Three interesting research projects have come out of the United Kingdom in recent months. The first looks at mapping proteins present in the brain of people diagnosed with Alzheimer’s disease. The second and third focus on the use of medicines, one new and one existing, that show potential in combatting neurodegenerative diseases.
Protein activity has been the subject of research into the most common cause of dementia – Alzheimer’s disease – for some time. Two proteins form unusual clumps in the brains of people with Alzheimer’s disease. These proteins are known as tau and beta amyloid. Tau deposits are found inside neurons, where they are thought to inhibit or kill them, whereas beta amyloid forms plaques outside brain cells.
Researchers at the University of Cambridge in the United Kingdom¹ have been examining tau activity in Alzheimer’s disease, and have used brain imaging techniques to map the build-up of tau. Results suggest the tau may spread in a similar way to influenza: the tau starts in one place and moves across neighbouring neurons and synapses to other places in the brain. This is called ‘transneuronal spread’ and has been demonstrated in mice but not people.
Understanding how the tau protein spreads across the neurons is a new approach to understanding Alzheimer’s disease. Unlocking this secret could inform the future development of medicines that could attack the protein and stop its spread, potentially halting its progression altogether.
The second research advance to report received coverage prior to Christmas, when the ABC reported on a ‘ground-breaking’ new drug able to target a toxic protein present in the brains of people diagnosed with Huntington’s disease². Huntington’s disease, a type of dementia, is a genetic and progressive neurodegenerative disease that usually surfaces between the ages of 30 – 50 years. Treatment breakthroughs in Huntington’s disease may have relevance to treating other types of dementia in the future.
The Huntington’s research takes a gene-altering approach and has now conducted clinical trials in humans. The new drug being trialled stops a gene producing a particular protein thought to be causing the destruction of the brain tissue. In a one-off process, researchers injected the drug into the spine of patients, which led to a reduction in the levels of the toxic protein that causes Huntington’s. However, the results are still early and the drug is yet to be trialled to see if it can slow progression of Huntington’s disease.
The drug has now been licensed by pharmaceutical company Roche. This research is cause for optimism given the results in clinical trials.
Meanwhile, an already existing drug originally developed to treat Type 2 diabetes has been found to significantly reverse memory loss in mice with Alzheimer’s disease. There is a known link between Type 2 diabetes and Alzheimer’s disease. Type 2 diabetes is considered a risk factor for Alzheimer’s disease that may cause the disease to progress more rapidly.
The drug was found to work by protecting the brain cells attacked by Alzheimer’s disease in three separate ways, rather than relying on a single approach³. In the trial the drug was seen to improve levels of brain growth factor, reduce the amount of amyloid plaques in the brain and slow down the rate of nerve cell loss. Researchers are now looking to test the drug on humans.
At Alzheimer’s WA, we support the pursuit of risk reduction, treatment and cure for dementia. There are currently no effective treatments for Alzheimer’s disease, only medications focused on managing symptoms. These are limited in their effectiveness, and there has been no new drug treatment for Alzheimer’s disease for over 20 years. While the global search for answers continues we will continue to focus on supporting those living with dementia, providing best practice support, advice and education where dementia experts are required.