World Alzheimer’s Month takes place every September and is dedicated to raising awareness of the disease and challenging the stigma associated with it. In our latest blog Dr Gareth Edwards, Senior Bioassay Scientist at Cellomatics discusses research into Alzheimer’s disease (AD) and the role in which neuroinflammation plays in AD pathogenesis.
Alzheimer’s Disease (AD) is one of the predominant forms of dementia (dementia is a set of symptoms induced by multiple progressive diseases which harm the brain). Cases of AD are increasing year on year, and it is now estimated that 1 in 3 people born in the UK will be diagnosed with dementia in their lifetime1. Prior to the COVID pandemic, 12.5% of deaths registered in England and Wales resulted from dementia and AD2.
There are multiple causes of AD at the genetic level: classically, harmful substances (amyloid and Tau) are deposited or abnormally phosphorylated in the brain, which loses the capacity to remove them before they can form damage-inducing plaques and tangles. This leads to shrinkage of the brain, inflammation, cell death, and changes in neurotransmitter-based signalling pathways. As the disease develops and damage builds up, there is a progressive onset of symptoms associated with dementia such as memory loss and inhibition of thought processes. Difficulties in performing simple everyday tasks increase, requiring extensive care and support. This places heightened workloads on the health service-and, much more importantly, on the relatives who are frequently the first-line carers of the person with AD.
Research is being performed on a global scale into the causes of AD and to identify potential treatments. To date, this has frequently focussed on slowing down disease progression3, for instance, by targeting the symptoms of the disease (e.g., neurotransmitter changes via acetylcholinesterase inhibitors such as Donepezil or Rivastigmine). Recently, interventions targeting the pathophysiological causes of AD have begun to reach the clinic (e.g. Lecanemab4, a monoclonal antibody which binds amyloidβ protofibrils, inducing their removal from the brain and preventing amyloidβ deposition). However, further progress in AD research is key: to date, many potential therapeutic compounds have demonstrated significant potential in the laboratory but have failed to reach clinical acceptance. It is thought that this may be due to a combination of factors, notably an ‘inadequate understanding’ of AD disease processes, and treatment commencing after the stage of the disease when it would have been most effective.5 Until the approval of Lecanemab by NICE, the development of new anti-AD therapeutics had reached an impasse.
Neuroinflammation plays a key role in AD pathogenesis, and increased levels of inflammatory markers can be detected in patients with AD.6 Taken together, this may identify a novel suite of potentially druggable targets which could be exploited in the development of new treatments for AD.7 Cellomatics Biosciences Ltd has significant expertise in the development and implementation of in vitro models of inflammation. This provides a strong basis for the development of platforms providing solutions to assist and enhance in vitro drug development pipelines targeting phenomena such as neuroinflammation in the context of dementia.8
To learn more about Cellomatics’ offering, please do not hesitate to get in touch with us today.
References
- https://www.alzheimers.org.uk/
- https://www.ons.gov.uk/peoplepopulationandcommunity/birthsdeathsandmarriages/deaths/bulletins/dementiaandalzheimersdiseasedeathsincludingcomorbiditiesenglandandwales/2019registrations
- https://www.nhs.uk/conditions/dementia/about-dementia/treatment/
- https://www.alzheimers.org.uk/blog/what-lecanemab
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7050025/
- https://doi.org/10.1038/s41582-020-00435-y
- https://doi.org/10.3390/cells13171426
- https://cellomaticsbio.com/posing-neuroinflammatory-questions-about-dementia/
