About 40 million people are affected by dementia, with the majority of people being over age 60; this measure is expected to be doubled after 20 years, until about 2050. About 60-70% of all cases of dementia are caused by Alzheimer’s disease. There is about 2.17 and 4.78 million people who are affected by Alzheimer’s disease; 46% of these individuals have a moderate or severe form of the disease.
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By the year 2050, there will be over 7.98 and 12.95 people affected by Alzheimer’s disease, which is four times the amount of Alzheimer’s disease currently. The rate of Alzheimer’s is much higher for developing countries than for the United States and Europe. Alzheimer’s is a progressive disease, and it can make it harder for an individual to participate in activities of daily living and instrumental activities of daily living. Alzheimer’s disease is irreversible, and it consists of two types, which is early onset Alzheimer’s disease, and late-onset or sporadic Alzheimer’s disease. Late onset Alzheimer’s disease is the most common type of the disease, and accounts for about 95% of all cases of Alzheimer’s disease. Alzheimer’s disease results in brain damage that causes memory loss, this is because the build-up of tau proteins and apical dendrites cause neurofibrillary lesions . There is currently no cure for Alzheimer’s disease, and treatments currently given only help the temporary relief and management of symptoms. Furthermore, it is difficult to assess Alzheimer’s disease because there is no diagnostic test that is set in stone, and the disease symptoms overlaps with other forms of dementia and cognitive deterioration. The symptoms of Alzheimer’s disease extend past just cognitive decline, and goes to other noncognitive symptoms such as depression, and behavioral changes. A person with this disease uses health care services at a much greater rate and have more accidents and falls than people without Alzheimer’s disease. There is an increased financial, physical, and psychological strain on informal caregivers of Alzheimer’s disease.
The costs of morbidity, premature death, and lost productivity results in about $38,000 every year, for each person, and a total of $65 billion on a national scale (Sloane et al., 2002). The costs will continue to increase, as the population of individuals with Alzheimer’s disease increases. Since informal caregivers contribute about one half to about two thirds of the financial cost of caring for a person with Alzheimer’s disease, it places a great financial burden on them. The typical informal caregiver spends on average 16.1 hours every week to provide care, and the burden increases as the disease gets to a more advanced stage. The typical amount of time an informal caregiver has to spend caring for a person who doesn’t have any disablements in activities of daily living is 5.9 hours a week, and that numbers rises to about 35.2 hours every week with people who have a severe disablement of activities of daily living (Sloane et al., 2002). There is a much higher cost of care when people are put in nursing homes, because it costs much money to care for individuals in these institutions. Since 1994, the cumulative cost of Medicaid for nursing home care for people who have Alzheimer’s disease has surpassed $8 billion (Sloane et al., 2002). The cost to take care of an individual with an advanced form of the disease is about 2.25 times higher than for patients with only a mild or moderate form of the disease. Diet-induced obesity, as a behavioral factor, has been shown to have a significant effect of the risk of cognitive deterioration and developing Alzheimer’s disease. People who become obese greater have insulin resistance and the dysregulation of the signaling of insulin, which is a risk factor that can cause cognitive impairment and Alzheimer’s disease. Specifically, central obesity in midlife can cause a neuronal environment that sets the grounds for Alzheimer’s disease. Diet-induced obesity makes the neuropathology and the negative cognitive effect of Alzheimer’s disease worse. Consistent high fat diets throughout life is shown to cause low metabolic dysregulation and cognitive deterioration. Diets high in fat and sugar, have been also shown to cause tau proteins to accumulate, process, and hyperphosphorylate at much higher rates. A reduction in brain glucose metabolism is a prime symptom of Alzheimer’s disease, this is because insulin signaling is altered. In people who are obese, insulin resistance causes a higher release of peripheral insulin, and the insulin concentrations in the brain are lowered, because of a decrease in insulin transport across the blood brain barrier. The environment is worsened when insulin signaling in the brain is diminished under average conditions. Elevated levels of adiposity cause increased neuroinflammation, which is a mechanism in Alzheimer’s disease. Vascular inflammation is a precursor to Alzheimer’s disease, and it is associated with hypertension and hyperlipidemia; all of these factors interact in an obese person to cause heightened levels of Alzheimer’s disease risk. The secretion of leptin increases as adiposity increases. Leptin is supposed to manage appetite; however, people who are obese have leptin resistance, which diminishes the hormones ability to modulate appetite. Leptin resistance is associated with the heightened pathogenesis of Alzheimer’s disease, whereas normal levels of leptin would reduce Alzheimer’s disease risk. As adiposity increases in obese people, the leptin response is lowered, and the satiety signal is not identified. Leptin resistance causes a disruption of the leptin signaling pathways and causes an increased level of inflammation in the hypothalamus.
People who have Alzheimer’s disease have lower plasma levels of leptin than people than people without the disease. Higher leptin levels cause a higher cerebral brain space and lowered levels of Alzheimer’s risk, these pathways can become dysregulated in the brain of an Alzheimer’s patient, where leptin levels are high, but the expression of leptin is not regulated properly. Leptin resistance is the mechanism in which people with diet-induced obesity have a higher risk of Alzheimer’s disease. Chronic stress, as a psychological factor, can cause higher tau phosphorylation, which can contribute to neuronal death and neuronal dysregulation, and is linked to Alzheimer’s disease. Cortisol is the major hormone linked to stress. Higher levels of cortisol in plasma, cerebrospinal fluid, and saliva have been discovered in people who have Alzheimer’s disease. The glucocorticoid 11 beta-hydroxysteroid dehydrogenase type 1, has been linked to a higher risk of developing Alzheimer’s disease (Caruso et al., 2018). This glucocorticoid is also called cortisone reductase, which speeds up the conversion of cortisol into cortisone. If an individual has a lack of functioning of cortisone reductase, they are more likely to develop Alzheimer’s disease because of elevated levels of cortisol at key target sites in the brain, such as the hippocampus. Cortisone reductase improves tau phosphorylation at Alzheimer’s disease re mechanism sites and increases the likelihood of a toxic neuronal effect as a result of Alzheimer’s disease. Chronic stress exposure, through the over secretion of glucocorticoids can increase the chance of onset and the progression of Alzheimer’s disease neuronal deterioration. Early life stress, associated with lower levels of maternal care, causes higher levels of DNA methylation of the expression of glucocorticoid receptors, lower feedback suppression of the hypothalamic-pituitary-adrenal axis (HPA) and a diminished stress response in adulthood. Acute stressors can activate the HPA axis, which causes higher levels of cortisol. Continued activation of glucocorticoid receptors by glucocorticoids linked to stress, can cause damage to the hippocampus. This can cause neurodegeneration and enhance the progression of the neuropathology of Alzheimer’s disease. Environmental factors such as heavy metals, are associated with the development of Alzheimer’s disease because of their capability of destroying metabolic pathways that are involved in the regulation of amyloid beta, which is a key plaque in causing Alzheimer’s disease. These metals are oxidative agents; the brain is susceptible to oxidative stress, because of a high glucose-based metabolic rate. These metals have high levels of polyunsaturated fatty acids, and enzymatic activity that is associated with transition metals that speed up the development of free radicals. Overexposure to Iron is associated with an elevated level in amyloid beta build up and hastens the process of advanced glycation end products (AGE), that can cause neurodegeneration. Phagocytosis of amyloid fibrils results in a higher secretion of pro-inflammatory cytokines, which can cause neuronal loss. Lead, another heavy metal has toxic neuronal effects. It can affect cognitive abilities, such as intelligence, memory, speed, processing, and motor functions. Lead also increases amyloid beta levels, by the reduction of the clearing of amyloid beta in the brain. It disrupts the transferring out of amyloid beta and can cause the plaques to build up over time. Mercury is another heavy metal that can cause neurotoxicity. It can interfere with brain development and causes cognitive disablement. Overexposure to mercury cause result in memory loss and changes in cognition. Mercury increases the production of amyloid beta levels and reduces the brain’s ability to clear the peptide. Inorganic arsenic is a toxic metalloid that has negative effects in neurocognitive development, and exposure to it can cause Alzheimer’s disease. Inorganic arsenic changes the amyloid pathway, and it is associated with inflammatory responses and oxidative stress, which can increase the development of Alzheimer’s disease pathology. Cadmium causes memory loss and mental retardation, and results in an increased production of amyloid beta and increases plaques in the cerebral cortex and hippocampus.
These metals activate the formation of amyloid beta in the frontal cortex, and also the hippocampus. A social factor of Alzheimer’s disease is race, and African-Americans are about two to three times more likely to develop Alzheimer’s disease than non-Hispanic whites of the same age. Older aged African-Americans perform more poorly in cognitive in comparison to non-Hispanic whites. Cognitive performance tests are one of the primary diagnostic procedures for Alzheimer’s disease, there are disparities in average results of performance for African-Americans. Although, African-Americans typically have a higher rate of survival ad lower decline for Alzheimer’s disease than do non-Hispanic whites, the performance on cognitive tests, that is weighed at only a single time point, causes many more diagnoses in African-Americans. If there are more measurements of performance over time, there would be more accurate rates of Alzheimer’s disease when comparing African-Americans with non-Hispanic whites. Because of a lack of proper data collection, and discrimination against African-Americans in research studies, African-Americans are purported to have higher rates of Alzheimer’s disease. The APOE e4 allele, which is associated with the heightened development of Alzheimer’s disease, is shown to be much higher in African-Americans than non-Hispanic whites. Alzheimer’s disease is associated with vascular conditions such as diabetes, and since African-Americans have higher rates of diabetes compared to non-Hispanic whites, this puts them more at risk of Alzheimer’s disease. Body mass index is also another risk factor of Alzheimer’s disease, and African-Americans are more overweight and obese than non-Hispanic whites, this contributes to the stronger effect that studies have, that purport African-Americans being more at risk for Alzheimer’s disease. In addition to this, African-Americans have less access to health care, less quality health care, poorer neighborhood conditions, and discrimination in general that reduces their ability to modify vascular conditions that are risk factors for Alzheimer’s disease. The influences chosen to interact with each other to contribute to Alzheimer’s disease because they all are in some way linked to the development of neuronal conditions that can cause the development of tau proteins, and amyloid beta accumulation that can lead to Alzheimer’s disease. Race and diet-induced obesity are related because being a certain race puts an individual more at risk of becoming obese, and being obese results in inflammation and insulin resistance, which contributes to Alzheimer’s disease. Race and environments with metal exposure interact because if a person is either African-American, Hispanic, or another minority group in America, they are more likely to grow up in an urban environment.
This environment may have more metals because of city development and just more technology and power plants in general. Individuals who live as African-Americans or Hispanics in low-grade environments with broken down, or shoddy houses are more at risk of having poor housing development, which can lead to over exposure to lead, zinc, and other heavy metals that can put an individual more at risk of Alzheimer’s disease. Stress is associated with race because being a minority such as African-American is linked with a higher prolonged acute stress response, this stress response can lead to a dysregulation of the HPA axis and also higher cortisol levels because of discrimination. All of these factors interact in causing a higher rate of development of Alzheimer’s disease. Moreover, the influence that is the best target for intervention is diet-induced obesity. This is because this is a modifiable risk factor, and individuals can be educated and shaped in a way that helps them have a better lifestyle in general. Reducing rates of obesity is pivotal to slowing down the development of Alzheimer’s disease. Obesity puts individuals at risk of diabetes, hypertension and other comorbidities that are shown to increase the risk of Alzheimer’s disease. Intervening in lifestyle choices such as diet is the best way to slow the development of Alzheimer’s disease. Incorporating employee education and participation programs is a way to plan an intervention for this influence. These programs encourage individuals to set goals, and give them self-help materials, and layouts of dietary plans, as well as group exercise programs. These programs are targeted at making sure an individual can reach a healthy weight after a certain amount of time. Employee health surveys are another way to prevent obesity. These services should be used in combination with counseling, personalized assessments, that give the guidance of a professional to change problem behaviors related to obesity and suggestions on how to control weight and manage dieting. Since obese people have problems with leptin signaling, they should also be given leptin shots in order to help them control their hunger, not only would this reduce food intake, but help individuals to feel more satiated and fuller. These programs could encourage individuals to eat less foods high in fat and sugar and opt for foods that have more fruits and vegetables and foods that promote a heart healthy diet.
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