ABSTRACT
This chapter begins where the previous one ended, with the promise of future pharmaceutical cures for the dementias. So far, we have taken “cure” as a rather self-explanatory concept, denoting the overcoming of the affliction in question. Here, I want to make “cure” far more malleable. To do so, I consider two key issues: the nature of the problem that we seek to solve and the nature of what it would mean for that problem to be solved. Ultimately, these are questions of what matters, to whom and why. Too often, biopolitics can make dementia meaningful to corporate stakeholders and thereby serve their concerns first and foremost. At worst, this can be at odds with, and potentially detrimental to, the interests of people affected by dementia. In response, I argue that a neurocritical dementia studies should attempt to reimpose those interests on dementia and dementia research. I hence advocate a reappropriation of dementia.
In the first section, I provide an overview of the contemporary push for a cure by 2025 and the initiatives that have grown around that ambition. These initiatives have contributed to a high-stakes research field, characterised by an intimidating failure rate but promising rich rewards for the first companies to develop successful treatments. The field has recently been ignited by the FDA approval of aducanumab, the first disease-modifying treatment for AD, and the controversies that have emerged around it. I argue that aducanumab represents a triumph of neuropsychiatric biopolitics over traditional scientific and clinical considerations and that this story exemplifies the capacity – and indeed necessity – for dementia studies to respond to the issues raised (e.g. corporate collusion, lobbying and data misrepresentation) if only it can abandon its neuro-agnosticism.
In the second section, I explore how the repeated failure of clinical trials has led to the reconfiguration of dementia in relation to both biomarkers and the lifecourse. Dementia drug discovery is characterised by growing interest in presymptomatic neuropathology and the development of molecular landmarks to circumvent the unreliability of cognition as a basis for operationalising dementia. I suggest that the move away from cognition and toward biomarkers represents a marked transformation of dementia as a technoscientific problem. The result is a new molecular imagining of dementia that is freed from the messiness of cognition and ageing and is therefore more amenable to traditional drug discovery research and the development of pharmaceutical products. Rather than finding a treatment that addresses dementia, dementia is made to fit the treatment.
Drawing on critical psychiatry, I argue that, in decoupling dementia from cognition, contemporary biomarker and drug discovery initiatives risk diagnosing and curing dementias, without having any meaningful impact on cognitive decline. In this context, it is increasingly difficult for trials to fail because the meanings of “failure” and “success” are themselves being reconfigured. In response to classic arguments that the amyloid hypothesis has become “too big to fail”, I instead argue that neuropsychiatric biopolitics is transforming dementia into a new type of problem that is, to some extent, too small to fail. That is, dementia is increasingly defined in such an abstract and limited manner as to be easily remediable. The danger here is that such remedies will offer little to people affected by what we would traditionally consider to be dementia. Finally, I consider the recent case of the drug lecanemab, which further complicates the question of how we understand success as our outcomes are made smaller.
