Alzheimer’s disease is a disease named after Alois Alzheimer who first described it in 1906. It is also known as Senile Dementia of the Alzheimer Type or Alzheimer’s and is the most common form of Dementia. It is an incurable, degenerative and terminal disease and is commonly diagnosed in people of over 65 years of age, however, there are traces of its onset in much earlier ages (Wegesin & Stern, 2004, p.646).The 2006 statistics indicated that 26.6 million people suffered from this disease world. The common symptoms for this disease are thought to be age related concerns or stress manifestations. The disease is characterized by memory loss, such as difficulty in remembering recently learned facts in earlier stages and confusion, mood swings, language breakdown, irritability and aggression and general withdrawal in the advanced stages.
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The causal effects for this disease are still unknown with fingers pointing to plaques and tangles in the brain. Most treatments available for this disease offer symptomatic benefit but fail to address the delay or progression of the disease. Since it’s incurable and degenerative, the management of patients is essential. The disease is known to place a great burden on caregivers who experience psychological, economic, social and physical pressures while taking care of sufferer’s of this disease. This disease is one of the most costly diseases in the developed world.
GuideAge Study: Trial of EGb 761 for prevention of Alzheimer’s disease among the elderly with memory complaints.
The primary objective of the study was to determine the effect of EGb761 in treatment on the rate of conversion from memory complaints to Alzheimer’s disease using survival analysis. The main targets for this study were ambulatory patients aged 70 years who exhibited memory complaints during a GP or memory centre consultation. Those with objective memory impairment or clinically relevant symptoms of anxiety and depression were however excluded. Participants were then required to make annual visits to a memory center where a series of neuropsychological tests were conducted to assess the cognitive function and cognitive status. The functional status was evaluated with the Instrumental Activities of Daily Living Questionnaire (Andrieu et. al., 2008, p.406).
The study recognized that primary and secondary prevention strategies are urgently needed for Alzheimer’s disease as its prevalence continues to rise in industrialized countries, with statistics showing that it has currently affected over 24 million people worldwide. There is also a high burden associate with this disease. The strategies have initially proved to be effective in reducing mortality, morbidity, and health care costs. Available treatments improve cognitive symptoms and estrogen or satin related treatments are secondary prevention strategies for Alzheimer’s disease (Wegesin & Stern, 2004, pp.647-648).
The basic science and clinical data indicate that estrogen therapy permeates healthy neurons with a survival advantage when challenged with a neuro-toxic agent. Greater benefit would therefore be predicted if estrogen therapy is begun while neurons are still healthy and not biologically compromised (p.650). The estrogen advantage to healthy neurons provides plausible explanation for why estrogen can be beneficial in preventing neurodegenerative diseases such as Alzheimer’s (Brinton, 2004, p.419).
In addition, in the treatment of AD, randomized placebo-controlled studies have provided evidence of efficacy. The study was spread out in a five year plan, and the primary objective was to determine the effect of treatment with EGb 761 on the rate of conversion from memory complaints to dementia of Alzheimer type using survival analysis. The study design: incorporated a network of physicians to recruit subjects; the eligibility criteria was validated in one of 25 reference memory centers. Coordination was by the hospital reference center located in Toulouse France (Andrieu et. al., 2008, p.407).
Age, residential location of patients, average socio-cultural and education levels, and spontaneous reporting of memory complaints were the main considerations for patient eligibility. Visual acuity and presence of drusen, abnormal pigmentary epithelium and vascularisation were considered in the diagnostic criteria for age related muscular degeneration. Apolipoprotein E, a genotypic determinant for treatment response was taken from blood samples while urine samples were taken to determine isoprostan, a potential biochemical surrogate marker of outcome. Spontaneously reported adverse effects were recorded for safety evaluation purposes (p.407).
In the treatment process, subjects were randomized at the validation visit by receiving EGb 761 or a matching placebo. Blinding was ensured by identical appearance of placebo and active drug while color marking was ensured by using a brown pigment. Behavioral assessment was through the administration of neuropsychological tests for assessment of cognitive function; the cognitive status was also evaluated fusing MMS and CDR; Functional status was evaluated using the Instrumental Activities of Daily Living Questionnaire. Other assessments involved balance disturbances, assessed by determining one’s ability to stand on one leg, posturography and diagnostic criteria for sarcopenia (pp.407-409).
Outcome measures entailed independent adjudication by four clinicians not connected to the study to ascertain uniform case results. Changes in CDR dementia scores and changes in performance on neuropsychological tests were considered in the secondary outcome measures.
The report described the cognitive function and disability in a population composed of 2854 patients who complained of memory problems. These patients were younger and better educated with high MMSE scores and longer durations of memory complaints. Primary care was the main context of the study. Patients who exhibited dementia, anxiety and depression symptoms were also excluded from the study so as to enrich the study sample in patients whose memory complaints were related to underlying cognitive difficulties other than emotional influences. From the screened population, over sixty percent scored 0.5 or more on the Clinical Dementia Rating Scale thus a relative degree of cognitive impairment was recognized. This therefore supported previous findings where majority of patients reported complaints in the general population thus evidence of overlap between elderly patients with subjective memory complaints and those with objective measures of cognitive impairment (p.410).
The results therefore imply that many elderly persons with cognitive impairment are undiagnosed within the community and that a pro active attitude from practitioners would help identify such people and pave way for provision of appropriate care. CDR would also be concluded as a sensitive means of detecting cognitive impairment amongst the elderly.
TheGuideAge is an important and innovative tool for prevention of AD in Europe. A recent study provided evidence of Gingko biloba extract effectiveness in preventing cognitive decline in elderly persons. To further determine the efficacy of Gingko biloba, the GuideAge study provided the required data from a large number of subjects. It would also be effective examining the evolution of cognitive function and consider risk factors as predictors of conversion from memory complaints to AD in the population.
From this analysis therefore, it can be concluded that preventive measures for AD are feasible owing to the ability to obtain data as well as initiate drug use in a large sample of the population.
Preventing Alzheimer’s disease: fact or fiction
The prevalence is Alzheimer’s disease is significantly increasing in the United States. Currently, the population of those with this disease stands at 4.5 million with an estimated increase of between 11 and 16 million in the next fifty years. In addition, explosive changes in technology would result in a great challenge in reflecting the mildest forms of cognitive deficit. The amyloid plaque in the brain remains the hallmark pathology of Alzheimer’s disease and the amyloid cascade, provides targets for interventions. The main aim of the interventions is to reduce damage resulting from amyloid plaque burden (Grossman & Dyk., 2008, p.887).
Significant positive approaches have been made, pivotal to the identification of symptomatic treatment of Alzheimer’s disease and the identification of conditions associated with increased treatment risks. The success of true prevention is however considered as fictitious as there is less data to support the claim that the aforementioned risks reduce the incidences of AD. Several advantages can be drawn from focusing on the prevention of the disease; first, it would expand the period of high quality of life in aging populations, a delay of onset of the disease by one year would significantly reduce its prevalence rate, and costs associated with the disease would be minimized (Grossman & Dyk, 2008, p.888).
Despite progress in the reduction of the disease, prevention strategies are still in the pipeline. Medical interventions for this disease are characterized as primary, secondary and tertiary. Primary: focus on disease prevention; secondary: on reduction in morbidity in presymptomatic individuals: and tertiary, on cure, palliation and rehabilitation. Grossman & Dyk (2008) recognize that current therapies for Alzheimer’s disease do exist. Tacrine was approved in 1993 by the US FDA as the first treatment for AD. The agency also introduced donepezil, rivastigime and galantamine as other treatment drugs. They further discuss that primary prevention refers to the prevention of disease in an unselected population trials to this need to enroll a large number of subjects with few exclusion criteria and infuse simple inexpensive evaluations of outcomes, with long observation and monitoring periods. The length of time for prevention trials and subjects’ enrolment, result into high expenses thus a permutation of the prevention trial, the ‘add on’ protocol permits the evaluations of multiple domains in a single clinical trial cohort (p.900).
Both primary and secondary prevention trials require careful attention to safety. The agents selected for prevention studies are frequently referred to as ‘neuroprotective.’ A term used to differentiate agents expected to reduce cognitive decline rather than relief of symptoms. Preventive mechanisms aim at reducing amyloid plaque by altering metabolisms or protecting cells from amyloid toxicity. These mechanisms are mostly proposed based on laboratory and animal studies as few markers of biological mechanisms available in humans exist. Several classes of agents with encouraging results have been tested. These are clearly discussed below.
First of all, statins, the HMG-CoA reductase are known to impact greatly on cognition, dementia and Alzheimer’s disease by reducing cholesterol levels in the body of humans (Sparks et. al., 2008, p.418). Secondly, tramiprosate, a 3-amino-1-propanasulfonic acid initially developed as a pharmaceutical treatment was examined in a two phased study of 58 patients with mild to moderate Alzheimer’s disease over three months. Patients receiving tramiprosate experienced a reduction in Alzheimer’s. Neurochem later reported that tramiprosate would be used as a nutraceutical. Thirdly, immunotherapy initiated by using fibrils for the development of Alzheimer’s vaccine was addressed in Schenk’s 1999 report as an option for regressing amyloid plaque. There was evidence of a patient demonstrating clearance of AÎ² trace deposits from their cortex, and a substantial microglial response. It was further concluded that displacement of AÎ², even when embedded in plaques, is possible in humans when immunotherapeutic techniques are used.
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Thirdly, is the use of enzyme inhibitors. Amyloid plaque remains a hallmark pathology for Alzheimer’s with the amyloid cascade providing targets for interventions to attack underlying mechanisms. Thus, interventions to reduce the amyloid plaque burden are widely proposed. Furthermore, the control of hypertension is evidence associated with reduced risk of cognitive impairment and dementia, characteristics of Alzheimer’s. Some studies have shown that effective control of hypertension is associated with cognitive benefit.
Hormone replacement strategies are also seen as beneficial mechanisms for the prevention of Alzheimer’s. There is an impression that estrogen may be beneficial in maintaining cognitive function and delaying dementia. The benefit of estrogen accrues from the fact that the hormone acts as a neurotrophin in the pyramidical cells of the CAI region which is known to degenerate in Alzheimer’s.Astrogen protects the hippocampal neurons thus reduces neural AÎ² generation.
Antioxidative strategies on the other hand employ the fact that oxidative stress plays a significant role in aging and Alzheimer’s disease. The use of antioxidants such as Vitamin C and E is associated with the reduction of risk of dementia. Nutritional supplementation, considers that dietary and nutritional supplements have an effect on the risk of Alzheimer’s. From several studies conducted, the use of Ginkgo biloba, a herbal supplement indicated an improvement in cognition. Another clinical trial on Salvia officinalis was studied for its potential benefit on cognition in patients diagnosed with Alzheimer’s. Significant benefits were observable between the endpoint and baseline scores on cognitive measures of the treatment group compared with the placebo group (Doraiswamy, 2002, p.816).
Lastly, nonpharmacological interventions such as physical exercise are observed as options to protect the elderly from cognitive decline. A Meta analysis conducted reported benefits from physical exercise on functional performance, behavior and cognition measures in patients with cognitive impairment and dementia. The implementation of Cognitive Motor Interventions on 38 patients in one year which involved cognitive exercise, social and psychomotor activities indicated an improvement in mood and subsequent scores against a control group (Kreil et. al., 2010, p.17).
Alzheimer’s disease is a common health concern amongst the aged. While effective treatment is available, the prevention mechanisms are not yet well understood. Cholesterol lowering, other cardiovascular risk reduction, amyloid metabolism and antioxidant mechanisms as well as environmental enhancements have proved as plausible prevention alternatives(Doraiswamy, 2002, p.818).
Evidence-based Approaches to Preventing Alzheimer’s disease.
Non modifiable risk factors for Alzheimer’s include: Age; this remains as the strongest risk factor for dementia, particularly for Alzheimer’s. The risk doubles every five years in individuals above 65 years. The risk however increases by close to 50%after 85 years. Family history; traces of Alzheimer’s in families’ accounts for 5% or less of cases. Hereditary or environmental factors related to families are major influences of this disease. Genetic factors; early Alzheimer occurring before 65 years accounts for 6-7% of all Alzheimer’s.13% of these clearly exhibit autosomal dominant transmission over more than one generation.30-70% of mutations are in presenilin-1 gene, 10-15% are in the amyloid precursor protein gene, and less than 5% are in the presenilin-2 gene (Bassil & Grossberg, 2009, p.30).
Modifiable risk factors on the other hand include cardiovascular risk factors such as hypertension, diabetes mellitus, hyperlipidemia, alcohol, depression, metabolic syndrome, smoking among others (Bassil & Grossberg, 2009, p.31). From studies conducted, the intake of statins indicated a reduction in dementia (Sparks, 2008, p.419). Other possible helpful agents to prevent Alzheimer’s include: Antioxidant vitamins, the brains of Alzheimer’s patients contain lesions typically associated with free radical exposure as well as elevated levels of endogenous antioxidants. Antioxidants reduce the toxicity of AÎ² in brain studies of Alzheimer patients. This therefore laid a basis for the assessment of the role of antioxidants such as vitamins E and C and curcumin for the prevention of Alzheimer’s. Curcumin has anti-inflammatory, anti- amyloid and antioxidant properties and is equally a promising agent in the prevention of Alzheimer’s from the ascertained data (Bassil & Grossberg, 2009, p.32).
Fish and Omega-3 fatty acids. Studies have shown that intake of saturated fat, total fat and total cholesterol increase the risk of dementia. Reduced level of Omega 3 fatty acids has been linked to increased risk of dementia thus high fish consumption would reverse the trend in risks related to dementia and cognitive decline (p.33).
Results form a community based study involving nondementaited individuals indicated that adherence to a traditional Mediterranean diet was associated with significant reduction in the risk of incidents related to Alzheimer’s disease. Fruits and vegetables are also associated with improved cognitive performance in elderly persons. Fruits are especially linked to reduction in dementia. Some studies have however associated high consumption of vegetables with reduction in cognitive decline (p.34).
Data on alcohol use and cognitive function in the elderly draws mixed results.
The complexity in these results is brought about by the dosage and type of alcohol taken. The moderate consumption of wine is associated with reduced risk of dementia and Alzheimer’s disease. On the other hand, high consumption of alcohol which results in alcoholism may lead to cognitive decline (p.34). A randomized controlled trial recently showed that moderate amounts of alcohol may delay age- associated cognitive decline. Others include; caffeine intake, hormone therapy, NonSteroid Anti-Inflammatory Drug (NSAID) therapy and homocysteine (Ho et. al., 2008, pp.86-88).
From this information it can be concluded that, dementia is the result of a set of underlying pathological processes, some which are preventable. Genetic factors, age and family history are disclosed as the major non-modified risk factors while modified risk factors range from alcoholism, hypertension, and diabetes mellitus to depression. All this contribute to the development of Alzheimer’s and plausible preventive solutions are therefore obtained from these problems. In addition, genetic vulnerability is seen to modify most of the risks associated with Alzheimer’s. Although there is insufficient evidence to cement primary prevention recommendations on dementia, physicians may advocate taking actions such as lowering cholesterol, blood pressure and homocysteine levels and controlling diabetes.
Three components of lifestyle, that is, social, mental and physical are associated with a magnificent reduction in the risk of dementia, and Alzheimer’s disease. Population based longitudinal studies have supported the hypothesis that social, cognitive and physical activity are inversely associated with the risk of dementia, Alzheimer’s disease and cognitive impairment. Physical exercise has been thought to enhance brain neurtotrophic factors and modify apoptosis. Dementia is lowered by preserving muscles mass as well as preventing falls and consequent head trauma (Kreil et. al., 2010,pp.18-19).
Evidence further shows that exercise can preserve optimal cardiovascular function, improve regional cerebral blood flow and deter stroke and micro vascular disease. NSAID therapy involves the treatment of Alzheimer’s with anti-inflammatory agents which slow the progression of dementia and inhibit its onset. NSAIDs portray increased possibilities of lowering levels of amyloidogenic AÎ²42 protein (Bassil & Grossberg, 2009, p.35).
From the above information, it is worth noting that Alzheimer’s disease can be prevented using both pharmacological and non-pharmacological alternatives. The integration of dietary options and physical exercise may also be efficient in achieving the preventive goal of Alzheimer’s disease.
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