Abstract
While the etiology of Alzheimer’s Disease (AD) is unknown, scientists have identified many risk factors, which will be examined in this review (Watwood, 2011). These risk factors include age, genetics, cardiovascular health, diet, sleep, mental health, education, and socioeconomic status (SES). In AD, a protein called beta-amyloid accumulates slowly over time, resulting in the risk of developing AD increasing with age (Jaroudi et al., 2017). Additionally, some individuals have genes that increase their risk of developing early-onset AD (Serrano-Pozo et al., 2021). During sleep, waste products and beta-amyloid buildup are cleared from the brain, highlighting the importance of sleep in AD progression (Cordone et al., 2019). Mounting evidence shows that other lifestyle factors, such as cardiovascular health and diet, affect one’s risk of developing AD (McGurran et al., 2019),(S. Pugazhenthi; L. Qin; P. Hemachandra Reddy, 2016). Besides physical health, depression affects an individual’s risk of AD, and is often a comorbid condition with AD (Novais & Starkstein, 2015). Furthermore, cognitive reserve plays an important role in delaying the onset of clinical symptoms of AD, and has been shown to increase with years of education (Xu et al., 2016). Finally, these risk factors will be discussed in the context of SES. Through discussion of AD and its risk factors, this paper aims to raise awareness of the influence of SES on the risk of developing AD and to suggest potential interventional strategies.
Keywords
Alzheimer’s Disease; Beta-amyloid; Socioeconomic Status; Diet; Cardiovascular Health; Glymphatic System; Genetics; Education; Aducanumab
Introduction
Alzheimer’s Disease (AD), the most common form of dementia, is a progressive neurological disease that diminishes the brain’s ability to form memories, control thoughts, and process language (Watwood, 2011),(CDC, n.d.). It is currently the sixth-leading cause of death in the United States, and has no cure (CDC, n.d.).
In AD, toxins called beta-amyloid and tau aggregate in the brain to create amyloid plaques and neurofibrillary (tau) tangles, which disrupt neural connections and damage neurons (Aging, n.d.-b). While tau is also involved in the process of AD, this review will mostly focus on the buildup of beta-amyloid. Beta-amyloid is a protein that is released when the transmembrane amyloid precursor protein (APP) is cleaved by ∝-secretase, β-secretase, and γ-secretase (Figure 1) (Breijyeh & Karaman, 2020). The isoform resulting from ∝-secretase cleavage will not aggregate, but the isoforms resulting from cleavage by β-secretase, and γ-secretase produce Aβ40 and Aβ42 (Breijyeh & Karaman, 2020). Though Aβ40 is more abundant in the human population, it is less likely to aggregate than Aβ42, which forms plaques more easily (Kwasi G. Mawuenyega, Tom Kasten, Wendy Sigurdson, 2013). This aggregation causes extracellular plaques, which can result in neuronal damage, and therefore the production of more Aβ40 and Aβ42 (Huang & Liu, 2020). Eventually, this positive feedback loop or “amyloid cascade” is followed by the aggregation of intracellular tau, neuronal loss, synaptic dysfunction, and eventually clinical symptoms of dementia (Huang & Liu, 2020). The accumulation of toxins occurs over decades, with few, if any, symptoms appearing at first.
AD primarily affects the hippocampus region of the brain, but as more neurons die, areas such as the entorhinal cortex (an area of the brain that is important to forming memories) and other cortical areas are affected, leading to global atrophy of brain tissue (Figure 2) (U.S. Department of Health and Human Services, 2016). Symptoms of AD include mood and behavioral changes, confusion, difficulty speaking, memory loss, and difficulty orienting oneself in time and space (Alzheimer’s Association, n.d.).
Alzheimer’s-like symptoms are observed in many conditions (brain tumors, head trauma, hydrocephalus, vitamin deficiencies, and depression, among others); therefore AD must be diagnosed using several methods: neuropsychological tests, brain imaging, and scanning, laboratory tests, psychiatric evaluations, and postmortem autopsies (Aging, n.d.-b).
AD has three stages: preclinical, mild cognitive impairment (MCI), and Alzheimer’s dementia (Aging, n.d.-a). Preclinical AD is defined by the presence of AD pathology (such as beta-amyloid buildup) without clinical presentation of AD symptoms, while MCI consists of unusual memory and executive function impairments without disrupting an individual’s independence (Aging, n.d.-a). Alzheimer’s dementia is the last stage of AD, and includes severe cognitive impairment (memory loss, word-finding, and visual and spatial processing difficulties) that disrupts an individual’s independent function (Aging, n.d.-a). The symptoms of AD can begin at various ages across individuals (usually between the ages of 50 until death), which scientists attribute to a number of risk factors, as well as cognitive reserve (Wada et al., 2018). Cognitive reserve is a measure of resilience, or the capacity of the healthy brain to maintain its function in the context of aging and disease (Wada et al., 2018). An individual with high cognitive reserve may incur the same disease process as an individual with low cognitive reserve and only develop symptoms much later in life (Wada et al., 2018). One of the main factors that increases cognitive reserve is education (Wada et al., 2018). While cognitive reserve plays a role in an individual’s risk of AD, other risk factors also contribute to the pathogenesis of AD, which will be examined in this paper along with the underlying factor of socioeconomic status (SES).
Figure 1: The Pathogenic cleavage of Beta-amyloid. This process is started when β-Sec cleaves APP, detaching the sAPPβ from the cell membrane. The remaining monomer is then cleaved by γ-Sec, which releases Aβ42 or Aβ40 monomers (Aβ42 shown in figure). These monomers eventually aggregate into beta-amyloid plaques.
Created with BioRender.com.
Figure 2: Pathology of Alzheimer’s Disease AD causes (a) brain atrophy and (b) extracellular beta-amyloid accumulation into diffuse and dense plaques and intracellular hyperphosphorylated tau accumulation.
Created with BioRender.com.
Age and Genetics
Age and genetics are both important risk factors for AD but cannot be modified by lifestyle choices.
Age is the most important risk factor for AD, and most individuals who develop this disease are over 65 years old. As individuals age, their body undergoes many changes: their muscle, bone, and brain mass decrease, cells are not able to repair themselves, and DNA damage begins to accumulate. In addition, synapses, the connections between neurons that are necessary for memories to form and be recalled, are lost with increasing age (Breijyeh & Karaman, 2020). Furthermore, cerebrovascular circulation can become impaired, leading to neuroinflammation and a further loss of synapses (Breijyeh & Karaman, 2020). Additionally, the aged brain has fewer resources with which to clear waste products such as beta-amyloid (Breijyeh & Karaman, 2020). All of these physical changes contribute to a decrease in cognitive reserve, which can accentuate the clinical symptoms of AD. While aging is an important contributor to the clinical progression of AD, several genetic factors also contribute to the speed and quantity of beta-amyloid accumulation in the brain, and the overall risk of AD.
The amyloid precursor protein (APP), which is found on chromosome 21, can have twenty-five unique mutations that cause an elevated accumulation of beta-amyloid (Breijyeh & Karaman, 2020). Studies in mouse models have found that these mutations increase the level of Aβ, Aβ40, and Aβ42, cause atrophy in different areas of the brain (namely the hippocampus and cerebral cortex), and contribute to the formation of amyloid plaques (Breijyeh & Karaman, 2020). Conversely, the mutation A673T protects against AD by decreasing the cleavage of Aβ, Aβ40, and Aβ42 (Breijyeh & Karaman, 2020).
Presenilin-1 (PSEN-1) is a protein that increases the production of Aβ from the APP. In studies of mice where the PSEN-1 gene was removed, synaptic dysfunction and memory impairment were present, suggesting that PSEN-1 is important to the maintenance of neurons and memory (Breijyeh & Karaman, 2020). Therefore, individuals with a mutated form of the PSEN-1 gene might be at a higher risk of developing AD. However, more research must be done to understand the PSEN-1 gene function in the human brain.
The APOE gene, which many researchers call the strongest genetic risk factor for AD, can either increase or decrease one’s risk of developing AD, depending on the APOE allele of that individual (Serrano-Pozo et al., 2021). The most common APOE allele is ε3, which has a prevalence of 77.9% in the general population (Liu CC, Kanekiyo T, Xu H, 2013). The other alleles, ε2 and ε4 have prevalences of 8.4% and 13.7%, respectively (Liu CC, Kanekiyo T, Xu H, 2013). The ε4 allele is the most dangerous, as individuals who have just one APOE ε4 allele are three to seven times more likely to develop AD, while being homozygous for the APOE ε4 allele increases the risk by a factor of 12 (Serrano-Pozo et al., 2021). This can be seen by the much higher prevalence of the APOE ε4 allele in AD patients (40% prevalence) compared to the general population (Liu CC, Kanekiyo T, Xu H, 2013). In addition, the APOE ε4 allele increases the buildup of tau and the inflammatory response of glial cells to aggregated proteins in the brain, leading to an earlier age of onset of AD (Serrano-Pozo et al., 2021),(Breijyeh & Karaman, 2020). Individuals with the ε3 allele are less likely to develop AD than those with the ε4 allele, but still more likely than those with the ε2 allele; studies show that the ε2 allele not only delays the onset of AD, but also reduces the risk of AD by 40%, even if the carrier is heterozygous and only has one ε2 allele (Serrano-Pozo et al., 2021).
Other genes that have an effect on the risk for AD include the ATP Binding Cassette Transporter A1 (ABCA1), the Clusterin (CLU) and Bridging Integrator 1 (BIN1) genes, the Evolutionarily Conserved Signaling Intermediate in Toll pathway (ECSIT), and the Estrogen Receptor gene (ESR) (Breijyeh & Karaman, 2020). These genes each play a role in the production and accumulation of beta-amyloid (Breijyeh & Karaman, 2020).
The effects of one’s genetics can be seen through the hereditary nature of AD. Early-onset AD is the rarest form of Alzheimer’s Disease, only affecting 1-6% of patients with AD, and is present most often in individuals whose families have had more than one individual in multiple generations develop the disease (Breijyeh & Karaman, 2020). Even late-onset AD, the more common form of the disease, is more common among families that have a history of AD (Breijyeh & Karaman, 2020).
Cardiovascular Health
Cardiovascular health is important for brain health and affects an individual’s risk of AD. The brain needs sufficient blood flow for oxygenation and to clear toxins like beta-amyloid and tau. If blood flow is reduced, the brain may receive inadequate nutrients and accumulate waste, increasing the risk of inflammatory processes that may contribute to protein aggregation (Duron & Hanon, 2008).
Many conditions can affect cardiovascular health, including hypertension, heart disease, smoking, type 2 diabetes, obesity, high cholesterol, and other metabolic syndromes. In addition, exercise plays an important role in maintaining cardiovascular health.
Longitudinal studies of individuals with chronic hypertension found that those with hypertension in midlife were more at risk of cognitive decline 15-20 years later (Duron & Hanon, 2008). High blood pressure may damage blood vessel walls over time, leading to poor circulation. Treatment can reduce the strain on the vessels, but it is not clear whether this treatment has any effect on the risk of AD: hypertension treatment can both increase and decrease one’s risk of developing AD (Duron & Hanon, 2008).
Smoking may be a risk factor for AD. Results from early case-control studies suggested that nicotine in cigarette smoke is protective against AD (Duron & Hanon, 2008). However, because smoking causes inflammation in blood vessels, increases the formation of atherosclerotic plaques in vessels, causes blood to clot, and restricts blood flow, it also increases the overall risk of developing AD (Duron & Hanon, 2008). This risk increase is shown in numerous studies, the first being the Honolulu-Asia Aging Study (Duron & Hanon, 2008). According to Tyas et al., the risk of AD increased with the duration of smoking at both medium (26.7-40.5 pack years) and heavy (40.5-55.5 pack years) levels (Tyas et al., 2003). In addition, the amount of plaque caused by beta-amyloid buildup increased with smoking level (Tyas et al., 2003).
Obesity is also an important risk factor of AD. A longitudinal study comparing sagittal abdominal diameter found that participants with the largest abdominal diameters were three times as likely to develop AD than those with the smallest abdominal diameters (S. Pugazhenthi; L. Qin; P. Hemachandra Reddy, 2016). However, according to other studies, being underweight also increases an individual’s risk of developing AD (S. Pugazhenthi; L. Qin; P. Hemachandra Reddy, 2016).
Type 2 diabetes has also been shown to increase one’s risk of AD. Insulin resistance leads to an increase in activation of a kinase called GSK3β that results in the hyperphosphorylation of tau (S. Pugazhenthi; L. Qin; P. Hemachandra Reddy, 2016). Furthermore, MRI studies have shown that diabetes results in decreased hippocampal size (S. Pugazhenthi; L. Qin; P. Hemachandra Reddy, 2016). Due to the reduction in brain mass, diabetes reduces cognitive reserve, which increases the risk of AD.
Since obesity and type 2 diabetes can be caused by lack of exercise, it can be reasoned that exercise can decrease the risk of AD. First, exercise improves circulation and reduces inflammation, resulting in a healthier brain. Moreover, in individuals with AD, a higher fitness level improved memory, reduced hippocampal atrophy, and increased grey matter volume(McGurran et al., 2019).
Genetics also play a role in cardiovascular health. The APOE protein transports cholesterol around the cell, and the ε4 allele is associated with atherosclerosis (Duron & Hanon, 2008). This may be because having the ε4 allele leads to higher levels of cholesterol, which creates arterial plaques and disrupts circulation (Duron & Hanon, 2008). The next section will discuss diet in relation to AD and cardiovascular health.
Diet:
Not only can a poor diet lead to cardiovascular diseases such as hypertension, high cholesterol, type 2 diabetes, obesity, coronary artery disease, and atherosclerosis, but it can also independently affect the risk of AD.
Lipids are important macromolecules: they are platforms upon which Aβ interacts with APOE and tau to influence the aggregation of plaques and hyperphosphorylated tau (Kao et al., 2020). In addition, lipids promote inflammation, meaning that a high-lipid diet can increase the risk of AD (Kao et al., 2020). Furthermore, a higher dietary intake of fatty acid lipid monomers has been shown to increase risk of AD and cognitive decline (Kao et al., 2020). More specifically, the risk of AD for those in the upper quintile of intake for saturated fat and trans-fat were 2.2 times and 2.5 times that of those in the lower quartile (Kao et al., 2020). This is because a high-fat diet leads to greater levels of free fatty acids in circulation, which can contribute to the accumulation of beta-amyloid and tau (Kao et al., 2020).
A study by Omar et al. demonstrated the effects of various diets on cognition (Omar, 2019). Diets such as the Mediterranean Diet and its other form, DASH, aim to reduce the prevalence of hypertension and neurological delay (Omar, 2019). Data from a DASH study showed a slower rate of cognitive decline, and DASH participants on a calorie-restricted diet showed improvements in memory, learning, and psychomotor speed, compared with the control group (Omar, 2019). Another diet called the Ketogenic Diet aims to reduce the amount of free fatty acids in the blood, and therefore the amount of beta-amyloid accumulation in the brain (Omar, 2019). Omar et al. found that participants in the Ketogenic Diet study had improved performance in the ADAS-cog and in verbal memory performance (Omar, 2019). However, the diet that performed the best was the MIND diet: Omar et al. observed a 53% reduction in the rate of AD, and that the MIND diet slows cognitive decline with age (Omar, 2019). Omar et al. also suggested that the MIND diet contributed to better cognitive protection for elderly individuals living in low to middle-income countries (Omar, 2019). The data suggests that the Mediterranean Diet and the Ketogenic Diet have a role in reducing the risk of AD. However, the results of studies analyzing the regular intake of lean meat, fruit, vegetables, and fish (which the Mediterranean Diet and Ketogenic Diets promote) were inconsistent (Omar, 2019).
The gut microbiome, which is influenced by diet, can also affect the risk of AD. Aging leads to gut dysbiosis, which leads to the misfolding of beta-amyloid and the formation of plaques (Kesika et al., 2021). In addition, an unhealthy gut microbiome can increase the presence of inflammatory cytokines that promote the aggregation of beta-amyloid (Kesika et al., 2021). Preclinical studies show that a gut microbiome that is bolstered by probiotic supplements reduces the risk of AD (Kesika et al., 2021).
The next section will examine the way sleep, much like diet, affects the risk of developing AD.
Sleep and the Role of the Glymphatic System
When sleeping, the brain is very active: recent studies have shown that the glymphatic system (GS) is responsible for clearing away waste products, including beta-amyloid, from the brain (Iliff et al., 2012). The GS, discovered by Iliff et al., consists of para-arterial spaces that surround blood vessels and allow for the flow of cerebrospinal fluid in and out of the parenchyma (Iliff et al., 2012). As shown in Figure 3, CSF leaves the perivascular space and moves through the parenchyma by bulk flow, clearing away beta-amyloid and other soluble waste products before leaving the brain through paravenous spaces surrounding veins (Iliff et al., 2012). Researchers have shown that the GS works during sleep, and more specifically during slow-wave sleep (SWS) (Cordone et al., 2019),(Iliff et al., 2012). Therefore, because the GS is most active during sleep and is instrumental in clearing beta-amyloid, the less sleep acquired by an individual, the less waste is cleared, allowing for more accumulation of soluble waste such as beta-amyloid and tau. Studies have shown that with chronic sleep deprivation, CSF Aβ42 levels are increased, and similar to mild sleep deprivation, memory worsens (Cordone et al., 2019). In addition, mice that underwent sleep deprivation for two months suffered the cognitive effects for three months (Cordone et al., 2019). These findings suggest that sleep deprivation is a risk factor for AD. However, other studies have shown that in the preclinical stage of AD, SWS is disturbed. Since SWS is the period of sleep during which the GS is the most efficient, this leads to a greater accumulation of beta-amyloid in the brain, which further disrupts sleep (Cordone et al., 2019). This vicious cycle continues as AD progresses, with decreased beta-amyloid clearance increasing protein deposition, and worsened AD causing further disturbances to SWS.
Other health issues can also affect the sleep cycle, such as insomnia and obstructive sleep apnea (OSA). OSA is sleep-disordered breathing that occurs when there is total or partial closure of the upper airway during sleep, and is associated with hemodynamic disruptions and recurrent brain arousals (Osorio, 2018). OSA causes disturbances of sleep (and therefore the GS), intermittent hypoxia (lack of oxygen delivery to the brain) and oxidative stress, intrathoracic and hemodynamic changes, and cardiovascular conditions, all of which increase the chance for AD (Osorio, 2018). OSA and AD are often comorbid conditions, or present in the same individual, with one meta-analysis finding that AD patients have five times the risk of developing OSA compared to individuals the same age as them, and that 50% of patients with AD experience OSA after being diagnosed (Osorio, 2018). However, the evidence is inconclusive as to whether OSA causes, worsens, and/or results from AD (Osorio, 2018).
In summary, more research is required to understand the GS and OSA in the context of AD.
Figure 3: The path of the glymphatic system. Cerebrospinal Fluid (CSF) leaves the perivascular space and moves through the parenchyma to clear away beta-amyloid and other soluble waste products. It then leaves the brain through paravenous spaces surrounding veins. Adapted from Iliff J. J. et al., 2012, with permission from the author.
Depression
Depression and cognitive impairment are often comorbid conditions, and are two of the most common disorders that affect the elderly (Bennett & Thomas, 2014). Various studies have examined whether early-life depression and/or late-life depression lead to AD. One longitudinal study with a 15 year follow-up found that late-life depression is a symptom of AD and that early-life depression does not affect one’s risk of developing AD (Bennett & Thomas, 2014). Conversely, other studies have shown that individuals who had depression early in their lives had reduced hippocampal volume, and more subcortical white matter lesions than individuals who had late-onset depression (Bennett & Thomas, 2014). This suggests that early-onset depression increases the risk of AD, as it decreases cognitive reserve. Furthermore, studies by Bennet et al. suggest that AD and depression are linked because they share symptoms such as inflammation, cardiovascular changes, and risk factors such as education level and SES (Bennett & Thomas, 2014).
Another analysis of epidemiological studies by Bennet et al. suggested that depression is independent of dementia and AD, as depressed individuals’ depression symptoms did not change as their dementia progressed (Bennett & Thomas, 2014).
While many studies have examined the relationship between AD and depression, more work is needed to fully understand the impact each has upon the other, and to find appropriate treatments. The next section will discuss how education affects the risk of AD.
Education
Cognitive reserve is defined as the acquired capacity of a functional brain’s adaptability and flexibility during aging (Wada et al., 2018). As previously discussed, an individual with high cognitive reserve may develop AD at the same time as an individual with low cognitive reserve, but only show symptoms of the disease much later in life. Because education is one of the main factors that increase cognitive reserve, it is important for decreasing the risk of AD (Wada et al., 2018).
A study using the AD Neuroimaging Initiative (ADNI) by Wada et al. found that more education was associated with a larger brain volume (Wada et al., 2018). Although education did not affect the amount of beta-amyloid and tau aggregated in the brain as measured by MRI and PET scans, the study suggests that education decreases the risk of AD by providing protection in the form of increased cognitive reserve (Wada et al., 2018). The study also found that while education prevents AD, it does not reverse it at any stage: patients who were educated during the MCI stage of AD were shown to have an increased brain volume and improvement of symptoms, while patients in the last stage of AD showed no improvement (Wada et al., 2018). Another conclusion from Wada et al. was that participants with a higher education had a higher cognitive reserve, and therefore a decreased risk of AD (Wada et al., 2018).
A study by Anderson et al. investigated whether education and intelligence lowered the risk of AD. The study found that the relationship between education level and intelligence is bidirectional, meaning that there is evidence of both education and intelligence affecting the risk of AD (Anderson et al., 2020). Anderson et al. also found that education increases intelligence. Therefore, more schooling and education, including independent learning outside of school or work, can lower one’s risk of AD (Wada et al., 2018),(Anderson et al., 2020).
Education is important for increasing cognitive reserve, and therefore decreasing the risk of developing AD, but might not be accessible to those of low SES.
Socioeconomic Status
While SES may seem unrelated to AD, it may have a large impact on one’s risk of developing AD. Low SES consists of low income and residence in disadvantaged areas (Chen et al., 2020). In the 2020 United States Census Bureau Income Report, low SES was described as an income between $13,465 (one individual household) and $50,035 (nine or more individual household) (EMILY A. SHRIDER, MELISSA KOLLAR, FRANCES CHEN, 2021). Low annual income can affect individuals by cutting off their access to clean water, food, and health care (Chen et al., 2020). Those with higher SES have access to healthier food, better healthcare, exercise, and clean air, resulting in better diets and cardiovascular health, thereby reducing their risk of developing AD (Chen et al., 2020).
Those with low SES have less access to health care, and may be more likely to have an unhealthy lifestyle (Fischer et al., 2009). They also may be less likely to utilize health care, even if they do have access to it (Fischer et al., 2009). Fischer et al. studied 217 patients from the Inner City Memory Disorders Clinic, of which most were classified as having low SES (46% of patients), and found that the low SES group had fewer years of education, greater levels of depression, and low annual income (Fischer et al., 2009). This study also found that low SES leads to an increased risk of all dementias, including AD (Fischer et al., 2009). As previously discussed, both low education and depression lead to an increase in risk of AD.
A separate study examined a Taiwanese database containing data from 99% of the population of Taiwan, and had similar findings (Chen et al., 2020),(National Health Insurance Research Database, n.d.). This study found that the 5-year survival rate for AD patients with low SES was 3.24 times lower than those who had a high SES (Chen et al., 2020). Therefore, low SES can not only increase the risk of AD, but may also have an effect on disease progression (Chen et al., 2020). Chen et al. also showed that low SES is associated with less hospital care and poorer symptom management (Chen et al., 2020).
Conversely to these studies, Yasuno et al. found that SES does not directly affect risk of AD. Rather, education and environmental factors during an individual’s early life affect risk of AD by influencing an individual’s mid and late-life SES (Yasuno et al., 2020). While this may seem like a contradictory result, this study highlights the importance of education and an individual’s childhood environment on later life access to healthcare, healthy food, and other factors that may influence risk of developing AD.
Conclusion
This review analyzed the risk factors of Alzheimer’s Disease, and the way SES affects all environmental risk factors for AD. Genetics and age play a large role in an individual’s risk for AD, but are not affected by lifestyle. Poor cardiovascular health leads to an increased risk of AD, and diet affects the development of AD by contributing to the health of both the cardiovascular system and the gut microbiome. Sleep and the GS are instrumental in clearing away beta-amyloid. Depression may be a result of AD or one of its risk factors, but requires further study to clarify this relationship. Education affects intelligence and cognitive reserve, both of which play a role in the likelihood of developing AD. This paper also discusses the ways SES may contribute to an individual’s overall health and risk of AD, and that those of lower in SES are more at risk of developing AD than those of higher SES.
Due to the lack of comprehensive data, future research should be directed towards different types of diets and their influence on the risk of AD, the seemingly protective effects of nicotine, and how the effects of depression and other mental health conditions affect the risk of developing AD. More research is also needed to answer the questions of how SES affects the risk of developing AD and how it interacts with other risk factors.
Future drug treatments should be made available at an affordable price. One of these treatments is Aducanumab, which helps clear beta-amyloid, and has been approved under the accelerated approval pathway by the FDA. As a result, research is needed to fully understand whether removing amyloid plaques will reverse the effects of AD, or simply prevent the disease from progressing.
Individuals at risk of AD, their health providers, and their caregivers should focus on developing environments that promote a healthy lifestyle. They should also find new ways to actively learn new information, such as online courses or reading the newspaper. Grocery stores and food manufacturers should make clean and unprocessed foods more accessible and affordable for all individuals. Finally, countries should make affordable healthcare, quiet housing, and education available to everyone, while also paying a livable wage to workers. Implementing these basic human rights will not only prolong health span, but also prevent the incidence of neurodegenerative disease affecting millions worldwide.
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