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Research grant to study Lewy body disease

Researchers at the University of Bristol’s Dementia Research Group have been awarded a grant to investigate the different forms of amyloid-β (Aβ) in Lewy body disease and its association with other diseases, such as Alzheimer’s and Parkinson’s.

The grant of over £80,000 has been awarded by local charity BRACE for the project “Contribution of Aβ to Lewy body disease”.  BRACE funds research into Alzheimer’s and other forms of dementia.

Lewy body disease is a form of dementia that shares characteristics with both Alzheimer’s and Parkinson’s diseases.

In Parkinson’s disease (PD) nerve cells form Lewy bodies, aggregates of the protein α-synuclein.  Lewy body formation is initiated by the addition of phosphate to α-synuclein.  Some variants of PD cause dementia and the brains of those patients usually accumulate Aβ, also found in Alzheimer’s disease (AD).

Seth Love, Professor of Neuropathology in the University’s School of Clinical Sciences, who will be leading the project, said: “This grant will help us to learn more about Lewy body disease and its association with other diseases and should help in the treatment of the disease.

“There is a lot of evidence to indicate that the Aβ exacerbates the dementia-associated variants of PD but the mechanism remains unclear.”

Mark Poarch, Chief Executive of BRACE, added: “The announcement of this project is a reminder that Alzheimer’s is not the only form of dementia that causes suffering to a great many people.  BRACE exists to fight dementia through medical science, and we are able to do so because of the fantastic support of local people over the past 24 years.  With their continued support, we can help to win this fight.”

Experimental studies suggest that some forms of Aβ may cause the addition of phosphate to α-synuclein, producing Lewy bodies and nerve cell damage.  At present, the levels of the different forms of Aβ (some of which are dissolved and not visible in tissue sections) that accumulate in the brain in PD or its variants are not known.

The study aims to measure the levels of the different forms of Aβ in the brain in these variants of PD, and the researchers will conduct studies to find out whether Lewy body formation and the toxicity of α-synuclein to nerve cells are increased by the Aβ.

Please contact joanne.fryer@bristol.ac.uk for further information.

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