Promising New Research on Alzheimer’s Disease

Previous clinical trials into the treatment and prevention of Alzheimer’s disease have been largely unsuccessful. Ralph Martins, Professor in the department of Biomedical Sciences at Macquarie University and international researcher into aging and Alzheimer’s disease, says the failure has been due to treatment being “too little, too late”, with the brain already being severely damaged.

Fortunately, new research into diagnosis and treatment looks very promising, with some methods claiming to catch Alzheimer’s twenty years before symptoms arise.

Alzheimer’s disease currently affects 413,000 Australians and this figure is predicted to rise to 536,000 by 2025. The exact cause is unknown, but the leading theory is that it is related to a protein fragment called beta-amyloid. Much like cholesterol, it is useful in small doses. However, when levels get too high it forms a neurotoxic sticky plaque that starts to kill brain cells.

“Until 1985, Alzheimer’s could only be definitively diagnosed through brain examination after death.”

This occurs for a number of reasons. Certain families have mutations that lead to the overproduction of beta amyloid, which causes early-onset of the disease. However, in the vast majority of cases, the disease develops later in life. In these circumstances, the body is not producing too much beta amyloid. Instead, it is not clearing it fast enough, often due to lifestyle causes, says Professor Martins.

Until 1985, Alzheimer’s could only be definitively diagnosed through brain examination after death. Thankfully, we now have the technology to examine the brain for the amyloid deposits during life.

In a study undertaken with various teams across Australia, 12,000 people were followed for twelve years to see if early diagnosis was possible. They found that at least 30% of people who had no memory issues had brains with high levels of amyloid deposits. This study was a “game changer”, says Professor Martins.

Amyloid deposits can be asymptomatic for years before diagnosis. This is called pre-clinical Alzheimer’s and new research has been focused on its early detection. There used to be “the notion that once amyloid was in the brain, it was there for life” states Professor Martins. However, this has been disproved through studies in mice. If deposits can be identified while still building up, they can be removed or reduced with a much better outcome. Professor Martins describes this as “the best time to intervene”. At this stage, there is a strong chance at success of preventing Alzheimer’s disease from developing and damaging the brain.

“Australian and Japanese scientists have created a highly accurate blood test that also detects the disease up to twenty years before symptoms.”

A developing form of diagnosis is a PET scan to detect amyloid presence. However, the problem with a brain scan is it’s cost, making it not feasible for many people. Mojtaba Golzan from the University of Technology Sydney has been looking into scanning the eye for signs of disease, including Alzheimer’s. “Our body is an integrated system,” he says, “One disease showing up in an area is likely to have an effect in another area as well”.

Professor Martins echoes this solution, which could detect the disease twenty years before symptoms arise. “Changes in the eye reflect changes in the brain,” he says, but acknowledges it’s still a work in progress. He hopes it will be the next game changer in the field, after a trial confirms its efficacy.

Other approaches include a blood test. Australian and Japanese scientists have created a highly accurate blood test that also detects the disease up to twenty years before symptoms. Colin Masters, Professor of Dementia Research at the University of Melbourne, states the main challenge is now developing treatment for the disease, rather than diagnosis. Despite the lack of treatment, he emphasises the importance of such tests because “in the early stages there’s no cognitive impairment so we are totally reliant on these objective biomarkers like blood tests to guide us in our search for a therapy.” Identifying the disease early provides a valuable opportunity for study, hopefully leading to a cure as soon as possible.

In terms of therapies, Professor Martin’s research is currently focused on the role of hormones and omega-3 in amyloid development. Omega-3 is well known in Alzheimer’s prevention, but Professor Martins is also investigating the role of testosterone. It may sound unusual, but testosterone has so far appeared to be a significant factor in Alzheimer’s development. This is because with age, testosterone levels decrease, and the major risk factor for the disease’s development is ageing.

Professor Martins seeks to investigate whether omega-3 can “synergise with testosterone to have an even greater effect” in individuals who have amyloid deposits but no memory loss symptoms. He hopes to see a profound effect on amyloid reduction and the delay or prevention of symptom formation altogether.

While a cure is still a while away, there are things you can do in the mean time. There are proven ways to reduce your own risk, says Professor Martins, as the disease is influenced by lifestyle factors. Adhering to a Mediterranean diet or increasing exercise can bring amyloid levels down, even with a genetic predisposition.

Professor Martins predicts the future of treatment will be integrated approaches such as the testosterone and omega-3 combination he is investigating. This has already been seen in cardiovascular disease and drugs for blood pressure. Perhaps an approach that uses these therapies along with positive lifestyle choices is the best way forward.

He has high hopes for both his and other current research, as does everyone affected by this disease.

Listen to the Leading Lights interview with Professor Ralph Martins here.

Listen to the follow-up interview with Professor Ralph Martins here.

Listen to the interview with Mojtaba Golzan here.

Listen to the interview with Professor Colin Masters here.

DATE POSTED
Wednesday 10th of October, 2018
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