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In the mind

Posted 22/05/2013 by sevans

This week is Dementia Week in the UK, designed to highlight the issues surrounding one of the major health problems facing the world today. Some might say that it is a problem only for the developed world where populations are ageing considerably, and not the youthful developing world. But ultimately we all get old, and thanks to the improvements in general healthcare and well-being that have followed the developments of the pharma sector, improved water supplies and nutrition and a host of other things, we are all living longer. And this trend is likely to continue and accelerate.

And in addition to the human cost, according to the UK Alzheimer’s Research Trust, dementia cost the UK economy over £23bn in 2010, more than cancer and heart disease combined. Last week, UK prime minister David Cameron used scientists and clinicians to work together to ‘improve treatments and find scientific breakthroughs’ to address ‘one of the biggest social and healthcare challenges we face’. 

Although much research has gone into the various causes of dementia, a solution has so far eluded researchers, as Dr Tuomas Knowles at Cambridge University in the UK points out: ‘There are no disease modifying therapies for Alzheimer’s and dementia at the moment. We have to solve what happens at the molecular level before we can progress and have real impact.’

But a timely announcement from the Cambridge department of chemistry research group, of which Knowles is a member, may have brought a ray of hope for the future. 

For the first time, the group has been able to map in detail the pathway that generates ‘aberrant’ forms of proteins that are at the root of neurodegenerative diseases, such as Alzheimer’s. They believe this discovery, which uncovers the earliest stages of the development of Alzheimer’s that drugs could target, brings us a vital step closer to increased capabilities for earlier diagnosis of these disorders and opens up the possibilities for a new generation of targeted drugs.

‘We’ve now established the pathway that shows how the toxic species that cause cell death. The oligomers, are formed,’ says Knowles. ‘This is the key pathway to detect target and intervene – the molecular catalyst that underlies the pathology.’

The neurodegenerative process that results in these diseases is triggered when the normal structures of protein molecules within cells become corrupted or misfolded and snag surrounding normal proteins to produce clumps of malfunctioning molecules. These masses can shape themselves into protein tendrils, called amyloid fibrils, which grow outwards from a focal point and form the foundation for the deposits or plaques that are visible in the brains of those suffering from Alzheimer’s and originally thought to be the cause of the disease. 

The new research shows that once a small but critical level of malfunctioning protein clumps have formed, then a runaway chain reaction is triggered thereby multiplying the number of clumps and activating new focal points through so-called nucleation. This secondary process produces ‘juvenile’ tendrils, which are small and highly diffusible ‘toxic oligomers’.

‘We are essentially using a physical and chemical methods to address a biomolecular problem, mapping out the networks of processes and dominant mechanisms to “recreate the crime scene” at the molecular root of Alzheimer’s disease,’ says Knowles.

Multidisciplinary science research is likely to be the watchword of the 21st century – and in this case the benefits could apply to one of the largest, and growing, patient groups.

Neil Eisberg - Editor

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