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The Earlier the Better: Alzheimer’s Prevention, Early Detection, and the Quest for Pharmacological Interventions

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Abstract

Although the risk factors, biomarkers, and medications for Alzheimer’s disease appear to be almost identical in 1993 and 2013, profound changes can de detected throughout this time period. This article maps these recent changes in the conceptualization of Alzheimer’s disease, especially the emerging trend toward prevention. While some preventive practices (e.g., brain training) and the search for early signs and biomarkers (such as APOEε4) have existed for a long time, the recent broadening of scope to include cardiovascular risk factors and their prevention, paired with pre-symptomatic detection of disease-specific biomarkers, has considerably impacted the conventional understanding of this syndrome and the possibilities for pharmacological and non-pharmacological interventions. The rationale for emphasizing multiple logics when explaining these changes is to avoid simplified argumentative pathways that exist among some scientists.

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Notes

  1. The Economist (2013, p. 13) recently published an article on “How science goes wrong,” stating that “modern scientists are doing too much trusting and not enough verifying… Last year researchers … found they could reproduce just six of 53 ‘landmark’ studies in cancer research… In 2000–2010 roughly 80,000 patients took part in clinical trials based on research that was later retracted because of mistakes or improprieties.”

  2. An example from the domain of Alzheimer’s research: The side effects of the traditional antipsychotic medications were the main reason for the marketing of the newer, pricier atypical antipsychotics. The latter, however, have also recently come under attack, because atypical anti-psychotics have “their ‘own’ adverse effects” (Van Melick 2004). “Ironically,” psychiatrists Peter Rabins and Constantine Lyketsos note (2005: 1964; emphasis added), “it was only because pharmaceutical companies were seeking an expansion of approved indications for antipsychotic drug use in dementia… that the risks came to widespread attention.” In addition, a recent study found that atypical antipsychotics are no more effective than certain older ones (Lieberman et al. 2005).

  3. In 1940, McMenemey (p. 232, quoted in Berchtold and Cotman 1998, p. 182) wrote: “That the pathological changes in this disease are not specific is generally agreed… Nevertheless, the presence of abundant plaques and neurofibrillary alterations together with extensive atrophy of the neurons is found only in Alzheimer’s disease and senile dementia” (emphasis added).

  4. As a comparison, Noel-Starr et al. (2013) describe the current landscape of dementia research as tightly linked to biomarkers, which need to get detected before the actual diagnosis of dementia: “The first category was the markers of brain β-amyloid (Aβ) deposition, such as low cerebrospinal fluid (CSF) Aβ42 levels and positive positron emission tomography (PET) imaging results using Aβ ligands. (…) The three major biomarkers in this [second] category included elevated CSF tau levels, decreased 18F-fluorodeoxyglucose (FDG) uptake on PET in the temporoparietal cortex, and disproportionate atrophy on structural magnetic resonance imaging (MRI) in the medial, basal, and lateral temporal lobe as well as medial parietal cortex. These biomarkers were also postulated to be useful for the diagnosis of mild cognitive impairment (MCI) caused by AD and the prodromal stages of AD” (p. e97, emphasis added).

  5. Alzheimer medications are also used as so-called smart-drugs in cognitively healthy individuals (see for example Mehlman 2004).

  6. Since this article refers to a long history in which the concept “Alzheimer’s disease” has changed a number of times, a short summary is included here: 1. Alois Alzheimer described in 1906 (Alzheimer 1907) the early-onset form, which Kraepelin coined Alzheimer’s disease (1910). Parallel to this, there existed the late-onset form, which was generally described as arteriosclerose. 2. Arteriosclerose then became vascular dementia in the 1970s, and infarcts in the brain (small AVCs), together with the “hardening of the arteries” were seen as the etiology. 3. Roth et al. in the late 1960s established the correlation between tau tangles and amyloid plaques as the main biomarkers of AD. 4. Katzman (1976) (and Butler who accepted this when he became the first director of the newly founded NIA, the National Institute of Aging) “unified” early-onset and late-onset dementia as Alzheimer’s disease, arguing that both are based on the same pathological pathway, while vascular dementia existed as a less important category parallel to AD. 5. Today, vascular dementia and AD are increasingly overlapping under the name of “Alzheimer’s disease” (or dementia), therefore, allowing a cardiovascular logic and prevention based on lifestyle (diet, exercise, etc.) that was previously almost exclusively linked to vascular dementia.

  7. The Dubois criteria establish that people who are cognitively normal but have a positive brain amyloid PET scan or an AD-like signature in their cerebrospinal fluid (CSF) would be viewed as being asymptomatic at risk for AD. Asymptomatic people who are known to get AD in the future because they carry a rare autosomal-dominant AD mutation are labeled as having “presymptomatic AD.” Further, those who show the typical symptoms of dementia, but not the typical biomarkers, would get a diagnosis of “prodromal AD” (see Fagan and Strobel 2011 for the distinction between these two diagnostic criteria sets).

  8. The American Heart Association and the American College of Cardiology have just released new cardiovascular prevention guidelines, in which statins play a major role: “Cholesterol-lowering statin drugs should now be prescribed to an estimated 33 million Americans without cardiovascular disease who have a 7.5 % or higher risk for a heart attack or stroke within the next 10 years.” In 2002, the federal cholesterol guideline recommended that people should only take statins if their 10-year risk level was higher than 20 percent for heart disease (stroke was not mentioned) (see American Heart Association 2013).

  9. Peter Whitehouse and Daniel George’s argument is, of course, more sophisticated. It is the general idea of non-existence that gets transmitted through such a choice of words that seems problematic to me. I have discussed this point on several occasions with Peter.

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    Annette Leibing

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Leibing, A. The Earlier the Better: Alzheimer’s Prevention, Early Detection, and the Quest for Pharmacological Interventions. Cult Med Psychiatry 38, 217–236 (2014). https://doi.org/10.1007/s11013-014-9370-2

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