Alzheimer’s Disease

Alzheimer’s Disease (AD) is a debilitating, progressive brain disorder, which gradually destroys a person’s memory, thinking and reasoning skills, and ultimately the ability to communicate. Discovered by Dr. Alois Alzheimer in 1906 (1), Alzheimer’s Disease has largely remained an enigma to scientists, as molecular biology research and clinical trials have only provided a small glimpse into the development of AD (1). It is estimated that Alzheimer’s is currently ranked as the third leading cause of death among older people (1). The increase in cultural concern on Alzheimer’s Disease, especially centered around the idea of loss of oneself, has led to increased activity not only within the research community, but within support organizations, the pharmaceutical industry, and even the federal government (5).

Biological Process/Definition

The NIH defines Alzheimer’s Disease as a “progressive, irreversible brain disorder that slowly destroys memory and thinking skills, and eventually the ability to carry out simple daily tasks” (1). Dementia is the loss of cognitive function, and Alzheimer’s is the most common cause of dementia among older adults (1).

In healthy people, all sensations, movements, thoughts, memories, and feelings are the results of signals that are sent through billions of neurons in the brain. Neurons are in constant communication with each other through electrical charges that travel down the cells causing the release of chemicals across small gaps to neighboring neurons. Other types of cells in the brain, such as astrocytes and microglia clear away debris and help keep neurons healthy. This healthy balance is destroyed by toxic changes in the brain of someone with Alzheimer’s (1).

Researchers believe this process involves two proteins, ß-Amyloid and tau, which become toxic to the brain through a complex series of molecular transformations (11). This abnormal tau accumulates in the brain, ultimately forming tangles inside the neurons, and ß-Amyloid clumps into plaques which gradually builds up between neurons. These two proteins work in tandem, as the level of amyloid reaches a critical mass, tau rapidly spreads throughout the brain (1).

Tau and ß-Amyloid are not the only factors believed to affect brain health. The vascular system may fail to deliver sufficient blood and nutrients to the brain and the brain may lack glucose needed to power usual activity (11). As these destructive changes progress, microglial cells fail to clear away debris and astrocytes react negatively to distressed microglia (1). Chronic inflammation sets in and neurons die, losing their ability to communicate. As neurons die, brain tissue begins to shrink beginning in the hippocampus, the part of the brain important for learning and memory function. By the final stage of AD the brain has heavily deteriorated its tissue has shrunk significantly (1).

Diagram comparing a cross section of a health brain (left) to the cross section of a brain affected by Alzheimer’s Disease (right) (12).

 

Memory problems are typically the first signs of cognitive impairment linked to AD, although memory problems are first diagnosed as mild cognitive impairment (MCI). Order of symptoms vary from person to person, however, the early stages of the disease are signaled by decline in non-memory aspects of cognition, including speech, reasoning/judgement, and vision/spatial senses. Mild symptoms include wandering, repeating questions, personality and behavioral changes, and taking a longer time to complete daily tasks. Moderate to severe staged Alzheimer’s produces symptoms that result from damage to areas of the brain that control language, sensory processing, reasoning, and conscious thought. Symptoms include worsened memory loss, trouble recognizing familiar faces, inability to learn new things or carry out multistep tasks, hallucinations, delusions, and paranoia. Total severity of the disease renders the individual unable to communicate and completely reliant on others for their case as their body shuts down (1).

Research…?

Scientists are not fully certain on the causes of Alzheimer’s (1). Basic science and epidemiological findings about late onset AD are continually subject to revision and are far from conclusive. Researchers have found a genetic component to some early onset cases: the presence of specific alleles that increase a person’s risk for AD. However, it is unanimously agreed that the presence of these alleles is neither necessary nor sufficient to cause AD for reasons that are still poorly understood (2). It has been theorized that late onset AD arises from a series of changes in the brain that occur over decades due to a combination of genetic, environmental, and lifestyle factors, and damage to the brain starts a decade or more before symptoms even appear (1).

Research focused on predicting late onset AD has been centered around amyloid and tau biomarkers since the 1990s (3). However, it has been shown that there is no straightforward correlation between quantity of amyloid plaques, tau tangles, and disease manifestations. It has even been noted that patients who displayed typical symptoms of AD had no accumulation of plaques and tangles in the brain, further puzzling the scientific community (1,11). Conversely, a study from the mid twentieth century found that 80% of individuals over 65 had typical plaques and tangles associated with AD, yet exhibited no AD symptoms (3). Additionally, given AD is most common in the aging population (1), anthropologists have proposed the notion that factors external to the body have significant effects on how the body ages; therefore, realistic predictions about risk for AD and dementia may not be possible other than the obvious and inevitable risk of aging itself (4).

Pulling together all the evidence the scientific community has confidently concluded about the disease, current research on AD is focused on therapies to target specific genetic, molecular, and cellular mechanisms (1). Embedded in all AD and dementia research is the importance of prevention and early detection, rather than reversing the effects of the disease (3), although multiple, ongoing clinical trials have found even more difficulty in recruiting potential subjects in advance without research bias (1,3).

Treatment

Pharmaceutical treatment of Alzheimer’s first began in the 1990s as drugs were released to enhance cognitive performance, however by 2005 it was shown that these medications had major side effects and only improved cognition for some, not all (3). These drugs, released on the basis of research teams hired by the pharmaceutical companies, were only as sound as the research behind them, but that did not stop the profit driven field. When it was clear these medications had limited to no effect in improving cognitive function, pharmaceutical companies worked with health professionals to widen the definition of AD and dementia to emphasize behavioral and psychological symptoms, rather than the dominating “cognitive paradigm” (3, p. 226). Previously existing drugs designed for cognitive enhancements were now being tested for non-cognitive outcomes, and these pharmacological interventions produced positive outcome studies which could then be published. Although this campaign was quickly abandoned as the medications became rapidly under fire due to dangerous side effects and misleading claims, the attempt to broaden the definition of Alzheimer’s persisted at the hand of external industries (3). Pharmaceutical intervention has continued with the repurposing of existing medications for the newly widened definition of Alzheimer’s and its proposed causes, such as diabetes medications, statins, and hypertensives, all of which have been linked to the newly evaluated cardiovascular risk factors for AD or vascular dementia (3).

Currently, several medications approved by the FDA are regularly prescribed to those with AD. These medications maintain mental function and manage behavior symptoms by regulating certain chemicals transferred between neurons. These drugs do not change the underlying disease process, they merely mitigate symptoms and temporarily slow damage (1).

Non-Pharmacological Care and Deterioration of the Mind

A new trend of AD analysis and research has been focused on the idea of the deterioration of a person’s true self (5,6). As a person loses their memories, relationships, and identity, their personhood is lost, as well. Many groups have sought to treat this perspective of AD over the past several decades, designing an approach to maintaining or restoring personhood through new methods and philosophies of care (6). These efforts include exposure to visual art and music as therapeutic programs to people suffering from AD. Such programs are a small anecdote for the larger movement to bring a variety of non-pharmacological treatment options to AD care.

Politics of Health

The societal view of Alzheimer’s Disease has transformed from the once narrow definition of loss of cognitive function, understood only by scientists, into a wide, anthropological disease, in which multiple groups of society are working to combat different aspects of the disease. Alzheimer’s is now culturally integrated, with social and cultural relevance on multiple levels. This movement was born with a mission to eliminate the ‘loss of self’ element, implicit in the current Alzheimer’s construct. The examination of ‘loss of self’ has been infused into popular culture, and the decay of familial relationships and friendships has been brought to the surface of many television shows, movies, and support groups. The AD movement served as a unifying conceptualization, which provided a focus for political action and a response by a social movement. Neuroscientists built their research careers around Alzheimer’s; representatives of the newly established National Institute of Aging sought congressional funding and support; caregivers and clinicians rallied to establish supportive services and a wide-reaching care network; and gerontologic and health policy activists lobbied for increased services for the affected elderly and their families (5). As the definition of Alzheimer’s transcended beyond molecular biology and became a social construct (7), those in the AD sphere had the opportunity to become biological citizens, as viewed by Adriana Petryna, and seek support from their state and community.

Additionally, AD is currently the most publicized health problem of old age, and defining Alzheimer’s as a disease, not just a normal part of aging, has led to multiple social, political, economic, and personal consequences. The increased activity around Alzheimer’s essentially medicalizes aging, which provides for the social control of the elderly through medical definition, management, and treatment (5). “Control” in the sense is justified as being good for the patient, especially in Alzheimer’s, which exemplifies the medicalization of social irregularity.

Lastly, with a disease that exhibits symptoms across multiple psychological and behavioral spectrums, the pharmaceuticalization of abnormal behavior will always be present. Given the lack of reliability in risk factors and biomarkers associated with AD, data gathered from researchers financed by the pharmacological industry cannot stand without doubt. There is a clear need for research that acknowledges numerous pathological explanations of cognitive decline, as profit driven pharmaceutical companies have and will promote pathways that guarantee sales for their medications.

 

Works cited:

1. “Alzheimer’s Disease Fact Sheet.” National Institute on Aging, U.S. Department of Health and Human Services, www. nia.nih.gov/health/alzheimers-disease-fact-sheet. Accessed 24 Sept. 2017.
2. Lock, Margaret. “Demoting the Genetic Body.” Anthropologica, vol. 51, no. 1, 2009, pp. 159–172. JSTOR, JSTOR, www.jstor.org/stable/25605464.
3. Leibing, Annette. “The Earlier the Better: Alzheimer’s Prevention, Early Detection, and the Quest for Pharmacological Interventions.” Culture, Medicine, and Psychiatry, vol. 38, no. 2, 2014, pp. 217–236., doi:10.1007/s11013-014-9370-2.
4. Lock, Margaret. “The Epigenome and Nature/Nurture Reunification: A Challenge for Anthropology.” Medical Anthropology, vol. 32, no. 4, 2013, pp. 291–308., doi:10.1080/01459740.2012.746973.
5. Herskovits, Elizabeth. “Struggling over Subjectivity: Debates about the ‘Self’ and Alzheimer’s Disease.” Medical Anthropology Quarterly, vol. 9, no. 2, 1995, pp. 146–164. JSTOR, JSTOR, www.jstor.org/stable/649114.
6. Selberg, Scott. “Modern Art as Public Care: Alzheimers and the Aesthetics of Universal Personhood.” Medical Anthropology Quarterly, vol. 29, no. 4, 2015, pp. 473–491., doi:10.1111/maq.12199.
7. Robertson, Ann. “The Politics of Alzheimers Disease: A Case Study in Apocalyptic Demography.” International Journal of Health Services, vol. 20, no. 3, 1990, pp. 429–442., doi:10.2190/c8ae-nyc1-2r98-mhp1.
8. Husain, Masud, and Mitul A. Mehta. “Cognitive enhancement by drugs in health and disease.” Trends in Cognitive Sciences, vol. 15, no. 1, 2011, pp. 28–36., doi:10.1016/j.tics.2010.11.002.
9. Åsberg, Cecilia, and Jennifer Lum. “PharmAD-Ventures: A Feminist Analysis of the Pharmacological Imaginary of Alzheimer’s Disease.” Body & Society, vol. 15, no. 4, 2009, pp. 95–117., doi:10.1177/1357034×09347217.
10. Kleinman, Arthur. “Four Social Theories for Global Health.” The Lancet, vol. 375, no. 9725, 2010, pp. 1518–1519., doi:10.1016/s0140-6736(10)60646-0.
11. Alzheimer’s Association Report. “2016 Alzheimer’s Disease Facts and Figures.” Alzheimer’s and Dementia, vol. 12, no. 4, pp. 459-509., doi: https://doi.org/10.1016/j.jalz.2016.03.001.
12. “Healthy Brain Versus Alzheimer’s Brain.” Alzheimer’s Association, www.alz.org/braintour/healthy_vs_alzheimers.asp.

Alzheimer’s Disease (AD) is a progressive, irreversible brain disorder that slowly destroys memory and thinking skills, and eventually the ability to carry out simple daily tasks. AD is the most common cause of dementia among older adults. There are multiple types of dementia, but in its barest forms, dementia is the loss of cognitive functioning (i.e. thinking, remembering, and reasoning) and behavioral abilities to the extent that it affects a person’s daily life and activities (1).

In healthy people, all sensations, movements, thoughts, memories, and feelings are the results of signals that pass through billions of neurons in the brain. Neurons are in constant communication with each other through electrical charges that travel down the cells causing the release of chemicals across small gaps to neighboring neurons. Other types of cells in the brain, such as astrocytes and microglia clear away debris and help keep neurons healthy. This healthy balance is destroyed by toxic changes in the brain of someone with Alzheimer’s (1).

Researchers believe this process involves two proteins, ß-Amyloid and tau, which become toxic to the brain through a complex series of molecular transformations. This abnormal tau accumulates in the brain, ultimately forming tangles inside the neurons, and ß-Amyloid clumps into plaques which gradually builds up between neurons. These two proteins work in tandem, as the level of amyloid reaches a critical mass, tau rapidly spreads throughout the brain (1).

Tau and ß-Amyloid are not the only factors believed to affect brain health. The vascular system may fail to deliver sufficient blood and nutrients to the brain and the brain may lack glucose needed to power usual activity. As these destructive changes progress, microglial cells fail to clear away debris and astrocytes react negatively to distressed microglia. Chronic inflammation sets in and neurons die, losing their ability to communicate. As neurons die, brain tissue begins to shrink beginning in the hippocampus, the part of the brain important for learning and memory function. By the final stage of Alzheimer’s, damage is widespread, and brain tissue has shrunk significantly (1).

Memory problems are typically the first signs of cognitive impairment linked to AD, although memory problems are first diagnosed as mild cognitive impairment (MCI). Order of symptoms vary from person to person, however. Decline in non-memory aspects of cognition, such as word finding, vision/spatial issues, impaired reasoning/judgement) signal the very early stages of the disease. Mild symptoms include wandering, repeating questions, personality and behavioral changes, and taking a longer time to complete daily tasks. Moderate to severe staged Alzheimer’s produces symptoms that result from damage to areas of the brain that control language, sensory processing, reasoning, and conscious thought. Symptoms include worsened memory loss, trouble recognizing familiar faces, inability to learn new things or carry out multistep tasks, hallucinations, delusions, and paranoia. Total severity of the disease renders the individual unable to communicate and completely reliant on others for their case as their body shuts down (1).

Scientists are not fully certain on the causes of Alzheimer’s (1). Basic science and epidemiological findings about late onset AD are continually subject to revision and are far from conclusive. Researchers have found a genetic component to some early onset cases, the presence of specific alleles that increase a person’s risk for AD. However, it is unanimously agreed that the presence of these alleles is neither necessary nor sufficient to cause AD for reasons that are still poorly understood (2, 165). It has been theorized that late onset AD arises from a complex series of brain changes that occur over decades – a combination of genetic, environmental, and lifestyle factors – and damage to the brain starts a decade or more before symptoms even appear (1).

Research focused on predicting late onset AD has been centered around amyloid and tau biomarkers since the 1990s (3, 220). However, it has been shown that the correlation between quantity of amyloid plaques, tau tangles, and disease manifestations is not entirely straightforward. It has been noted that patients who displayed typical symptoms of AD had no accumulation of plaques and tangles in the brain. Conversely, a study from the mid twentieth century showed that 80% of individuals over 65 had typical plaques and tangles associated with AD, but exhibited no AD symptoms (3, 220). Additionally, given AD is most common in the aging population (1), anthropologists have proposed the notion that factors external to the body have significant effects on how the body ages; therefore, realistic predictions about risk for AD and dementia may not be possible other than the obvious and unde1ble risk of aging itself (4, 299).

The pharmaceutical treatment of Alzheimer’s first began in the 1990s as drugs were released to enhance cognitive performance, but by 2005 it was shown that these medications had major side effects and improved cognition for some, not all (3, 221). When it became clear that these cognitive enhancers had only limited effect, pharmaceutical companies worked with health professionals to widen the definition of AD and dementia to emphasize behavioral and psychological symptoms, rather than the dominating “cognitive paradigm” (3, 226). Previously existing drugs designed for cognitive enhancements were now being tested for non-cognitive outcomes, and these pharmacological interventions produced positive outcome studies which could then be published. Although this campaign was quickly abandoned as the medications became rapidly under fire due to dangerous side effects and misleading claims, the widening of a once narrow definition of AD and dementia continues to exist at the hand of external industries (3, 226). Pharmaceutical intervention continues with the repurposing of existing medications for the new conceptualization of Alzheimer’s disease, such as diabetes related agents, statins, and antihypertensives, all of which have been linked to the new focus on cardiovascular risk factors (3, 227).

Currently, several medications approved by the FDA are regularly prescribed to those with AD. These medications maintain mental function and manage behavior symptoms by regulating certain chemicals transferred between neurons. These drugs do not change the underlying disease process, they merely mitigate symptoms and temporarily slow damage (1).

A new trend of AD analysis and research has been focused on the idea of the deterioration of a person’s true self (5,6). As a person loses their memories, relationships, and identity, their personhood is lost, as well. Many groups have sought to combat this perspective over the past several decades, designing an approach to maintaining or restoring personhood through new methods and philosophies of care (6, 475). These efforts include exposure to visual art and music as therapeutic programs to people suffering from AD. Ultimately, this branch of treatment seeks to provide a more diverse set of non-pharmacological technologies to Alzheimer care.

Current research on Alzheimer’s is focused on therapies to target specific genetic, molecular, and cellular mechanisms (1). Embedded in all AD and dementia research is the importance of prevention and early detection, rather than reversing the effects of the disease (3).

As Alzheimer’s Disease became assessed less and less as a biomedical disease, and more as a medical anthropological disease, a movement was born with a mission to eliminate the “loss of self” element, implicit in the current Alzheimer’s construct. The AD movement served as a unifying conceptualization, one which provided a focus for political action and a response by a social movement. Neuroscientists built their research careers around Alzheimer’s; representatives of the newly established National Institute of Aging sought congressional funding and support; caregivers and clinicians rallied to establish supportive services and a wide-reaching care network; and gerontologic and health policy activists lobbied for increased services for the affected elderly and their families (5, 150). As the definition of Alzheimer’s transcended beyond molecular biology and became a social construct (7), those in the AD sphere became had the opportunity to become biological citizens and seek support from their state.

Additionally, AD is currently the most publicized health problem of old age, and defining Alzheimer’s as a disease, not just a normal part of aging, has led to multiple social, political, economic, and personal consequences. The increased activity around Alzheimer’s essentially medicalizes aging, and the mechanisms of medicalization are shown to provide for the social control of the elderly through medical definition, management, and treatment (5, 152).  “Control” in the sense is justified as being good for the patient, especially in Alzheimer’s, which exemplifies the medicalization of social irregularity.

Lastly, with a disease that exhibits symptoms across multiple psychological and behavioral spectrums, the pharmaceuticalization of abnormal behavior will always be present. Current struggles surrounding profound interventions targeting Alzheimer’s disease shows not only the recent changes in interpreting risk factors and biomarkers associated with AD, but also highlights doubts surrounding data gathered from researchers financed by the pharmacological industry. There is a clear need for research that acknowledges numerous pathological explanations of cognitive decline, as profit driven pharmaceutical companies have and will promote pathways that guarantee sales for their medications.

 

Works cited:

1. “Alzheimer’s Disease Fact Sheet.” National Institute on Aging, U.S. Department of Health and Human Services, www. nia.nih.gov/health/alzheimers-disease-fact-sheet. Accessed 24 Sept. 2017.
2. Lock, Margaret. “Demoting the Genetic Body.” Anthropologica, vol. 51, no. 1, 2009, pp. 159–172. JSTOR, JSTOR, www.jstor.org/stable/25605464.
3. Leibing, Annette. “The Earlier the Better: Alzheimer’s Prevention, Early Detection, and the Quest for Pharmacological Interventions.” Culture, Medicine, and Psychiatry, vol. 38, no. 2, 2014, pp. 217–236., doi:10.1007/s11013-014-9370-2.
4. Lock, Margaret. “The Epigenome and Nature/Nurture Reunification: A Challenge for Anthropology.” Medical Anthropology, vol. 32, no. 4, 2013, pp. 291–308., doi:10.1080/01459740.2012.746973.
5. Herskovits, Elizabeth. “Struggling over Subjectivity: Debates about the ‘Self’ and Alzheimer’s Disease.” Medical Anthropology Quarterly, vol. 9, no. 2, 1995, pp. 146–164. JSTOR, JSTOR, www.jstor.org/stable/649114.
6. Selberg, Scott. “Modern Art as Public Care: Alzheimers and the Aesthetics of Universal Personhood.” Medical Anthropology Quarterly, vol. 29, no. 4, 2015, pp. 473–491., doi:10.1111/maq.12199.
7. Robertson, Ann. “The Politics of Alzheimers Disease: A Case Study in Apocalyptic Demography.” International Journal of Health Services, vol. 20, no. 3, 1990, pp. 429–442., doi:10.2190/c8ae-nyc1-2r98-mhp1.
8. Husain, Masud, and Mitul A. Mehta. “Cognitive enhancement by drugs in health and disease.” Trends in Cognitive Sciences, vol. 15, no. 1, 2011, pp. 28–36., doi:10.1016/j.tics.2010.11.002.
9. Åsberg, Cecilia, and Jennifer Lum. “PharmAD-Ventures: A Feminist Analysis of the Pharmacological Imaginary of Alzheimer’s Disease.” Body & Society, vol. 15, no. 4, 2009, pp. 95–117., doi:10.1177/1357034×09347217.
10. Kleinman, Arthur. “Four Social Theories for Global Health.” The Lancet, vol. 375, no. 9725, 2010, pp. 1518–1519., doi:10.1016/s0140-6736(10)60646-0.

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