Trauma Induced Neurodegenerative Diseases: Reimagining dementia?

Written by Greg Hollin

Knowledge regarding the causes of dementia have changed considerably over the course of the last hundred-or-so years. Nonetheless, since the discovery in the 1990s of gene variants that alter the risk of getting neurodegenerative disease, Alzheimer’s-related dementias have been understood in primarily genetic terms, and social scientists have persuasively argued that a ‘genetic imaginary’ continues to dominate scientific and medical visions of Alzheimer’s (Lock, 2013; Milne, 2020). On July 30th, 2020, however, a Lancet Commission formally recognised Traumatic Brain Injury as a ‘[s]pecific potentially modifiable risk factor’ for dementia (Livingston et al., 2020, p. 417). 

Around half of us will experience traumatic brain injuries, such as concussions, in our lifetime. Falls and motor accidents the most common causes (Sandel, 2020), but there are numerous groups at high-risk for brain injury: victims of domestic violence (Saulle and Greenwald, 2012), the elderly, infants, military personnel (Goldstein et al., 2012), professional athletes (Mackay et al., 2019; McKee et al., 2009), prisoners, and the homeless (Sandel, 2020) amongst them.

The suggestion that Alzheimer’s-related dementias may be, in part, environmental conditions promises to transform scientific understandings of dementia and to have significant social and political consequences. Particular spaces—such as the home or the workplace—may become medicalized and bound to neurodegenerative disease, while particular accidents and activities within those spaces—from trips and falls, to car accidents, to domestic violence—are newly rendered as risks for dementia.

Brain: lateral view. Colour lithograph by Brocades Great Britain Ltd.. Credit: Wellcome CollectionPublic Domain Mark

These newly medicalized places and acts, in turn, pave the way for novel forms of intervention: from new forms of pharmaceutical treatment, to regulation targeted at those now understood as being ‘at-risk’. The changes represent perhaps the most significant re-conceptualization of Alzheimer’s in thirty years and with potential effects that cascade across classification, diagnosis, therapeutics, and regulation, with space opened for new forms of social activity, be they attempts to surveil risky populations; regulate the risk of neurodegenerative disease within the home; or bring litigation against employers as a result of disease linked to the workplace. These are matters not only crucial for, and applicable to, contemporary understandings of dementia research but to wider discussions of the direction and implications of the contemporary life and biomedical sciences.

For the next five years, and following a Wellcome Trust University Award, I will be investigating this fast changing landscape at the Department of Sociological Studies and iHuman. I will undertake ethnographic research with three groups of scientists (neuropathologists, molecular neuroscientists, and sports scientists) who each have a stake in the classification, diagnosis, treatment, and regulation of brain-injury induced dementias. These scientific communities often approach the matter of brain injury with diverse and conflicting samples, methods, and underlying assumptions, and, perhaps unsurprisingly, often reach very different conclusions about the risk associated with particular persons or activities. It is through these interdisciplinary relations and tensions, as much as the findings of any one discipline, that novel understandings of dementia are forged and this project will be amongst the first to trace these highly contentious scientific terrains which offer to transform understandings of dementia.  


DeKosky, S.T., Asken, B.M., 2017. Full article: Injury cascades in TBI-related neurodegeneration. Brain Injury 31, 1177–1182.

Goldstein, L.E., Fisher, A.M., Tagge, C.A., Zhang, X.-L., Velisek, L., Sullivan, J.A., Upreti, C., Kracht, J.M., Ericsson, M., Wojnarowicz, M.W., Goletiani, C.J., Maglakelidze, G.M., Casey, N., Moncaster, J.A., Minaeva, O., Moir, R.D., Nowinski, C.J., Stern, R.A., Cantu, R.C., Geiling, J., Blusztajn, J.K., Wolozin, B.L., Ikezu, T., Stein, T.D., Budson, A.E., Kowall, N.W., Chargin, D., Sharon, A., Saman, S., Hall, G.F., Moss, W.C., Cleveland, R.O., Tanzi, R.E., Stanton, P.K., McKee, A.C., 2012. Chronic Traumatic Encephalopathy in blast-exposed military veterans and a blast neurotrauma mouse model. Science Translational Medicine 4, 134ra60-134ra60. https://doi.org/10.1126/scitranslmed.3003716

Livingston, G., Huntley, J., Sommerlad, A., Ames, D., Ballard, C., Banerjee, S., Brayne, C., Burns, A., Cohen-Mansfield, J., Cooper, C., 2020. Dementia prevention, intervention, and care: 2020 report of the Lancet Commission. The Lancet.

Lock, M., 2013. The Alzheimer Conundrum: Entanglements of Dementia and Aging. Princeton University Press, Princeton, New Jersey.

Mackay, D.F., Russell, E.R., Stewart, K., MacLean, J.A., Pell, J.P., Stewart, W., 2019. Neurodegenerative disease mortality among former professional soccer players. N Engl J Med NEJMoa1908483. https://doi.org/10.1056/NEJMoa1908483

McKee, A.C., Cantu, R.C., Nowinski, C.J., Hedley-Whyte, E.T., Gavett, B.E., Budson, A.E., Santini, V.E., Lee, H.-S., Kubilus, C.A., Stern, R.A., 2009. Chronic Traumatic Encephalopathy in athletes: Progressive tauopathy after repetitive head injury. Journal of Neuropathology & Experimental Neurology 68, 709–735. https://doi.org/10.1097/NEN.0b013e3181a9d503

Milne, R., 2020. The rare and the common: scale and the genetic imaginary in Alzheimer’s disease drug development. New Genetics and Society 39, 101–126. https://doi.org/10.1080/14636778.2019.1637718

Sandel, E., 2020. Shaken Brain: The Science, Care, and Treatment of Concussion. Harvard University Press, Cambridge, MA & London.

Saulle, M., Greenwald, B.D., 2012. Chronic Traumatic Encephalopathy: A review. Rehabilitation Research and Practice 1–9. https://doi.org/10.1155/2012/816069

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