Cambridge scientists unveil breakthrough in research into Alzheimer’s and Parkinson’s

Megan Hughes 17 May 2014

Scientists at the University of Cambridge have isolated conditions which facilitate the spread of neurodegenerative diseases in a pair of studies published this week. It is hoped that the research, which further advances our understanding of the triggers of these conditions, could be used to develop treatments for Alzheimer’s and Parkinson’s.

The breakthroughs were discovered through a collaboration between several teams of scientists which focus primarily on protein “misfolding” diseases, headed by Dr Tuomas Knowles, Dr Chris Dobson and Dr Michele Vendruscolo. The news comes a year after the same group made significant headway in mapping the channels which produces the “aberrant” forms of proteins which cause certain neurodegenerative diseases to occur.

Evidence from the first study suggests that acidic conditions within cells encourage proteins to clump together, the cause of these diseases. By isolating the parts of the brain which are more acidic, scientists plan to target treatments in these areas in order to prevent the spread of dementia and other illnesses.

Head of the Knowles Group in the Department of Biophysics and Biophysical Chemistry, Dr Tuomas Knowles said that the first study “takes us much closer to understanding how the disease might spread.” A fellow at St John’s, Knowles emphasises last year that researchers “have to solve what happens at the molecular level before we can have real impact”.

The second study looks at how the role of molecular “chaperones” might be enhanced to counter the development of protein “misfolding” diseases. Scientists have found ways of increasing the efficacy of these “chaperones” in preventing these proteins from causing damage within the brain, which could counter the onset of neurodegenerative conditions.

Dr Janet Kumita, a senior research associate in the Dobson Group, described the role of the chaperone as “like a warning flag for the cell, telling it that something is wrong.

“If we could find a way of developing a drug that introduces the same structural alterations, we would have a therapeutic intervention capable of increasing this protective activity in patients with Alzheimer ’s Disease.”

Dr Chris Dobson, head of the Dobson Group, reaffirmed the fundamental importance of the studies. The research, he argued, “will undoubtedly provide vital clues to the development in due course of new and effectives drugs to combat these debilitating and increasingly common disorders”.