy studies have revealed that nearly 100% of people with Down syndrome who live beyond the age of 40 years have cerebral neurofibrillary tangles and neurotic plaques which are the characteristic features of Alzheimer’s disease. It is however estimated that only about 40% of adults who have Down syndrome have behavioral symptoms and memory loss which are characteristic of Alzheimer’s disease. It is not clear why some individuals with Down syndrome fail to develop the external manifestations of Alzheimer’s disease despite the fact that their brains show the neuropathological features of this disease (Hersen, 1998).
Diagnosis of Alzheimer’s: A Neurological Examination
There are no accurate diagnostic methods, however, a neurological examination of the patient’s movement or the motor system; for instance agitation and retardation, sensory functioning, walking (gait) and co-ordination with the purpose of detecting problems with the nervous system that may be responsible for the problems with behavior and thinking.
There are no other diagnostic methods other than post-mortem. Only probabilistic statements can be made about whether or not there is dementia can be made in a given patient. Any Alzheimer’s disease changes in the post-mortem brain such as neurofibrillary tangles, neuritic plaques or diffuse amyloid are considered to be abnormal and should be recorded as such. The presence of Alzheimer’s disease lesions and their amount in the postmortem brain cannot be predicted with certainty but inferred when the case of progressive dementia has been recorded ante-mortem in an elderly individual (Rosenberg, 2005).
Treatment of Alzheimer’s: Drugs
Early treatment of Alzheimer’s improves the quality of life of patient. Pharmacological treatment is used in the early stages of the disease and is quite helpful in improving cognitive disorders and also helps in slowing down the advancement of the deficit and also reduce the psychiatric symptoms for example psychosis, agitation and depression. Non- pharmacological treatments on the other hand, include caring for the patient through the implementation of psychotherapeutic and stimulation interviews. Psycho education is important because it can result in behavioral changes and may therefore diminish the need for a symptomatic treatment in the same way that an organized routine can be set up, the cognitive stimulus when possible, the avoiding of isolation and affective contention( Monczor, 2005). This paper will discuss about effective psychotherapy as opposed to sports counseling.
Music therapy is the clinical based use of music interventions as a form of therapeutic relationship by an individual (or professional) who has completed an approved music therapy program. Music therapy is designated to help promote interaction for patients with the Alzheimer's disease. Music is known to manage stress, alleviate pain, enhance memory, promote wellness and improve communication. Research in music therapy indicates that music can facilitate movement and physical rehabilitation, increases motivation to continue treatment, creates an outlet for expression feeling and provides emotional support for the affected people and their families. Unique outcomes are possible from music therapy due to its non-threatening medium.
This pharmacological group is the most studied for the treatment of Alzheimer’s disease. They improve the cholinergic transmission thereby inhibiting the enzyme in three ways; reversible, pseudoreversible or irreversible way. During the early stages of the disease, they moderate the effects of the disease and its long term use delays the advance of the cognitive deteroriation. The cholinesterase inhibitor medications are: donepezil, rivastigmine, tacrine, and galantamine (Monczor, 2005).
Tetra-hidro-aminoacridine (THA) is a reversible inhibitor of the cholinesterase. Tacrine is metabolized in the liver and has a half life of 2 to 4 hours. Side effects of tacrine are nausea, stomach ache, anorexia, vomits, bradicardia, ataxia,mialgias and an increase in hepatic enzymes such as the transa-minase glutamic-oxalacetic in about 40% of the cases that have already been studied. Tacrine however, cannot be used in patients with hepatic hepatic deficiency. Increased hepatic enzymes are produced during the first 12 weeks of treatment and occur more frequently in women. When treatment is halted, enzyme levels go back to normal levels within 4 to 6 weeks. There has to be weekly controls of the enzymes for the first 6 weeks, then monthly after2 months and then every 3 months. The increase of the dosage must be of 40mg every 6 weeks. Almost 90% of the patients were able to tolerate the drug (Monczor, 2005).
It is a reversible inhibitor of cholinesterase that is more potent than tacrine. In two double-blind studies that involved 900 patients who had slight to moderate dementia and were between the ages of 50 and 90 years, a cognitive improvement was observed; there was a detention of thedecline as was evaluate by the ADAS scale between 15 to 30 weeks. The doses used were 5-10mg daily. It is absorbed almost 100% orally and has a peak of between 3 to 4 hours after taking it. It is metabolized in liver and is not saturated. It is however not known if it can induce the hepatic enzymatic system. The average half life is about 70 hours and therefore it can be taken once a day. The side effects of this drug are nausea, vomit, diarrhea, cramps, fatigued and anorexia. Increase of gastric heartburn, bronchospasm, bradicardia, syncope and convulsions are however not that frequent. In high doses, it seems that there is some tolerance to the negative side effects because after 6 weeks, there was a reduction of the negative side effects (Monczor, 2005).
It is an inhibitor of the brain selective carbamate acetylcholinesterase and its function is pseudoreversible. Itmakes the inhibition of acetylcholinesterase persistentalthough the drug has been eliminated. The half life of this drug is 1 hour the effect duration is 10 hours. It is most effective in patients with Alzheimer’s in slight to moderate degrees with the most effective dosage being between 6mg to 12mg. its side effects are minor and include nausea, vomits, anorexia, diarrhea, dizziness, migraine, agitation, shaking, fatigue and insomnia (Monczor, 2005).
It is the newest reversible inhibitor of the cholinesterase and it has an allosteric modulatory action on the nicotine receptors. The presynaptic activation of the nicotine receptors leads to an increase in the release of acetylecholine, glutamate, monoamines and GABA. It therefore has a dual action and is most effective over cognitive symptoms and psychiatric symptoms. It has a half life of 7 hours. Negative side effects are: nausea, anorexia, shaking and vomits and is well tolerated when the dose is gradually increased (Monczor, 2005).
It has been observed that women who have taken estrogen after menopause have a reduced risk of developing Alzheimer’s. Estrogen is believed to have a protective effect against Alzheimer’s by activating cholinergic neurons, diminution of plasmatic levels of APOE, increase in the use of glucose by neurons and the promotion of neuronal survival. Its use is however controversial more so when one considers the risks versus the benefits of hormonal therapy. The risks are breast cancer, endometria’s cancer and deep vein thrombosis. Its benefits are over the memory and over cardiovascular diseases.
Vitamin E blocks the lipidic peroxidation and is a potent antioxidant. It has been observed that it produces impairment cognitive delay under daily doses of 400 to 3,000 UI. It is easily tolerated and negative side effects are relatively rare that is cataract and hemorrhage risk in patients with vitamin K deficit and syncope. It would however have a protective effect on the immunological response and on heart diseases.
The incidence of Alzheimer’s is significantly low in patients treated with anti-inflammatory drugs just as the cognitive deficit. Clinical studies carried out in recent years with ibuprofen, aspirin, indomethacin and prednisone have proved beneficial effects. Other drugs that are still being studied include colchichines, the methotrexate and hidroxichloroquine. Prednisone and colchicines when used have shown a decrease in cognitive decline (Monczor, 2005).
Selegiline helps in aminergic transmission because of its antioxidant effect and therefore it improves cognition and delays the declination. It has been proved to delay the progression of the illness. Its most frequent side effect is the orthostatic hypotension thus causing crisis with irritability and anxiety.
Ginko Biloba stops the cognitive decline in patients with mild Alzheimer’s due to its protector effect. Its results are however controversial. In a double-blind study with ginko biloba (160 or 240mg/d) with 214 patients with Alzheimer’s, vascular dementia and Age Associated Memory Impairment, at 24 weeks it was not effective.
Memantine is a non-competitive NMDA antagonist. It blocks the calcium channels of such receptor thereby stopping the entrance of calcium to the neurons and the toxicity that it produces. In double-blind studies an improvement in the cognition and in behavior has been observed. It is now in phase III studies in the United States. The dose is 15 to 20mg daily. Its side effects are dizziness, restlessness, vomits, tiredness and vertigo.
Alzheimer’s disease being a degenerative brain disease can cause immeasurable pain and suffering to the patients and their family members. Technological advances have greatly improved diagnosis of Alzheimer’s disease for example through imaging has played a key role in tackling this illness. New drugs that will among other things modify the pathology of Alzheimer’s disease are now at the stage of clinical trials. Many experts now believe that early diagnosis of the disease is important for any kind of treatment to be effective. There is a need to allocate more resources towards research in Alzheimer’s disease. Any vaccine whether active or passive will greatly help in stopping the ravages of this disease.
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