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Abstract
This paper provides a comparison of how genetic biomarkers are used (or not) in three contexts: clinic-based diagnostic work with people; lab-based research on mice and their marbles; and lab-based research on thrashing nematodes. For all the worldwide drive to find biomarkers that can be used in the detection of early, presymptomatic dementia, there is little research on how or when the association between biomarkers and a definitive disease are being made to “hold.” First, we show the disjuncture between the animal modeling that underpins laboratory attempts to stabilize genetic biomarkers and the paradigms that inform clinical diagnosis. Secondly, we develop this theme to show how in our third site, an epigenetics “worm” laboratory, neurodegenerative changes are explored as located in specific gene-environment interactions over time. We speculate whether such an enactment brings us closer to a notion of “situated biology,” to undercut possibilities of making genetic biomarkers of preclinical dementia hold.
Highlights
There is an ongoing challenge for biomedicine to firm up biomarkers that can be used in the early detection of dementia (King 2018)
One of our aims has been to explore the disjuncture between the animal modeling that underpins laboratory attempts to stabilize genetic biomarkers of Alzheimer’s disease and other dementias (ADAD) for early detection and the paradigms that inform clinical diagnosis
We discussed how pressure for early detection technologies are critiqued by medical doctors as well as social scientists for their reduction of dementia to biological mechanisms in ways that do not account for how minded and situated personhood unfolds over time
Summary
There is an ongoing challenge for biomedicine to firm up biomarkers that can be used in the early detection of dementia (King 2018). This research presses the relationship between gene expression and age (early and later in life), and makes some attempt to situate the biology of dementia, but does not attribute worms with any form of mindedness Both these laboratory studies attribute no mindedness to the animals they use, rather neurological symptoms are conceived of as “behavior” and attributed to what is hardwired cognition. Where the laboratory science seems to be moving towards conceiving of biological processes that underpin particular pathologies as located in gene-environment interactions across the lifespan of the animal, including possibilities for variation, plasticity and even reversibility of neurodegenerative effects, do genetic biomarkers as is the case in the clinic, need to be treated as always provisional?
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