Dr Mason explains: ‘In neurodegenerative diseases such as Alzheimer's or Parkinson's, aggregation (or clumping) of proteins into toxic fibrils (or chains) is considered to be the key pathogenic event.
However, no therapeutic agents currently exist to control this process. In particular, two proteins known as ß-amyloid and a-synuclein aggregate into fibrils, forming amyloid plaques and Lewy bodies that are characteristic of these diseases. A problem arises, however, in antagonist development; in recent years it has become established that small soluble (protofibrillar) forms of amyloid are the neurotoxic species, and that larger fibrils rather serve as reservoirs for these smaller protofibrils.’
‘Unfortunately, peptides and drugs designed to prevent amyloid have until recently been concerned with removing these larger fibrillar deposits. If compounds designed to breakdown amyloid are only partially effective then the balance will be shifted in the direction of smaller protofibrillar forms, rendering the amyloid more toxic in the process. We will use our expertise in the amyloid, protein-protein interaction, and library screening and design fields to combat this.’
This grant application follows on from Dr Mason's previous experience in the field. There are currently 700,000 people living with dementia in the UK, this will rise to more than a million in less than 20 years. At present, dementia costs the UK around £17 billion each year. Development of drugs capable of slowing or stopping the onset of Alzheimer’s or Parkinson's disease would improve the lives of millions of sufferers worldwide.
Victoria Bartholomew | alfa
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