Like so many people who are routinely awakened by an alarm clock, I recover from the experience with a review of the morning’s news. Many of my friends do the same, and if they come across an Alzheimer’s disease story, they immediately forward it on to me knowing that my research focusses on dementia. With this in mind, last month a rare event occurred. I stumbled upon an article entitled “Alzheimer’s Preventative Drug Hope” (1) before a single person had messaged me something along the lines of, “Looks like you’re out of a job.”

Behind the eye catching title, the news article went on to explain that researchers had prevented the accumulation of beta-amyloid plaques in roundworms. These “plaques” are sticky lumps of protein in the brain and are widely believed to lead to Alzheimer’s. Indeed, in the original article (2) the researchers unequivocally assert that plaques lead to Alzheimer’s and that their results suggest potential treatment pathways.

Similar headlines and research are not a rarity. My Twitter feed often appears entirely dedicated to announcing the imminent eradication of Alzheimer’s. Behind the fanfare, this usually means that somebody has reduced plaques in an unfortunate mouse. Whilst the results are presented as revealing a cure, I am not yet “out of a job.”

The truth is, the plaques model is flawed. At post-mortem, many people diagnosed as having Alzheimer’s disease whilst alive, have no plaques. Likewise, many older people who showed no signs of Alzheimer’s whilst alive have brains riddled with plaques. This discrepancy runs at 10% to 40% depending on the study (3,4,5). One research project successfully removed plaques from the brains of people with dementia with no effect on their symptoms (6).

Evidently the model is inadequate. Plaques might cause Alzheimer’s, they might contribute, they might be completely uninvolved or they might be the brain’s protective mechanism against Alzheimer’s. The immediate tragedy of this is that reliance on a flawed model comes at the expense of carers, both in terms of recognition and resource allocation, as I outline in a previous Ageing Issues post (7). Despite the uncertainty and harm, the plaques model is often perpetuated as fact by the medical community and subsequently the media. But why?

As with most good answers, this one arrived in the pub. Speaking with a medical student, I discovered that medical education often presents the plaques model as absolute truth. This does a great disservice to the medical students themselves, well intentioned and working feverously, only to be taught falsities. More worryingly, it undermines the possibility of future medical advances, as medical students become researchers and unwittingly re-enact the inadequacies of their training.

This student asked me, “Why does this continue?” I automatically engaged my standard sociological response, replying that the answer is cultural, political and economic. Culturally, veneration of individualism and rationality supports cure over care, the former representing independence and logic, the latter interdependence and emotion (8,9). Politically, the plaques model has been employed to evidence the importance of gerontological and medical interests (10). Economically, in a competitive grant market, researchers must decide whether to market their study as investigating either “beta amyloid proteins” or “a cure for Alzheimer’s.” Which description is more likely to attract funding?

Satisfied with my answer, I returned the question, “Why do you think it continues?” Her answer was perceptive and straightforward. Lecturers teach the model as fact because it was taught to them as fact, by lecturers who were themselves taught it as fact. There is a cumulative chain of reinforcement. Medical students have so much to learn that questioning the mass of material delivered to them is an unrealistic expectation, particularly as a hierarchical culture discourages dissent.

This is an invaluable observation warranting significant contemplation. Its practicality offers potential solutions to the plaques problem, yet poses difficult questions. To what degree can we expect over-burdened practitioners, and researchers desperately pursuing funding, to step back and deconstruct the consensual wisdom of their superiors? Conversely, in a field characterised by alienating jargon, status and power, to what extend can the non-medical community meaningfully challenge the status quo? These questions are vast, and have ramifications far beyond Alzheimer’s.

For the time being, the truth is that every time I awaken to an Alzheimer’s cure headline, my likelihood of being “out of a job” decreases a little more.


  1. BBC News (2016) ‘Alzheimer’s preventative drug hope’, BBC News. Available at: [25.02.16].
  2. Habchi, J. et al. (2016) ‘An anticancer drug suppresses the primary nucleation reaction that initiates the production of the toxic Aβ42 aggregates linked with Alzheimer’s disease’, Science Advances, 2 (2) e1501244.
  4. Woods, B. (2005) ‘Dementia’, in Johnson, M.L. (ed.) The Cambridge Handbook of Age and Ageing. New York: Cambridge University Press.
  5. Turner, R.S. (2006) ‘Alzheimer’s disease’, Seminars in Neurology, 26 (5) 499-506.
  6. Homes, C. et al. (2008) ‘Long-term effects of Aβ42 immunisation in Alzheimer’s disease: Follow-up of a randomised, placebo-controlled phase I trial’, The Lancet, 372 (9634) 216-223.
  7. Fletcher, J.R, (2015) ‘The “costs” of dementia’, Ageing Issues. Available at: [26.02.16].
  8. Post, S.G. (2006) ‘Respectare: Moral respect for the lives of the deeply forgetful’, in Hughes, J.C., Louw, S.J. & Sabat, S.R. (eds) Dementia: Mind, Meaning and the Person. Oxford: Oxford University Press.
  9. Radden, J. & Fordyce, J.M. (2006) ‘Into the darkness: Losing identity with dementia’, in Hughes, J.C., Louw, S.J. & Sabat, S.R. (eds) Dementia: Mind, Meaning and the Person. Oxford: Oxford University Press.