Clive’s current study RESIST is comparing people with Rheumatoid Arthritis on immunosuppressive anti-inflammatory drugs also known as “biologics” with those on traditional disease modifying anti-rheumatic drugs with early memory problems to see if there are differences in cognitive decline over 18 months. The justification for this study was published: Mason, A., Holmes, C., & Edwards, C. J. (2018) Inflammation and dementia: Using rheumatoid arthritis as a model to develop treatments? Journal of Autoimmunity Reviews, 17, 919-925. The take home messages from the article are:
“The systemic inflammation seen in rheumatoid arthritis may hasten deterioration in dementia and make this an important model to study therapies for dementia in an accelerated fashion”
“Interventional studies are now ongoing to assess whether the use of these immunosuppressive therapies could delay or halt cognitive deterioration in adults with a diagnosis of early dementia” (Mason et al., 2018; pp. 923)
The full article can be found at: https://www.sciencedirect.com/science/article/pii/S1568997218301617
Professor Clive Holmes c-director of the Memory Assessment & Research Centre professor at the University of Southampton
Clive has also recently had a paper accepted by the Brain Journal. This paper was based on work conducted at MARC which started back in 2003. The study explored an amyloid- β immunisation that removed amyloid plaques associated with Alzheimer’s Disease from the patients’ brains. This was evident at post-mortem, however the progression of dementia remained which the authors concluded was potentially due to continued tau in the brain. The study provides important information about the causes of dementia and has the potential to inform future treatment options.
The abstract for the paper, currently in press, can be found here: Nicoll, J., Buckland, G., Harrison, C., Page, A., Harris, S., Love, S., ... Boche, D. (Accepted/In press). Persistent neuropathological effects 14 years following amyloid-β immunisation in Alzheimer’s disease. Brain, [BRAIN-2018-01483.R2].