Research has revealed more about the way Alzheimer’s disease progresses in the brain, upending previously held beliefs. Scientists believe the discovery will help reshape the way the disease is treated in its early stages.
Alzheimer’s disease is the most common form of dementia in Australia, accounting for around 70 per cent of the more than 400,000 dementia sufferers living in the community.
The disease has been traditionally thought to originate from a single point in the brain, where a ‘chain reaction’ is started and leads to the death of brain cells.
But an international research team, led by the University of Cambridge, has demonstrated that Alzheimer’s actually reaches several different parts of the brain early. How fast the disease progresses from there depends on how quickly it begins to produce clusters of toxic cells in these different areas of the brain
Read: Australian research identifies likely cause of Alzheimer’s
The researchers believe their study will assist understanding of the progress of Alzheimer’s and other neurodegenerative diseases, and assist in the development of new treatment methods.
“In Alzheimer’s disease and many other neurodegenerative diseases, like Parkinson’s disease, proteins that are normally part of healthy brain cells start sticking together in microscopic clumps,” lead study author Dr Georg Meisl wrote for The Conversation.
“These clumps of protein, called aggregates, form in patients’ brains, killing off brain cells and leading to symptoms such as memory loss.
“The thinking had been that Alzheimer’s develops in a way that’s similar to many cancers: the aggregates form in one region and then spread through the brain, but instead we found that when Alzheimer’s starts there are already aggregates in multiple regions of the brain, and so trying to stop the spread between regions will do little to slow the disease.”
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The results may explain why Alzheimer’s and other types of dementia are notoriously hard to treat, with many pharmaceutical companies opting to stop researching medicines to treat the condition.
The study used post-mortem brain samples from Alzheimer’s patients, as well as PET scans from living patients. In particular, the team aimed to track the aggregation of ‘tau‘, one of two key proteins thought to be responsible for Alzheimer’s.
The researchers are hopeful that their methodology could be used to develop new treatments that target this tau protein aggregation process. Additionally, they hope the method could be applied to other neurodegenerative diseases, such as Parkinson’s disease.
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“The key discovery is that stopping the replication of aggregates rather than their propagation is going to be more effective at the stages of the disease that we studied,” Professor Tuomas Knowles, co-author of the study, told ScienceDaily.
The researchers are now planning to look at the earlier processes in the development of the disease, and extend the studies to other conditions, such as traumatic brain injury and progressive supranuclear palsy, where tau aggregates are also formed.
Are you buoyed by the work being done in this area? Do you think scientists are edging ever closer to a credible treatment? Why not have your say in the comments section below?
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