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About 40 million people are affected by dementia, with the majority of these individuals being over the age of 60. This number is expected to double in the next 20 years, reaching around 80 million by 2050. Approximately 60-70% of all dementia cases are caused by Alzheimer’s disease, affecting between 2.17 and 4.78 million people. Out of those, 46% have a moderate or severe form of the disease. It is estimated that by 2050, between 7.98 and 12.95 million people will be affected by Alzheimer’s disease, which is four times the current number. The rate of Alzheimer’s is significantly higher in developing countries than in the United States and Europe.
Alzheimer’s is a progressive disease that makes it difficult for individuals to participate in activities of daily and instrumental living. It is an irreversible condition that consists of two types: early-onset Alzheimer’s disease and late-onset or sporadic Alzheimer’s disease. Late-onset Alzheimer’s disease is the most common type, accounting for about 95% of all Alzheimer’s cases.
How it works
Alzheimer’s disease results in brain damage leading to memory loss; this occurs due to the build-up of tau proteins and apical dendrites, which cause neurofibrillary lesions. There is currently no cure for Alzheimer’s disease, and existing treatments only provide temporary relief and management of symptoms. It is challenging to diagnose Alzheimer’s disease, as there is no definitive diagnostic test, and the disease’s symptoms overlap with other forms of dementia and cognitive deterioration.
The symptoms of Alzheimer’s disease extend beyond cognitive decline to include non-cognitive symptoms like depression and behavioral changes. Individuals with Alzheimer’s use health care services at a far greater rate and are more prone to accidents and falls than those without the disease. The disease also places an increased financial, physical, and psychological burden on informal caregivers.
The costs of morbidity, premature death, and lost productivity result 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 progresses to a more advanced stage.
The typical amount of time an informal caregiver spends caring for a person who doesn’t have any impairments in activities of daily living is 5.9 hours a week, and that number rises to about 35.2 hours every week with people who have severe impairments of activities of daily living (Sloane et al., 2002). The cost of care increases significantly when people are placed in nursing homes, because these institutions are expensive to maintain. Since 1994, the cumulative cost of Medicaid for nursing home care for people with Alzheimer’s disease has surpassed $8 billion (Sloane et al., 2002). The cost to care for 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 significantly affect the risk of cognitive deterioration and developing Alzheimer’s disease. People who become obese typically have insulin resistance and a dysregulation of insulin signaling, which can cause cognitive impairment and Alzheimer’s disease. Specifically, central obesity in midlife can create a neuronal environment conducive for Alzheimer’s disease. Diet-induced obesity exacerbates the neuropathology and the negative cognitive effects of Alzheimer’s disease. Consistently high-fat diets throughout life have been shown to cause metabolic dysregulation and cognitive deterioration.
Diets high in fat and sugar also cause tau proteins to accumulate, process, and hyperphosphorylate at significantly higher rates. A reduction in brain glucose metabolism is a prime symptom of Alzheimer’s disease because insulin signaling is altered. In obese people, insulin resistance causes a higher release of peripheral insulin, and the insulin concentrations in the brain are lowered due to decreased insulin transport across the blood-brain barrier. The condition worsens 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 is associated with hypertension and hyperlipidemia. All of these factors interact in an obese person to heighten the risk of Alzheimer’s disease.
The secretion of leptin increases as adiposity increases. Leptin is supposed to manage appetite, but obese people often have leptin resistance which diminishes the hormone’s ability to regulate appetite. Leptin resistance is associated with an increased risk of Alzheimer’s disease, whereas normal levels of leptin would reduce this risk. As adiposity increases in obese people, the leptin response lessens, and the satiety signal is not recognized. Leptin resistance disrupts the leptin signaling pathways and incites an increased level of inflammation in the hypothalamus.
People who have Alzheimer’s disease have lower plasma levels of leptin than those without the disease. Higher leptin levels cause a larger cerebral brain space and lowered Alzheimer’s risk. These pathways can become dysregulated in the brain of an Alzheimer’s patient, where leptin levels are high, but leptin expression is not properly regulated. Leptin resistance is the mechanism in which people with diet-induced obesity have a heightened risk of Alzheimer’s disease.
Chronic stress, as a psychological factor, can cause a significant increase in tau phosphorylation, which contributes to neuronal death and dysregulation, and is linked to Alzheimer’s disease. Cortisol is the primary hormone linked to stress. Elevated levels of cortisol in plasma, cerebrospinal fluid, and saliva have been found in individuals with Alzheimer’s disease.
The glucocorticoid 11 beta-hydroxysteroid dehydrogenase type 1 has been associated with a higher risk of developing Alzheimer’s disease (Caruso et al., 2018). This glucocorticoid is also known as cortisone reductase, which accelerates the conversion of cortisol into cortisone. If an individual has dysfunctional cortisone reductase, they are more likely to develop Alzheimer’s disease due to raised cortisol levels at key target sites in the brain, such as the hippocampus. Cortisone reductase enhances tau phosphorylation at Alzheimer’s disease mechanisms and increases the probability of a toxic neuronal effect resulting from the disease.
Chronic stress exposure, mainly due to the oversecretion of glucocorticoids, can heighten the chances of Alzheimer’s disease onset and its neuronal deterioration progression. Early life stress, linked with lower levels of maternal care, causes a significant increase in 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, leading to higher cortisol levels. Continuous activation of glucocorticoid receptors by glucocorticoids associated with stress can damage the hippocampus, causing neurodegeneration and enhancing the progression of Alzheimer’s disease neuropathology.
Environmental factors such as heavy metals are associated with Alzheimer’s disease development due to their ability to damage the metabolic pathways involved in the regulation of amyloid beta, which is a key plaque-causing agent for the disease. These metals are oxidative agents; the brain is susceptible to oxidative stress due to a high glucose-based metabolic rate. These metals have high levels of polyunsaturated fatty acids and enzymatic activity associated with transition metals that hasten free radical development.
Overexposure to iron is linked with increased levels of amyloid-beta build-up and accelerates advanced glycation end products (AGE), which can significantly contribute to neurodegeneration. Phagocytosis of amyloid fibrils results in heightened secretion of pro-inflammatory cytokines, leading to neuronal loss.
Lead, another heavy metal, has toxic neuronal effects impacting cognitive abilities such as intelligence, memory, speed, processing, and motor functions. Lead also increases amyloid beta levels, reducing amyloid-beta clearance in the brain. It disrupts the transfer of amyloid beta, leading to plaque build-up over time. Mercury, another heavy metal, can also cause neurotoxicity.
It can interfere with brain development and cause cognitive disablement. Overexposure to mercury can 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 on 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, increasing plaques in the cerebral cortex and hippocampus.
These metals activate the formation of amyloid beta in the frontal cortex and the hippocampus. A social factor of Alzheimer’s disease is race. African-Americans are about two to three times more likely to develop Alzheimer’s disease than non-Hispanic whites of the same age. Older African-Americans perform more poorly on cognitive tests in comparison to non-Hispanic whites. Cognitive performance tests are one of the primary diagnostic procedures for Alzheimer’s disease, and there are disparities in the average results for African-Americans.
Although African-Americans typically have a higher rate of survival and lower decline for Alzheimer’s disease than non-Hispanic whites, their performance on cognitive tests, weighed at only a single time point, causes many more diagnoses. If there were more measurements of performance over time, there would be more accurate rates of Alzheimer’s disease when comparing African-Americans with non-Hispanic whites. Due to a lack of proper data collection and discrimination against African-Americans in research studies, they 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 in 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 at a higher risk of Alzheimer’s disease. Body mass index is also another risk factor of Alzheimer’s disease, and as African-Americans are more overweight and obese than non-Hispanic whites, this contributes to studies purporting that African-Americans are more at risk for Alzheimer’s disease.
In addition to this, African-Americans have less access to healthcare and poorer neighborhood conditions, and face discrimination that reduces their ability to modify vascular conditions that are risk factors for Alzheimer’s disease. The risk factors chosen interact with each other to contribute to Alzheimer’s disease because they all are linked to the development of neuronal conditions that can cause the accumulation of tau proteins and amyloid beta, leading to Alzheimer’s disease.
Race and diet-induced obesity are related because being of a certain race increases the risk of obesity, which in turn results in inflammation and insulin resistance, contributing to Alzheimer’s disease. Race and environments with metal exposure interact because African-Americans, Hispanics, and other minority groups in America are more likely to grow up in urban environments.
This environment may have more metals due to city development and an increase in technology and power plants. Individuals who identify as African-Americans or Hispanics and live in low-grade environments with broken down or shoddy houses are at a higher risk of poor housing development. This can lead to overexposure to lead, zinc, and other heavy metals that increase the risk of Alzheimer’s disease. Stress is associated with race because minorities, such as African-Americans, experience higher levels of prolonged acute stress. This stress response can lead to a dysregulation of the HPA axis and higher cortisol levels due to discrimination. All of these factors contribute to a higher rate of Alzheimer’s disease development.
Moreover, the best target for intervention is diet-induced obesity. This risk factor is modifiable, and individuals can be educated to adopt better lifestyle habits. Reducing obesity rates is critical for slowing down the development of Alzheimer’s disease as obesity increases the risk of diabetes, hypertension, and other comorbidities that elevate the risk of Alzheimer’s disease. Intervening in lifestyle choices, such as diet, is the most effective way to slow the disease’s progress.
Implementing employee education and participation programs is one method of planning an intervention. These programs encourage individuals to set goals and provide self-help materials, dietary plan layouts, and group exercise programs. These programs aim to ensure an individual can achieve a healthy weight within a specific time frame. Employee health surveys are another preventative measure against obesity. These services, combined with counseling and personalized assessments, provide professional guidance for changing problematic behaviors related to obesity and offer suggestions on how to control weight and manage diet.
Since obese people often have issues with leptin signaling, they could also benefit from leptin shots to help control their hunger. These shots would not only reduce food intake but also help individuals feel more satiated. The aforementioned programs could encourage individuals to consume fewer high-fat and high-sugar foods and opt for a diet higher in fruits and vegetables and foods that promote a heart-healthy diet.
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