Data from European Academy of Neurology (EAN) - Curated by EPG Health - Date added 05 July 2019
Early treatmentis the key to beating Alzheimer’s disease in later life
(Oslo, Sunday, 30June, 2019)World-renowned neuroscientist Professor Bart De Strooper will deliver the prestigious ‘Brain Prize Lecture’today at the 5th European Academy of Neurology (EAN) Congress in Oslo, Norway, and outline why we need to intervene much earlier if we want toprotectpeopleagainst the symptoms of Alzheimer’s disease in later life1.
This approach is based on decades of researchon the causes of hereditary forms of Alzheimer’s disease2 and,unfortunately, disappointing clinical trial outcomes so far.
Over the past decades, Professor De Strooperhas made important contributions to our understanding of the mechanisms of Alzheimer’s disease. This included uncovering thatgene mutations in presenilin –part of the γ-secretase protein complexthat ‘cuts’ other proteins into smaller pieces –lead to the production of abnormal amyloid to formplaques in the brains of people with Alzheimer’s disease.
His discoveries mark breakthrough findings in the dementia field, furthering the understanding of how Alzheimer’s disease may begin and provide potential new mechanisms to target with drug therapies in the future.
Professor De Strooper, Director of the UK Dementia Research Institute, Londonand group leader at the VIB-KU Leuven Center for Brain & Disease Research, Leuven, was awarded the Lundbeck Foundation Brain Prize for his work in this area last year and explained that understanding how these mutations drive dementia is important in developing new therapies. “We need to understand what is going on in the brain and how the brain operates while these changes occur”, he commented. “Treating amyloid at a very early stage could protect against symptoms later on and we must target these processes if we want to make the most effective treatments.”
The amyloid hypothesis works on the assumption that the accumulation of peptide amyloid-β plaquesis the main cause of Alzheimer’s disease by triggering neurogenerative processes. This leads to the loss of memory and cognitive ability and has guided research into dementia treatments for the past 25 years.
Professor De Strooper commented, “For decades we have studied Alzheimer’s disease in its final stages. We now know that the disease process in the braincan start decades before the first symptoms arise. Studying the cognitive abnormalities in Alzheimer’s disease patients has indeed taught us a great deal about the disease, but we are always looking at an advanced stage or evenpost-mortem. You could compare this to studying cancer but only reviewing the metastatic disease, completely missing the stage where the disease actually originates and begins to spread. Needless to say, in both cases the chance of clinical success and making a meaningful change in treatment for patients, would be in those earlier stages.”
Trials for new Alzheimer’s drugs have, until now, often been tested in patients with advanced disease and it is therefore difficult to change the disease course. Professor De Strooper argues that we need tounderstand what happens before the plaques form in the cellular phase. “Scientists need to shift their focus to the earlier stage of the disease and think about the cellular environment in which the disease develops”, he observed.
Although budgets have been cut in dementia research, Professor De Strooper added there is still room for plenty of optimism due to the discoveries made on the neurodegenerative process. “Even though the situation is more complex than previously anticipated, if we compare the budgets and publication numbers inthis disease area with those for cancer, it is simply not true that the success rate is exceptionally low. We just need to continue to invest heavily in new, innovative research to provide patients with optimal outcomes.”
References - 1. The Brain Prize Lecture: The prodromal, cellular phase of Alzheimer’s Disease: towards a novel understanding of the disorder. Presented on Sunday, 30 June, 2019, at The 5th European Academy of Neurology (EAN) Congress in Oslo, Norway. 2. Alzheimer’s-Causing Mutations Shift Aβ Length by Destabilizing γ-Secretase-Aβn Interactions: https://www.cell.com/cell/fulltext/S0092-8674(17)30811-5.