Enzyme unravels Alzheimer’s protein in mice

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By Philip Tubby | Tuesday 27 June 2017

Researchers from the US and Germany have found that a naturally occurring protein, called CyP40, can reduce features of Alzheimer’s disease in mice. The research, published today (27 June 2017) in the journal PLOS biology involves support from an international collaboration of research funders including Alzheimer’s Association, the Weston Brain Institute, and Alzheimer’s Research UK.

Alzheimer’s disease involves a number of complex brain changes including a build-up of the proteins amyloid and tau. These two hallmarks of Alzheimer’s are thought to play a key role in driving damage to nerve cells, and approaches that prevent or reverse their build-up are a key goal for researchers working to develop new treatments.

The researchers in this study carried out a series of experiments to explore whether an enzyme called CyP40 could influence clumps of tau protein. CyP40 occurs naturally in the body and is involved with the way that proteins form and order themselves.

The study team found that when they introduced CyP40 to tau in a dish in the lab, the tangled tau proteins began to break apart. They followed this up by working with mice that develop key features of Alzheimer’s disease, including a build-up of tau protein in the brain. The researchers injected a group of these mice with a dose of CyP40, finding that this group performed better in tests of memory and thinking ability than untreated mice. When they analysed the brains of the mice, they discovered lower levels of tau protein and a greater number of healthy nerve cells in those that received injections of CyP40.

The researchers suggest that finding out more about the exact mechanism could open the possibility of developing drug treatments that promote or replicate the activity of CyP40.

Dr Rosa Sancho, Head of Research at Alzheimer’s Research UK, said:

“The build-up of tau in the brain is a hallmark of Alzheimer’s disease as well as other forms of dementia and understanding how to manipulate these proteins could be key to tackling these devastating diseases. Though this research in mice is in the very early stages, the study

opens the door to new directions in research. Future studies will need to explore how CyP40 influences tau and what this tells us about the way Alzheimer’s develops and how it could be tackled.

“Research like this is vital as there are currently no treatments that can stop or slow the progression of Alzheimer’s, a disease that affects millions of people across the world. Dementia is an urgent and global medical challenge that needs to be met with concerted global action. Alzheimer’s Research UK is proud to help support this important work through a collaboration of international research funders.”


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Philip Tubby