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Graphic showing build-up of amyloid plaque between nerve cells in the brain.
Amyloid plaques can build up between nerve cells in the brains of people with Alzheimer's disease.

Published in the journal Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring, the study looked at two US-based long-term health studies and found what appears to be a 'switch-on' moment in later middle-age when the protein accumulation begins to accelerate.

The research adds to the growing interest in the rate of protein accumulation in the brain and suggests scope for further research – particularly the need to pinpoint new and better biomarkers that can identify those prone to accumulation and thus help towards earlier diagnosis and treatment of Alzheimer's disease.

Writing in The Conversation, Dr Koychev said: 'The past three decades saw a dramatic improvement in our understanding of what brings about Alzheimer's disease. Two proteins are thought to be responsible: amyloid and tau. The most widely accepted theory is that a critical level of amyloid in the brain triggers the build-up of the more toxic tau protein. This has led to several studies testing drugs and vaccines that remove amyloid and tau to see if they can improve or even prevent dementia. Results have been disappointing.

'Over the same period, studies in people destined to develop the condition because of a genetic mutation reported that the changes leading to dementia begin up to 25 years before any symptoms. One logical interpretation is that attempts to find a cure for dementia may have failed because the patients in drug trials were treated too late in the disease process.

'Researchers have shown that people who are yet to reach the critical level of amyloid but are accumulating the protein at an accelerated rate, show early signs of dementia-related brain changes, such as changes to mental ability.

'Our team wanted to know if such a group of "fast protein accumulators" can be identified among healthy ageing adults. The implication is that these people would be the ones who would benefit most from a drug that interferes with the dementia process, before any damage has set in.

'We were able to demonstrate that some people are on a particularly aggressive course of build-up of either amyloid or tau, or both. Importantly, there seemed to be a "switch-on" moment in the participants' late 50s when the accumulation suddenly ramped up.

'Having a genetic variant that is well known to predispose people to dementia (the e4 version of the APOE gene) made it more likely that the person would be on the aggressive protein-accumulation path and have their "switch-on" moment five years earlier, compared with those without an APOE e4 gene version.

'We found that the "switch-on" moment happens at roughly the same age for both the amyloid and tau proteins. This contradicts the theory that "a brain full of amyloid" is needed to start the cascade leading to dementia. Instead, the processes that lead to dementia run concurrently.'

Dr Koychev said we now need to find the best ways of identifying people on a 'fast track' to developing dementia. For example, this information could come from wearable devices that measure gait or track sleep patterns.

He added: 'A number of such digital technologies are being developed and, hopefully, in the not-too-distant future, we will have access to such solutions in both routine clinical practice as well as studies testing new treatments that delay or even prevent dementia.'

Read the full article in The Conversation.