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Preventing Dementia?
Critical Perspectives on a New Paradigm of Preparing for Old Age
Annette Leibing, Silke Schicktanz, Annette Leibing, Silke Schicktanz
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eBook - ePub
Preventing Dementia?
Critical Perspectives on a New Paradigm of Preparing for Old Age
Annette Leibing, Silke Schicktanz, Annette Leibing, Silke Schicktanz
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The conceptualization of dementia has changed dramatically in recent years with the claim that, through early detection and by controlling several risk factors, a prevention of dementia is possible. Although encouraging and providing hope against this feared condition, this claim is open to scrutiny. This volume looks at how this new conceptualization ignores many of the factors which influence a dementia sufferers' prognosis, including their history with education, food and exercise as well as their living in different epistemic cultures. The central aim is to question the concept of prevention and analyze its impact on aging people and aging societies.
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PART I
The Discursive and Social Practices of Dementia Prevention
1 A WINDOW TO ACT?
Revisiting the Conceptual Foundations of Alzheimerās Disease in Dementia Prevention
Lara Keuck
Introduction
THROUGHOUT THE TWENTIETH CENTURY AND up till the present, Alzheimerās disease has served as a working title. This chapter offers a historical and epistemological perspective that allows us to locate and evaluate the promises of dementia prevention that allude to Alzheimerās disease as a much feared medical condition and simultaneously capitalize on the idea of a window to act (before it is too late).1 The current popular scientific understanding of Alzheimerās disease presents the long inconspicuous trajectory of a pathology that ultimately results in devastating symptoms of dementia, such as severe mental decline and the loss of the capacity to lead oneās life autonomously.2 Accordingly, the notion of a window to act refers to a biologically defined time frameānamely, before an irreparable pathological process has caused perceivable cognitive and functional deficits. This chapter argues that this picture is based on shaky grounds, and that it represents a collage of different ways in which the disease has been conceptualized within the last century. Alzheimerās disease has acted as an ambiguous term for the diagnosis of a very severe mental disorder with dramatic effects for affected patients, their families, and care givers, as well as for the underlying, yet-to-be-fully-characterized biological process that presumably starts many years, even decades, before the manifestation of symptoms. This chapter shows that the conceptual foundations of the medical category of Alzheimerās disease rest on a history of shifting question marks concerning the relation between the pathological process, clinical symptoms, and nosological category. The window to act might serve as a sound scientific hypothesis; however, it can transform into a questionable justification for assigning a broad range of people the responsibility to take action and adopt preventive or early intervention strategies against developing dementia. If the proposed actions come with potential negative side effects (like taking a drug after an earlyāuncertainādiagnosis), this is even more problematic. To give an example, the mobilization of concerned potential patients was marketed in an online advertisement campaign of the pharmaceutical companies Pfizer (who closed its Alzheimerās disease research and development program in 2018) and Eisai, which presented a middle-aged, healthy, and determined-looking man vis-Ć -vis a teeth-baring tiger and the slogan āface the fear of Alzheimerās disease,ā along with these lines: āthe earlier you diagnose Alzheimerās disease, the sooner you can do something about it / fighting Alzheimerās disease right from the start / AriceptĀ® donepezil hydrochloride (click here for healthcare professional information on prescribing and adverse event reporting).ā This advertisement, which went online in 2009, evokes a picture of a clearly identified enemy. However, medical experts have redrawn the composite sketch of this enemy several times from the first description of Alzheimerās disease to the most recent formulation of a research framework.
This chapter successively presents and discusses three of the most influential sketches of Alzheimerās disease: those found within the proposals of Emil Kraepelin and Alois Alzheimer around 1910; of Bob Katzman around 1976; and of the recently published NIH-AA work group for a new research framework on a biological definition of Alzheimerās disease (Jack et al. 2018). It shows that the key questions framed by the respective research programs differed significantly from each other, yet none of them could so far be answered conclusively: the relationship between Alzheimerās disease and senile dementia, the identification of the pathological process, the biological definition of the diseaseāall of the enquiries remain open. However, every agenda replaced unresolved questions with working assumptions in order to probe new avenues for solving the ongoing problem of determining a diagnosis of Alzheimerās disease, and finding a way to manage, cure, or prevent it.
I have selected the mentioned positionings of Alzheimerās disease for this analysis because the respective approaches and actors already figure prominently within the existing historiography of Alzheimerās disease and have been assigned argumentative roles especially in the context of discussing the origins of, and possible measures against, the frustrating futility of research on effective treatments against Alzheimerās disease and other dementias.3 Drawing on my own historical and philosophical research, I suggest a different understanding of the reconceptualizations of Alzheimerās disease that focuses more on the shifting epistemological roles that have been assigned to this purported medical entity. Against this background, I have considered how the acclaimed new paradigm of dementia prevention differs from past and present conventional dementia research. I will conclude that this question must be answered case by case, but that many dementia prevention strategies draw on the above depicted āwindow to actāāan epistemology that also motivates the current research framework toward a biological definition of Alzheimerās disease, even if the aims and means to act may differ largely in the case of general recommendations for healthy aging versus biomarker profileāspecific interventions.
The main conceptual shifts between the three research frameworks and a fourth framework that some proponents of prevention seem to embrace and that questions the coherence of the past centuryās approach to classifying diseases altogether will be illustrated in simple figures in the four succeeding sections of this chapter. Like all simplifications, they must be handled with care. The reality is always more complex, and the influence that the discussed proposals and their antecedent or succeeding variants have had can only be explained by looking more closely into the contexts, conditions, and incentives of using and propagating these programs. All of the discussed proposals have been controversially discussed within their times by psychiatrists and medical scientists from various institutions. This chapter restricts itself to providing a comparative representation of the conceptual foundations in which Alzheimerās disease has figured within the selected frameworks. The aim is to visualize what has remained and what has changed between them. The concluding section details why the medical category of Alzheimerās disease can be best conceptualized as a working title, and exemplifies how this perspective helps us to raise meaningful questions for evaluating present promises of dementia prevention.
In Search of a Nosological Position: Alzheimerās Disease around 1910
This section reassesses the introduction of Alzheimerās disease more than a century ago to highlight how this category was used as a working title to encourage research in histopathology and clinical psychiatry with the aim of better classifying mental disorders. Against this background, the remaining part of this chapter discusses the continuities and changes in the premises and promises of succeeding programmatic approaches to dementia research.
In 1910, Alzheimerās disease was first presented within the senile dementia section of the eighth edition of one of the most influential textbook classifications of the time, authored by German psychiatrist Emil Kraepelin (1856ā1926) (Kraepelin 1910: 624ā629).4 Four years earlier, Alois Alzheimer (1864ā1915), who worked in Kraepelinās psychiatric university clinic in Munich and headed the institutionās microscopic laboratory, had discussed the clinically and histopathologically āpeculiar caseā of a female patient who had died in her fifties of a severe form of dementia. The woman, Auguste D[eter] (1850ā1906), later became known as the first case of the disease that Alzheimer ādiscoveredā and that Kraepelin ābaptizedā (Alzheimer 1907).5
Within their time, however, Alzheimer and Kraepelin remained cautious about claiming a new disease entity. For sure, they marked their stakes: their publications feature detailed descriptions of both the clinical picture of an accelerated, progressive, ultimately fatal mental deterioration and the histopathological autopsy of plaques, tangles, and degenerated cortex tissue. Alzheimerās disease was regarded as an organic brain disease that gave rise to severe symptoms of dementia and that left its pathological traces in the anatomical substrate of a patientās brain. Similar to the characterization of infectious diseases such as syphilis and rabies that could give rise to madness, the pathological anatomy of organic brain diseasesāfor instance, arteriosclerosis in brain vesselsāwas regarded as proof of principle that psychiatry could become increasingly scientific and thereby legitimate itself as a medical university discipline. While the theoretical potential of the classification of Alzheimerās disease was ambitious, its actual realization remained underdetermined. In none of their publications did Alzheimer and Kraepelin take a definitive stance on whether the small group of āpeculiar casesā should be regarded as atypical variants of senile dementia or as a distinct entity. Rather, they presented this question of how to relate Alzheimerās disease to senile dementia and other organic brain diseases within a clinical theory of diseasesāthe nosologyāas a task for further research.
The patient records of the Munich clinic provide further evidence for the use of Alzheimerās disease as a clinical diagnosis, which did not serve to settle a medical issue but to mark interesting cases and recommend, if possible, examination of the patientsā brains postmortem: not only was the diagnosis regularly accompanied with question marks and corrections, but also the parameter that most historians of psychiatry considered to be a clear defining feature of Alzheimerās diseaseānamely, the presenility or comparably young age of the patients (in their forties or fifties) at the onset of dementiaāwas not a criterion of exclusion for an Alzheimerās diagnosis. In general, the category was rarely applied: the clinic records from 1909 to 1912 list more than eight thousand patients, out of which seven received a clinical diagnosis of Alzheimerās disease. Within this small group were patients that were in their late sixties, and in the case of a 63-year-old female patient, the diagnosis was even named āsenile Alzheimersche Krankheitā (see Keuck 2018a).
FIGURE 1.1. Schematic representation of the nosological puzzle that Alzheimerās disease presented in 1910. Picture referring to clinical symptoms: āAuguste Deter aus Frankfurt am Main,ā unknown photographer, 1902 (public domain, Wikimedia Commons, https://commons.wikimedia.org/wiki/File:Auguste_D_aus_Marktbreit.webp); picture referring to the pathological process: Alois Alzheimer, 1911, āĆber eigenartige KrankheitsfƤlle des spƤteren Alters,ā Zeitschrift fĆ¼r die Gesamte Neurologie und Psychiatrie 4: 356ā385, plate IV, figure 2.
Figure 1.1 schematically represents my reconstruction of the conceptualization of Alzheimerās disease at the time of its incorporation in Kraepelinās textbook. Two aspects are salient: first, the triadic structure constituting this psychiatric category, which connects clinical symptoms with a pathological process and a nosological category; and, second, the unsettledness of the very place of this category vis-Ć -vis the umbrella classes of senile dementia and organic brain disorders. As mentioned above, Kraepelin (and Alzheimer, who provided all the microphotographs for Kraepelinās book) discussed the āpeculiar casesā alongside a handful of other organic brain diseases as exemplars for the general potential of using pathological anatomy (alongside other service sciences that had already been incorporated into Kraepelinās vision of clinical psychiatry) to scientifically found psychiatric nosology and guide clinical differential diagnosis: when postmortem examinations showed distinctions within a clinically lumped group of patients, these should guide the clinician to search for matching differences in the symptomatology of living patients.
From the point of view of Kraepelinās clinical psychiatry and Alzheimerās cortex pathology, most of the mental disease categories were considered provisional.6 The use of these categories served nonetheless important purposes for compiling statistics to call for more funding, for managing and overseeing the flow of in-patients from the clinics to cheaper asylums for long-term stays, and for establishing psychiatry as a sound medical discipline that strives for systematic knowledge. The latter was based on an equally systematic recording and archiving of diagnostic procedures and evaluations during the initial anamnesis at admission, the psychiatristsā visitations during the clinic stay, the epicrisis (i.e., the final medical judgment of the case after the patient was released or had died), and the review and reassessment of this empirical material in light of new theories within the qualification works (habilitation theses) of aspiring professors of psychiatry.7
Alzheimerās disease was presented as a nosological puzzle and used as an exploratory category in a specific way: it was left open whether the closer examination of related āpeculiar casesā would give more insights into the pathological process responsible for the development of dementia symptoms in general, or whether these cases only superficially resembled forms of senile dementia and rather constituted a pathologically distinct entity. In other words, the solution to this nosological puzzle would either contribute to a refined histopathological description of senile dementia or to the characterization of Alzheimerās disease as an etiopathologically and prognostically differentiable classification. Kraepelin and Alzheimer did not take preconfigured sides on this issue; rather, they discussed potential in-between nosological positions that Alzheimerās cases could representāfor instance, as atypical forms of senile dementia. Operating with provisional categories opened up room for speculation while remaining circumspect about present conclusions: Kraepelin mused that the occasional early onset could either indicate that the symptoms associated with senile dementia were actually independent from senility or that these patients aged too early. Evidence of a āsenium praecoxā would strengthen the conceptual connection between the pathological process of dementia and its association with aging.
The psychiatrists could operate the triadic structure between clinical symptoms, pathological process, and nosological category as an epistemic machine: if we imagine the three aspects as cogs, in which the teeth of each cogāthe specific symptoms, pathological aberrations, categorical descriptionsāare worked on, are filed and oiled, we can look at how the movement of each cog changes when one of them is altered. Awkward clinical symptoms (cog 1) directed the clinician-histopathologist to look into deceased patientsā brains, where plaques and tangles were identified (cog 2). If such alterations appeared exclusively in a subgroup of patients, clinicians should look for matching differential diagnostic symptoms in living patients (moving cog 1) and revise their provisional taxonomy accordingly (moving cog 3). New categoriesālike that of Alzheimerās diseaseāwere then used to label patients in the clinics, which again provided the empirical basis for testing and refining the specificity and questioned relations between a putative pathological process and the presentation of significant symptoms...