DOI: 10.31038/ASMHS.2022613

Abstract

Depression is one of the mental health conditions identified and projected to be the second leading cause of burden of disease in late life and unfortunately concerns for its debilitating consequences have birthed the need for continuous studies into its etiology, risk factors and management options (WHO, 2017). As the world aged population increases (by 2 billion persons in the next 30 years from 7.7 billion currently to 9.7 billion in 2050), number of older adults aged 65 years and over is projected to proportionately grow by 50% from about 727 million in 2020 to more than 1.5 billion by 2050 (United Nations, 2020) invariably implying that one in six people worldwide will be aged 65 years and over. Averagely, the number of older adults manifesting symptoms of mental disorders such as depression is set to increase proportionately among the estimated population.

The sudden but precipitated increase in incidences of depression across all ages had necessitated the need for constant reviews of mental health disorders. Factors that informed the mental health decisions of community dwelling older adults are hinged on their personal convictions on the presence of the disease and not just another somatic related illness. These convictions are quite germane to the kind of treatment they sought for and could invariably be the major reason why geriatric depression has consistently been misdiagnosed or undertreated very often among community dwelling older adults.

Keywords

Late life depression, Mental health, Burden of disease, Community dwelling older adults

Introduction

Depression is one of the mental health conditions identified and projected to be the second leading cause of burden of disease in late life and unfortunately concerns for its debilitating consequences have birthed the need for continuous studies into its etiology, risk factors and management options across all populations and samples [1]. As the world aged population increases (by 2 billion persons in the next 30 years from 7.7 billion currently to 9.7 billion in 2050), number of older adults aged 65 years and over is projected to proportionately grow by 50% from about 727 million in 2020 to more than 1.5 billion by 2050 [2] invariably implying that one in six people worldwide will be aged 65 years and over. Averagely, the number of older adults manifesting symptoms of mental disorders such as depression is set to increase proportionately among the estimated population. Good news however is that mental health issues in late life has been explored within different population of older adults globally.

Specifically, literature exploring late life depression in community samples and in clinical trials have been widely explored [3-7]. Though comparison in case reports from continents varies as limited number of accounts of depression among older adults in Africa constitute a major setback in reports and management [7]. Despite the disparities in reports and studies conducted all over the world, the goal of research in bridging gaps in findings had been successfully achieved; studies had established the etiology of late life depression, consequences of untreated depression and management options had also been widely appraised. This review will address types of depression relative to older adults, diagnosis and complications of undiagnosed late life depression, the interpretation and assessment of depressive symptoms and experience of depression in some Nigerian communities will also be explored. Publications on the psychological management and implications of culture on the expression of depression in community samples of older adults will also be appraised in relation to their clinical and research implications.

Late Life Depression

Psychological issues have remained an issue met with lots of reluctance and ignorance which older adults are always embarrassed to describe. Presentation of depression in late life which often include insomnia (complaints about difficulties in recall and identification), social withdrawal (lack of interest in social activities and behavioural changes characteristic of hostility (irritability), frequent unexplained falls, hallucination, agitation etc. are often missed for age-related illnesses or somatic complaints [8]. The Diagnostic and Statistical Manual of Mental Disorders (DSM–5), gave a clear description of Major Depressive Disorder (MDD) as: “a manifestation of multiple major depressive fits”. A depressive fit is described in the DSM-5 as mood change characterized by variations in emotions resulting in a continuous manifestation of multiple characteristics of depressive behaviours usually exhibited concurrently for two weeks. Other accompanying symptoms may include daily display of a characteristically low emotional state observed either by the sufferer or observation made by others [9]. Anhedonia, described as an identifiable attention shift from all or from about all activities of choice, spanning throughout the day or on daily basis. Drastic loss or gain of body weight, daily amnesia or hypermnesia [10], daily mental degeneration, daily burnout (feeling stressed), excessive or inappropriate self-attribution of guilt and or cognitive retardation [11].

There must be an accompanying diagnosable distress or discomfort and social withdrawal following the listed symptoms to meet the criteria of the DSM-5. Of the five symptoms, the sufferer must either have a “depressed mood” or totally lose interest in pleasure or social activities. Other symptoms typical of late life depression include somatic complaints, cognitive impairment, persistent anhedonia or loss of pleasure, behavior changes and the pronounced presentation of negative personality traits [12,13]. There has been an age long societal misconception about aging and its accompanying misery. Coincidentally, this reflection has been documented in literature, myths and beliefs of people across diverse communities all over the world [9]. [14] in his argument for the inclusion of counseling sessions in the proper diagnosis and treatment of age related physical and mental illnesses established that many physical manifestations of late life depression could mimic the symptoms of illnesses peculiar with old age making depression diagnosis relatively difficult [10].

Depressive Disorders in Late Life

Major Depression

Major depression, also referred to as depression is a mental health disorder characterized by at least two weeks of consistent negative mood swings observed across the individual’s activities of daily living. It is characterized by poor self-esteem, loss of interest in normally enjoyable activities, fatigue, and bodily ache [15]. There is a close similarity between the DSM-IV-TR [16] criteria for major depression in both old and younger individuals and the DSM-5. Major depression in older adults may be preceded by cognitive impairment that may develop after the onset of depression, this condition is described in [17] as dementia syndrome of depression, because of the obvious cognitive deficits.

Vascular Depression

Vascular depression is the comorbid presence of heart related complications in depressed older adults diagnosed with their first onset of depression [18]. There is the hypothesis that manifestation of late life depression with associating vascular risk factors is complicating to both the sufferer and the clinicians. The risks of misdiagnosis for clinicians are higher, medication interference, and nihilistic attitude from the patient are all compounding for vascular depressive patients [19].

Psychotic Depression

Clinically diagnosed psychotic depression is any form of depression associated with physical characteristics like hallucination, delusions and violent agitation. Psychotic depression is most common in late life; it includes many difficult to treat symptoms like hallucinations, delusions paranoia, and weight loss due to not eating and dehydration due to not drinking [20].

Dysthymia

Late onset of dysthymia in late life have a higher prevalence and comorbid factor of cardiovascular disease but are otherwise similar to older patients with late onset depression [21]. Dysthymia is a psychological disorder with presenting symptoms closely mimicking depression with a repeated occurrence lasting through several days or years. Dysthymia is associated with the risk of the development of major depression in older adults, so-called “double-depression,” and may be particularly treatment resistant [18].

Diagnosis and Complications Late Life Depression

Depression assessment for older adults can be challenging, especially in the physically frail and cognitively impaired. Coexisting medical conditions typical with old age can increase older adult’s susceptibility to depression [22]. Proper assessment to rule out the possibilities of other physical health conditions such as hypothyroidism, alcohol use, incontinence, falls, partial and total stroke, cardiac related issues, drug abuse etc. that may contribute to depression need be done before the major depressive disorder diagnosis [23]. Researchers and caregivers are daily challenged on the choice of assessment techniques, diagnosis and identification of depression pointers. For clinicians working with older adults, identifying the prognostic consequences of comorbid medical illnesses in geriatric depression is essential to management and treatment planning [20]. These accompanying medical illnesses poses great difficulties in diagnosing depression having established the interference of medical conditions overlapping affective disorder symptoms. Clinicians must attain a balance when assessing older adults for depression between assumptions [24] (misunderstanding the psychomotor decline in Parkinson disease for a depressive disorder) and outrightly exclusive (erroneously dismissing an older adult’s mood swings as “understandable” and typical with old age).

Additionally, for the geriatric population, a number of medications are believed to have interactive effect on their emotions and psychological dispositions thereby igniting a depressive disorder. Use of prescribed medications in old age if not religiously taken may have associating consequences [10]. Depression is a state of emotional disequilibrium which can be managed with clinically prescribed antidepressants. Antidepressant use is known to have a higher interference effects with other medications prescribed for use in old age. [25] reported that sampled cases, market survey reports and reflective studies have carefully examined the relative effects of medications like antipsychotics, corticosteroids, endocrine-altering medications, stimulants etc. with late life depression. Other factors hindering proper diagnosis of geriatric depression may include poor and incoherent communication skills in the elderly [24], presence of multiple somatic complaints not well expressed (Isabella & Henrietta, 2008), time constraints during clinical visits among others.

Geriatric depression left untreated or undiagnosed predisposes older adults to chronic effects of the disorder. Complications of untreated geriatric depression identified in literature may include:

Worsening Emotional Well Being

Old age is presumably a time when older adults are assumed to observe lots of fun activities to relieve already suppressed emotions. It is presumed to be a time to reminiscence and relish the accompanying relief of leaving an active phase of life. Unfortunately, aging and its accompanying complexities are not always perfect as assumed. Sporadic turn of events accompanying physical frailty, systemic degeneration, osteoporosis, incontinence etc. are not in totality very tolerable, they tend to weigh heavily on older adult’s psychological disposition [27]. Geriatric depression is a psychological disorder that requires a balance in cognition, attitude and genetic composition. Older adult’s inability to maintain a balanced emotion are at a greater risk of having a depressive episode with its associating risk factors [28].

Suicidal Ideation, Act and Behaviour

Suicide is unarguably the commonest and an extreme psychiatric emergency [29]. The World Health Organization (2000) definition of suicide as a self-attempt to kill and deliberately terminate life initiated and orchestrated by the individual having a full knowledge of the consequences and fatality is just a total summation of the act and its consequence. [30] in their documentation of the incidence and prevalence rates of suicide in the geriatric population presented a figure that is non-comparable with the younger population across most countries. Expressively implying that older adults are at a greater risk of death by self-suicide than the younger population. For every suicide attempted, the margin of those successfully completed is higher in the geriatric population as with a suicide reported in about twelve attempts, four will be effectively completed [31]. In other words, suicide attempts among the geriatric population should be seen as a serious health concern.

Reports on suicide and suicidal attempts in Nigeria taking instances from the stories of an unidentified medical doctor’s suicide on the Third Mainland Bridge in Lagos reported by [32], the story of a final year student of Ladoke Akintola University of Technology, Ogbomosho, with a ‘First Class’ who died of self-poisoning, a woman reported to have been rescued from suicidal attempt on the same mainland bridge who confessed to hearing voices calling her to come to the bridge and jump etc. The disappointing part of these stories which foregrounds the difficulty in tackling depression-induced deaths was the comment of an unnamed friend of the medical doctor whose case seemed to be most recent, about the deceased being very funny and lively [24]. In advanced stage of depression especially in older adults, they cover up with laughter and tend to be extroverted when around people so as to hide deeper psychological ‘injury’. Sadly, this type of comment follows virtually every case of suicide reported in Nigeria, [32]. Psycho-pathologically, in a deeply cultural and religious Nigerian society where awkward death by suicide are never taken as a possible negative response of mental disorders, it is not surprising to see people attributing suicide to witchcraft. While the possibility of such a cause cannot be entirely ruled out due to the deep connection Nigerian society shares with religious rites and the belief in metaphysical powers, the fact that it cannot be scientifically proven makes it unreliable [33].

Interpretation and Assessment of Depression in Some Nigerian Communities

Owing to the diversities in culture and traditions in Nigeria, clinicians and medical professionals have reported ethnic variances in reporting and diagnosing geriatric depression. [34] in his report of the nature and diagnosis of depressive disorders in Nigerian elderly highlighted differences in older adult’s expression of depression based on cultural diversities, religion and social groupings. Over sixty percent of the Nigerian population will readily employ the services of traditional healers before consulting the conventional medical experts. This submission reported by [35] alluded to the general consensus that traditional or alternative medicine is widely perceived as a more affordable and accessible form of health care than the highly overrated conventional medicine. [36] argued the sensitivity of traditional health care services offered by traditionalists like sorcerers, witches, diviners etc. to the human emotional, environmental and spiritual consciousness. Their argument considered in some quarters to have been stretched beyond biological influences of medical practice, has unfortunately remained highly efficient and available in every society till date.

Postulations from the World Health Organization [37] about depression assuming a widespread status of highly acclaimed mental illness by 2020 invariably projecting depression as a fast-rising epidemic. [38] believed that cultural beliefs and societal values will dictate the behavioural trends, individual conceptualization, modes of treatment and pattern of recovery to be adopted by individuals towards depression and its consequences. This supposition is further buttressed by Kessing referenced in [39] whose definition of culture encompasses a cluster of ideas, laws and interpretations underlying human existence and interactions. His definition further expressed a clear understanding of individual’s views of his surroundings, his expression of emotions towards events, occurrences, people around and beyond, towards higher beings, spiritual forces and his ability to maintain an equilibrium. Cultural studies across the world however presents a contrasting opinion on the influence of culture on the expression of depression. In their view, culture can be interpreted and accepted differently, in other words presenting the uniqueness of culture to different people across tribes and settlements. For instance, depressive mood in a community context in Nigeria is often ascribed to contravention of cultural interdictions, spiritual truculence, evil machinations, intrusion of objects, afflictions by god/sorcery, spiritual/religious influence, family retribution, cultural traditional abuse, consequences of disobedience to traditional beliefs [36]. Community dwelling older adults may be limited in their need to seek help for mental health conditions that seemingly defy ordinary reasoning. There are however alternative traditional means employed over time and documented in literature to be traditionally effective in managing mental health related issues some of which are use of purgatives, making bodily incision, offering sacrifices/appeasing the Gods, fasting and prayers, organizing deliverance sessions, performing exorcisms etc. Comparatively, [40] reported that African traditionalists will report symptoms of geriatric depression as gloominess, head/lead formication, neuralgic sensations, bloating etc. Contrary to these beleifs, depressive symptoms as listed in [41] are indicative of consistent emotional roller-coaster, disappointment, loss of self-esteem and boredom.

Late Life Depression Management

The disadvantage for adults diagnosed with depression might have been considered enormous due to conflicts in diagnoses, identification, management and treatment. Advocacy for proper management and treatment plans for depression implores clinicians to take into cognizance the patient’s treatment of choice, anecdotal records, entry data, mental and physical health status in relation to age and socio-economic status. Before initiating diagnosis, it behoves of clinicians to investigate patient’s reactions to treatment models available and put into consideration their fear of medication and treatment reaction. Older adults need to be reassured about their worries of drug dependence and addiction. Contrary to the general misconceptions, antidepressants are not inhibitors. Obvious emotional reactions to a loss of a significant other, to poverty and wants cannot be suppressed by antidepressant or medication use [42]. Concerns and issues relating to depression management can be resolved successfully by a thorough and not selective listening, awareness and regular reassurance.

Available evidences indicated that geriatric depression can be effectively managed in and out of a clinical environment with psychotherapies, pharmacotherapies, electroconvulsive therapy (ECT) or more effectively psychotherapies can be combined with pharmacotherapies for enhanced results [43,44]. A general specification employed by geriatric psychiatrists globally proposed the use of the combination of drugs (antidepressants) with psychological interventions (CBT, reminiscence therapy, interpersonal therapy etc.) for effective outcome of a reduced depression [45]. There was an initial classification of antidepressant use as a standalone treatment regimen considered as another management option for depression [10]. Electroconvulsive therapy became another relative management option for chronic depressive disorders in the event of antidepressant use and psychotherapeutic failure or on occasion of the presence of suicidal intentions or life-threatening medical comorbidities. Psychotherapy is a talking treatment between the psychotherapist and a client i.e. the depressed individual. However, the topic and the treatment plan depend on the type of therapy being utilized.

Pharmacotherapy

In Nigeria, over twenty antidepressants (depression induced medications) have been authorized and certified safe by the National Agency for Food, Drug Administration and Control (NAFDAC) for depression in the elderly [46]. Antidepressants had been the official prescription for depression in most health facilities in Nigeria. Its wider acceptability is not void of complaints of side effects like excessive weight gain, dizzy spells, bowel irritation, anxiety etc. Although complaints of complications from the use of antidepressants in old age have been received in various quarters, complications of medications for geriatric depression treatment can be fueled by different factors which include multifarious use of medications more than the younger population, increased potential interactions of multiple prescriptions and age [47].

Electroconvulsive Therapy

The efficacy of the electroconvulsive therapy in a number of controlled studies on late life depression have been expressed in a percentage range of 60-80% [43,45]. Electroconvulsive therapy is a psychological intervention that involves the passage of tiny voltage of electric current through to the brain triggering a short but reflexive seizure, the procedure is generally done under anesthesia. ECT is selectively suggested for patients with diagnosable resistant depression whose cases is considered a risk to self and people around. It is a form of psychotherapy that involves a complete alteration of the brain composition causing an immediate reverse of depressive symptoms. Treatment duration is usually between six to twelve weeks of hospital stay which in most cases is in a psychiatric facility. ECT intervention is not totally free of treatment side-effects, patients record complaints of mild to severe headache, delusion, temporary amnesia all of which persists for few days and responds to analgesics and corresponding medications. In severe cases of side effects, mortality rates for the utilization of ECT is minus 1% death in 10,000 depressed patients treated putting the ratio at 1:10 [43]. Experts thus advise that following each session of ECT, a maintenance medication should immediately be commenced to avert and put in check consequent relapse.

Psychotherapy

The talking treatment as it is referred to in some climes, psychotherapy is the process of engaging in an in-depth discussion (sessions) with a patient referred to as client to obtain facts and information regarding his current emotional state. Studies on depression in both young and older populations have established the effectiveness of psychotherapies as a treatment regimen. Its efficacy in resolving psychological disorders have established its empirical relevance across cultures [24]. Cognitive behavioral therapy, interpersonal psychotherapy, cognitive reminiscence therapy, problem-solving therapy are few empirically supported psychotherapies effective for managing geriatric depression. Other evidence-based therapies established to be adequately effective but not extensively explored for the management of geriatric depression carefully considering cognitive challenges, cardiac implications, limitations in function and physical illness in old age include supportive therapy, laughter therapy, psychodrama, music therapy, dance and movement therapy, humor therapy etc. Psychotherapies are structured discussion between a professional trained in the act and a client, psychotherapeutic sessions are usually between six to twelve sessions delivered within a period of six to eight weeks. Comparisons in the effectiveness of psychotherapies and pharmacotherapy cannot be effectively established in literature as about 45%-70% patients who underwent a therapeutic session recorded success rate that is quite similar to statistics observed across patients treated with antidepressants [48].

Conclusion

The sudden but precipitated increase in incidences of depression across all ages had necessitated the need for constant reviews of mental health disorders. Factors that informed the mental health decisions of community dwelling older adults are hinged on their personal convictions on the presence of the disease and not just another somatic related illness. These convictions are quite germane to the kind of treatment they sought for and could invariably be the major reason why geriatric depression has consistently been misdiagnosed or undertreated very often among community dwelling older adults. There is a constant basis for disagreement between mental health professionals, medical experts and psychotherapists alike on the construction of experience of depression especially by rural community dwellers. This is particularly relevant in Nigeria especially in communities surrounded with diverse cultures and beliefs confirming the age long belief in herbal mixtures and concussion, which seems to be appealing and realistic enough to be accepted as the immediate choice of health care. More studies exploring assessment, diagnosis and management of late life depression in rural community samples of older adults are therefore necessary to further establish their needs.

Acknowledgments

The author will like to acknowledge the University of Ibadan for the resources

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DOI: 10.31038/ASMHS.2022612

Abstract

Even though French sociology has long been interested in Alzheimer’s disease, most studies have been carried out “for” or “in support of” disease treatment, with the aim of analyzing the impact of the disease on the life of patients. This article offers some elements for the sociological study “of” Alzheimer’s disease. Based on a literature analysis centered on the information file on Alzheimer’s disease published by INSERM and on scientific articles and communications addressing the etiology of the disease, this paper aims to show how the entity “Alzheimer’s disease” is constructed today. After examining the way the figures on the disease have been produced, it will show how the etiology is constituted by advances in “diagnostic techniques” and research protocols.

Keywords

Sociologie, Alzheimer, Étiologie, Sociology, Alzheimer, Etiology

Introduction

It is now nearly 30 years since the first studies on Alzheimer’s disease referring to sociology or drawing from its methods were published. Apart from the work of [1], these first articles were often written by doctors working in the field of gerontology and public health [2,3], using methodologies (i.e. focus groups) derived from the social sciences. They focused, among other things, on the way in which the disease impacts the patient’s life course and his/her social network and the way in which he/she learns to cope with the illness. In France, the first sociological publications dealing specifically with Alzheimer’s disease date from the early 2000s [4,5]. After the disease was placed on the political agenda following the 2001 Girard report [6] and with incentives being given to conduct multi- or even inter-disciplinary research, numerous research projects have developed in sociology on the “big issues” model, reflecting the influence of the Anglo-Saxon model on the world of French research.

To obtain funding, sociologists have thus been invited to submit proposals to calls from large associations such as Médéric Alzheimer or France Alzheimer or from public funders such as the Caisse Nationale de Solidarité à l’Autonomie (CNSA – National Solidarity Fund for Autonomy) and the Fondation de Coopération Scientifique pour le plan Alzheimer (Foundation for Scientific Cooperation for the Alzheimer Plan). They have also taken part in programmes led by biomedical science or clinical research laboratories. Patient associations have been largely instrumental in ensuring that research should not confine itself to providing medical answers but should also answer the specific social needs of patients. The third (2004-2007) and fourth (2008-2012) Alzheimer Plan resulted in calls for even more inter-disciplinary research.

In such context, French sociological research has mostly been working “for” or “in support” of disease treatment, rather than dealing with the sociological study “of” the disease : while sociological work “in support” of Alzheimer’s disease treatment mainly aims to shed light on the experience of the patient (which is often little understood by medical professionals), sociology “of” the disease needs to examine the historical, social and scientific construction of what is called Alzheimer’s disease. Despite their theoretical and methodological differences, the former studies shared the common objective of furthering understanding of the disease. They have challenged strictly medical interpretations by showing, among other things, the way in which social context and social status (gender, age, family or professional status) have an impact on the announcement and reception of diagnosis and on adherence to treatment, and, more broadly, on the strategies devised by patients and their relatives to cope with their conditions. They have also shed light on the experience of caretakers and patients which had hitherto been overlooked areas of study [7]. This type of sociological work could also be described as sociological studies of sickness or illness, with “sickness” referring to the social role of sick people as defined by their relatives and professional colleagues and “illness” to the subjective experience of patients.

This paper, on the other hand, undertakes a sociological analysis of Alzheimer’s disease in the sense that it aims to question the way “Alzheimer’s disease” – a disease with biological and/or clinical specificities – has been constituted. Its approach is inspired by the sociology of science approach taken by [8] and Lock [9]. Based on the idea that “the facts of science are made, constructed, modeled and refined to produce data and a stable meaning” [8] p. 182) and that the sociologist’s role is to describe and decode them (Pestre, Ibid), I wish here to examine a few elements related to the etiology of the disease. In order to do so, I use the information file on Alzheimer’s disease published by the Institut National de la Santé et de la Recherche Médicale (INSERM- National Institute of Health and Medical Research). This file synthetizes the scientific knowledge on the disease and is mainly, though not exclusively, based on French research. As it is produced by the leading health research centre in France and signed by prominent French specialists in the field, it qualifies as scientific authority [10]. The aim of this paper is to examine the information presented in this report using scientific publications and presentations and show what data and hypotheses it rests on. I will first take a look at the figures (the prevalence) of the disease and the links with age. This will shed light on the way the figures have been “constructed” and suggest the way age has been used as one of the “explanatory” factors of the disease. Then I will discuss the issues raised, among other things, by advances in “diagnostic techniques” as to the etiology of the disease. Finally, I will suggest that some of the methodological limitations in the clinical investigation of sporadic forms result in the development of scientific protocols that ultimately reinforce the idea of biological and genetic causality.

Age and the Number of Patients

Age is very often used in the literature on Alzheimer’s disease to account for the prevalence of the disease among different age groups as well as to generate hypotheses as to its etiology.

Estimated Prevalence of the Disease by Age

After a short introduction, the section “understanding the disease” in the INSERM file opens with the following paragraph:

Rare before the age of 65, Alzheimer’s disease begins with loss memory, followed over the years by more general and disabling cognitive disorders (…) After 65, the incidence rate of the disease rises from 2 to 4% of the general population. It rises rapidly to reach 15% of the population at age 80. About 900,000 people suffer from Alzheimer’s disease in France today. The number should reach 1, 3 million in 2020, given the increase in life expectancy.

It should first be observed that there are no explanations given for the two age limits chosen – 65 and 80 – which merely seem to refer to the distinction that is commonly made in everyday language between senior citizens and elderly dependents. Age is only considered here in a chronological way. This understanding of age thus seems to derive from convention rather than scientific results or hypotheses about biological deterioration or the effects of social or psychological aging.

As for prevalence, the reading of scientific papers helps trace the way the figures have been established. The most widely cited paper [11] (i.e. cited about 150 times) estimated the proportion of sick people to be 17,8% among people aged 75 or more in 2003, which amounted to 769,000 people. A later, also much cited (47 times), paper [12] indicated that there were about 850,000 cases of Alzheimer’s disease and related syndromes at the time. To support these figures, the second paper referred to the same source as the first one, a survey entitled Personne âgée quid (Paquid). This population-based cohort study, initiated in 1988, targeted 3,777 people aged 65 or more in towns and villages of the Gironde and Dordogne departments and consisted in an epidemiological study of cognitive and functional aging. Dementia and its level of severity were measured using a clinical test, the Mini Mental State (MMS). The number of sick people given by the Paquid survey was then estimated through a projection by age to the general population. The 900,000 cases announced in the INSERM report thus do not correspond to diagnosed cases – I will come back to the meaning of this term below – but to estimates based on a clinical test carried out on a limited sample as pointed out by [13].

Population and Diagnostic Differences Behind Age

As Ankri pointed out, the epidemiological studies giving the incidence and prevalence rates of the disease by age present strong methodological limitations. Apart from the fact that it is difficult to constitute representative samples, they are based on very different patient populations. Ankri explains that the estimated rates often result from the collection of data from surveys of populations affected by very different physio-pathological types of dementia. Moreover, the diagnoses and measurement tools differ depending on the protocols used:

Estimates are most frequently based on nonrepresentative samples and case identification procedures vary with the evolution of diagnostic criteria and the availability of imaging or biological markers. Moreover, whether studies of mild or severe forms of dementia or residents of institutions are included or not can have a strong impact on the results (Ankri, op.cit. p. 458)

While age groups are considered as uniform categories, they include people suffering from different degrees and sometimes even types of dementia. Under chronological age are subsumed different cases, as if people from the same age group were “medically comparable” even though there can be a great number of different risk factors associated to different types of dementia (vascular, Lewy Body, Alzheimer). Moreover, from a methodological point of view, the motivations for taking part (or refusing to take part) in a survey are known to be diverse and to have an impact on the results of clinical tests. When age – merely viewed in its chronological aspect – is used to constitute groupings, researchers lose sight of its social dimension and of its potential influence on the data collected.

Age: A Mere Variable or a Risk Factor?

When these epidemiological data are used, chronological age is considered as a risk factor since incidence rate seems to increase with age. In statistical terms, age even appears to be the main risk factor. Let us look more closely at the findings of epidemiology [14]. The works based on cohort analysis confirm that age is the main risk factor and add that incidence doubles “practically for every five-year age group after 65” (Ibid., p. 738). They also confirm that the incidence rate is higher among women, while indicating that “In the Paquid survey, the incidence of Alzheimer’s disease was higher among men than women before 80, whereas the reverse was true after 80” (Ibid., p. 739). The difference between men and women is accounted for in the following way:

Life expectancy, which is higher for women than men, might explain the results, assuming that men, with increased longevity, are more resistant to neurodegenerative diseases. It can be observed that in some countries like the United States where the gap between life expectancy for men and women is smaller, there is no gender difference in the incidence of Alzheimer’s disease. (Ibid., p. 739)

This is a classical hypothesis in longevity research, which suggests that the selection effect might be stronger for men and that, as a result only the most physically and cognitively strong might reach advanced age [15].

Moreover, interpreting these age-related findings is a complex task because a risk factor means a notable frequency of simultaneous occurrence of two variables, here age and a negative result in a clinical and/or neuropsychological test like the MMS. The risk factor is measured for a population but implies no causality at the individual level. In order to interpret this correlation as causality, other aspects of age must be considered beside its mere chronological reality.

Age as a Cause of the Disease?

Since the literature on Alzheimer’s disease is mostly based on medical and biological research, age is viewed from a physiological point of view. The passage of time is considered as responsible for physiological wear and tear and biogenetic damage and alterations of the human body and brain. It is believed, then, that alterations multiply with age, which is why the prevalence of dementia is understood to increase with chronological age. According to some researchers [16], most of the clinical studies that have investigated the cognitive capacities of centenarians have concluded that 50 to 75% of them suffered from “cognitive impairments”. Although they are a rapidly growing population, centenarians have so far rarely been considered as subjects for the study of Alzheimer’s disease. There are many reasons for this. First, they are considered to be statistically too few in number and to have too short a life expectancy for cohort analysis, and, second, they seem difficult to study. [13] drew the following conclusion:

Finally, because of the increase of prevalence and incidence with age, another source of uncertainty lies in the low representation of the very elderly (over 90 years old) in epidemiological studies, which makes estimation of prevalence and incidence at the most advanced ages uncertain. (…) the lack of data about the very elderly leaves two questions open: either there is an exponential increase of incidence in dementia with age, which means for some that it is an aging-related phenomenon rather than a disease; or the decrease of incidence beyond a certain age, after quasi-exponential growth, shows that it is rather an age-related disease.

The quasi-linear increase of dementia prevalence with age remains a major focus of reflection since it raises questions about the very essence of what is called “Alzheimer’s disease”. According to some researchers [17], what is called Alzheimer’s disease is not in fact a disease (i.e. a clearly defined pathology with a proven etiology), but rather a syndrome, i.e. a set of more or less unified symptoms grouped under the same generic term. These symptoms might then simply be an effect of senescence and manifest themselves with great interindividual variety. This hypothesis stands all the more if the diagnosis – and the subsequent labelling process [18] – rests on clinical tests in which failure is correlated with senescence. As [19], this hypothesis questions the social and political construction of the disease, which is based on a distinction between Alzheimer’s disease, senility and senescence.

In such context, diagnosis is a crucial stage to distinguish between “Alzheimer’s disease” and other possible causes of dementia. Yet diagnostic procedures are intrinsically linked to the etiology of the disease: they depend one on the other.

The Etiology and Diagnosis of the Disease

To understand “diagnostic procedures” and the etiological issues they raise, it is useful to trace the history of the way the disease was defined.

Senile or Presenile Dementia?

One of the oldest and most famous debates about the etiology of Alzheimer’s disease also has to do with the link between age and disease. In his history of Alzheimer’s disease, [20] charts the process of construction of what is called “Alzheimer’s disease” and points out that it was first considered as “presenile dementia”. There were many reasons for this. Continuing the work of Aloïs Alzheimer on the “first patient” Auguste D, Perusini observed correspondences as well as morphological (cerebral modifications) and symptomatic differences with senile dementia. Yet this is not what really motivated the distinction. Berrios (1989, quoted by Gzil. Op. cit.) points out that the anatomopathological features (amyloid plaques and neurofibrillary tangles) that Aloïs Alzheimer considered to be possible specificities had already been identified by Ficher and that he considered them to be relatively frequent occurrences in dementia in elderly people. He therefore proposed the name of “presbyophrenic dementia” for all types of senile and presenile dementia in which plaques and sometimes fibrillary alterations could be observed. The reasons why Alzheimer’s disease was distinguished from senile dementia lie first in the fact that Aloïs Alzheimer had no occasion to conduct histological examinations of elderly patients (as he himself recognized). Another reason was the then popular conception of mental illness, inherited from Kahlnaum (Krepelin’s mentor, Krepelin being himself Alzheimer’s mentor), according to which there were specific diseases for every stage of life. As Gzil points out, in the 19th century, many psychiatrists believed that mental disease was related to age.

The table presented by [20] listing the cases of Alzheimer’s disease published between 1907 and 1914 can provide further insights. The table lists 22 cases, with the youngest patient having been diagnosed at 32 and the oldest at 63. The average age at diagnosis was 57 and, apart from 3 cases, they were all diagnosed after 48. Today most of these people would be considered as young patients, but what did these ages mean in the early 19th century in biological, demographic and social terms? In demographic terms, with life expectancy at birth being about 50 at the time, it is debatable whether these patients could be described as young. If the average age at diagnosis were 7 years higher than life expectancy at birth today, it would be 87. Would the people diagnosed at that age be considered as young patients? Moreover, biologically (wear and tear) and sociologically (status and role in society) speaking, were these people young? It is quite difficult to answer this question, which in turn raises the issue of how to define old age [21].

Whether Alzheimer’s disease is a form of senile or presenile dementia was not decided on the basis of age but of the anatomopathological features of the disease. While clinicians believed there were two separate diseases, at the end of the 1960s, anatomopathologists justified the “merging” of the two on account of their biological manifestations. [19] showed that community and pharmaceutical lobbying also supported this classification under a single label. Today, the only age-related distinction is based on genetic arguments and establishes a separation between autosomal (genetic) and sporadic forms.

Biological Markers: The Causes of the Disease?

The features that Aloïs Alzheimer identified in Auguste D (and Fischer in other patients), i.e. amyloid plaques and neurofibrillary degeneration, are still considered today as the hallmarks of Alzheimer’s disease. The INSERM file indicates that:

Study of the brains of patients with Alzheimer’s disease shows the presence of two types of lesions which make diagnosis of Alzheimer’s disease a certainty: amyloid plaques and neurofibrillary degeneration.

It is important to insist on the fact that these biological features are what makes diagnosis certain because diagnosing the disease is not an easy task as Pr. Philippe Amouvel, one of the French experts of the disease, explained: “Today, we are used to referring to any memory disorder as Alzheimer’s disease while in reality, it takes a very long, very complex work to make a diagnosis” [22]. While in Aloïs Alzheimer’s time, such “alterations” (amyloid plaques and neurofibrillary tangles) could only be identified post mortem, new medical techniques have been developed in order to trace the lesions at the root of cognitive disorders that can then be identified through the use of clinical tests. Two main types of “diagnostic techniques” can be distinguished: the identification of biological and/or genetic markers thanks to lumbar puncture and medical imaging. These examinations are performed on living subjects, either subjects experiencing clinically assessed health problems, or healthy subjects being tested for research purposes. As underlined by some publications [23], the possibilities offered by these technical advances have reinforced a biological understanding of the disease, in which biomarkers are considered both as signs and causes of the disease. This so-called improvement in diagnosis certainty actually results in enhancing the biological aspects of “Alzheimer’s disease” and supporting an etiology based on the “amyloid cascade” hypothesis. This hypothesis posits that the deposition of amyloid-beta peptide in the brain leads to brain disorders. Although this hypothesis is sometimes debated [24], the causal process it describes constitutes the focus of most of the research today. The INSERM file specifies that:

Amyloid beta protein, naturally present in the brain, accumulates over the years under the influence of various genetic and environmental factors, until it forms amyloid plaques (also called “senile plaques”). According to the “amyloid cascade” hypothesis, it would seem that the accumulation of this amyloid peptide induces toxicity in nerve cells, resulting in increased phosphorylation. (…) Hyperphosphorylation of tau protein leads to a disorganization of neuron structure and so-called “neurofibrillary” degeneration which will itself lead, in the long run, to the death of the nerve cell.

While a few years ago, diagnosis was based on the clinical signs of the disease, today clinical-biological criteria are used, leading to an ATN classification system. The deposition of amyloids (A), Tau protein (T) and Neurodegeneration (N) (cerebral modifications) are considered as both biomarkers and causes of the disease. Medical neuroimaging (magnetic resonance imaging and positron emission tomography) makes it possible to visualize cerebral atrophies and hypometabolism which are considered as signs of neuronal and synaptic dysfunction [25].

From a clinical point of view, it is important to detect the biomarkers at an early stage in order to identify “the people who have these biomarkers and are worried about their memory and to offer them, long before they decline, long before they enter the clinical disease stage, strategies to avoid cognitive decline” (Dr. Audrey Gabelle, Pr. of neurology and neuroscience, University of Montpellier, 01/04/2021).

Biological Lesions and Clinical Disorders: An Etiological Paradox?

The significance of early detection rests on the theory that there is a prodromal stage of Alzheimer’s disease in which biological signs are present in the brains of the “patients” even though they do not experience any problem or present any clinically identifiable symptom. Yet some studies have suggested that there is no such clear link between biomarkers and clinically assessed disorders:

Several studies have shown that the extent of neuropathological changes and the degree of cognitive impairment were poorly related in the very elderly. In examinations conducted on centenarians it has been shown that several subjects did not present any cognitive impairment despite extensive neuropathological abnormalities and conversely, that several subjects who presented significant cognitive impairment did not have neuropathological abnormalities. In this context, even beyond the issue of correct interpretation of the epidemiological data, some have raised the conceptual question of whether dementia should be considered as an age-related phenomenon (generally occurring around a specific age) or a normal consequence of aging [26].

On this point, the “Nun Study” sparked considerable discussion in the scientific literature, especially the case of Sister Mary [27]. The study was based on a population of 678 nuns aged from 75 to 103. It focused on nuns in order to better control the environmental (social status) and behavioral (tobacco and alcohol consumption) factors that can have an impact on cognitive impairment. Sister Mary died at 101. Until her death, she had had high scores in cognitive tests and appeared to be “cognitively intact”. Yet the autopsy (the currently used “diagnostic techniques” were not as advanced then as they are now) of her brain revealed large numbers of neurofibrillary tangles and amyloid plaques. Sister Mary is not, in fact, an isolated case. Several studies based on post mortem anatomopathological data have shown that in a significant number of cases, there is no link between the presence or absence of amyloid plaques and neurofibrillary degeneration and the presence or absence of cognitive disorders. The study conducted by Zekri et al. (2005) on 209 autopsied subjects (100 demented and 109 non-demented subjects) indicated that “even more surprising were the observations made in 109 non-demented subjects: in 33% of the cases, the density of neurofibrillary degeneration of the isocortex was equivalent to that of demented subjects” (p. 253). In this study, the brains of 1/3 of the subjects with no clinical sign of dementia had the same biophysiological markers as those of subjects with Alzheimer’s disease.

While the idea that there is a pre-symptomatic stage of the disease has been challenged by these studies, on account of the mismatch between the number of lesions and the presence of cognitive disorder, some suggest that this paradox might be explained through the notions of brain plasticity and cognitive reserve. They believe that some brains have the ability to offset or stave off lesions and continue to function “in a normal way”.

Towards a “Geneticization” of Alzheimer’s Disease?

Another explanation is also used to account for this paradox, whose effect is to redefine the etiology and reinforce the idea that the disease might have genetic origins.

Genetic Causes for the Appearance of Biological Lesions?

In their analysis of the origins of Alzheimer’s disease, some researchers [28] underline the fact that while there is no correlation between the presence of amyloid peptide and the existence of symptoms, the symptoms are correlated with neuronal death which they believe is caused by an abnormal amount of Tau protein. This leads to a rather different causal pattern. In this perspective, genetic factors – particularly the APOE gene [29] – and environmental factors are believed to be responsible for the amyloid cascade and the abnormal production of amyloid peptide affecting Tau protein and leading to neuronal death. This gives rise to a much clearer causal pattern with the following successive, rather than concomitant, stages: genetic (and environmental) factors à amyloid à Tau à neuronal death à clinical symptoms. It should be said that this causal pattern is causing debate among researchers for several reasons. First, some studies [30] point out that the causal succession of amyloid plaques and Tau phosphorylation must be reexamined since Tau protein can appear before the plaques do. Moreover, accumulated Tau protein can also be found in “the brains of elderly and cognitively healthy subjects but in relatively moderate quantities” (Wallon, op. cit). Yet these observations do not call into question the idea that there is a pre-symptomatic stage during which the disease develops in invisible ways. There have been much cited hypotheses and models [31] to describe this development process but researchers do not have sufficient longitudinal data to confirm them yet.

From Genetic Models to Sporadic Forms

Faced with this methodological problem which makes it difficult to confirm or refute the hypotheses and models being discussed, some researchers have turned to genetic models. The first genetic model is based on autosomal Alzheimer’s disease. According to the INSERM file: “Hereditary forms of Alzheimer’s disease account for 1,5% to 2% of the cases. They almost always occur before 65, often around 45 years old. In half of the cases, rare mutations have been identified as the root of the disease”. Researchers have been able to follow the evolution of the disease in these patients carrying a rare genetic marker causing the development of lesions (amyloid and Tau), leading them to think that the pathology might begin 15 years before the clinical signs appear. On this basis, the genetic forms of the disease have been considered as a model to approach sporadic forms. Yet this approach can be questioned since in the general population, 50% of the study subjects with biomarkers (amyloid and Tau) of the disease did not develop any symptom over a ten years’ period [32].

The other genetic model used is an animal model. Several studies of Alzheimer’s disease, including those which gave rise to the amyloid cascade hypothesis [33], are based on in vitro experiments conducted on the brains of mice or other marsupials such as mouse lemurs. They rely on the assumption that the results obtained from mouse brains can be “transferred” to the human brain. Yet comparing the two is by no means easy since mice do not “naturally” develop Alzheimer’s disease as it is today defined and it is debatable whether clinical tests performed on animals can be assimilated to those used to make a diagnosis on human subjects. The mice used in laboratories are “models”, i.e. they have been genetically modified so as to develop Alzheimer’s disease. The studies in immunotherapy carried out by [34] made this point very clear. The mice used, APPswe/PS1ΔE9 models, overexpressed mutated forms of the human APP gene and the human PSEN1 gene and were compared to so-called “wild-type” mice from the Jackson Laboratory.

In addition to the fact that this model appears to be far removed from the reality of sporadic Alzheimer’s disease, it is also questionable whether its results can be used because it completely overlooks “environmental” risk factors in order to promote an exclusively genetic explanation. The limitations inherent in investigations of human and sporadic forms of the disease thus result in the construction of models which are based on comparison and end up eliminating one of the factors that was initially considered as responsible for the disease. This paper suggests that the development of such models is to be understood within a broader movement towards defining the elderly as biologically specific individuals.

Conclusion

Through analysis of the etiological construction of Alzheimer’s disease, this paper provides some insights for a sociological study of Alzheimer’s disease, following previous work in anthropology [35] and sociological studies of other biomedical subjects such as procreation [36]. This approach reveals that natural sciences – however hard they may be considered to be – also construct their research subjects on the basis of technical advances and out of the necessity of bypassing existing methodological obstacles.

This paper has shown that the way age is understood and used in research on Alzheimer’s disease can result in shortcuts, whereby statistical correlations are transformed into causal links, and in classification of the patients into falsely unifying categories. It has also questioned the boundaries between early dementia, late dementia and senescence by showing that the difficult interpretation of chronological age and the almost total lack of data about certain age groups are barriers to reflection and raise questions as to the very nature of what we call “Alzheimer’s disease”.

The medicalization of society which has long been observed by health sociologists is today compounded, in the case of Alzheimer’s disease (but not only), by increasingly biological [37] and genetic interpretations of the human being. Yet, while study of the biomarkers triggering amyloid cascade can yield helpful results, this line of research needs to be carefully scrutinized just as research seeking to identify prognostic biomarkers for psychiatric disorder in children has been [38]. Individuals in the asymptomatic phase are not, clinically speaking, sick. The desire to prevent development of the disease should not blind researchers to the possible social and human consequences. Similarly, advances in genetics should not cause unquestioning acceptance of genomic medicine [39-42] and its probabilistic interpretations of individual fates. I believe that, even before looking at the possible social and political effects of biomedical paradigms and practices on society and individuals, a sociology of Alzheimer’s disease should focus its attention on the research being conducted and show its historicity, constructions and controversial issues as a way to shed light on the modern forms of biopower. Yet, this type of work doesn’t appear to be in line with funders’ and research institutes’ demand for interdisciplinary research. Multi-disciplinary research, which means looking at the same subject from different points of view based on specific epistemological principles, certainly needs to be pursued; on the other hand, inter-disciplinary research, which means orienting different types of disciplinary research towards the same direction, appears to me to be highly counter-productive while trans-disciplinarity (which blurs or erases historical and epistemological differences between disciplines) can be considered as dystopian.

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