Researchers have discovered that the enzyme, endothelin converting enzyme-2 (ECE-2), may cause the decrease in blood flow in the brain seen in Alzheimer's disease and contribute to progression of the disease.
The study by Jennifer Palmer, BRACE/Reverend Williams PhD Scholar and colleagues at the University of Bristol's Dementia Research Group is published in the current issue [July 2009] of the American Journal of Pathology.
Alzheimer's disease is the most common form of dementia, affecting over half a million people in the UK - a figure expected to double in the next 20 years. Aβ peptide, which accumulates in the brain of Alzheimer's disease patients, is thought to lead to narrowing of the blood vessels and reduction of blood flood in the brain. ECE-2 may contribute to the disease by converting an inactive precursor to endothelin-1, which constricts blood vessels and further reduces blood flow.
Jennifer Palmer said: "Our findings raise the possibility that drugs that can block the actions of endothelin-1 and which are already licensed for treating other diseases may also be of benefit for the treatment of Alzheimer's disease."
Much of the funding for Jennifer Palmer's work comes from Bristol-based charity BRACE. The charity's Chief Executive, Mark Poarch added: "This is real progress and opens up new areas for research. It is also good news for the thousands of local people who have raised money to try to beat Alzheimer's. BRACE is stepping up its fundraising to help scientists press on and find a cure."
The researchers had been studying ECE-2 in human brain tissue that was donated to the South West Dementia Brain Bank at the University of Bristol because the enzyme is also able to break down Aβ peptide, which accumulates in Alzheimer's disease. They found that ECE-2 was markedly elevated in Alzheimer's disease. ECE-2 was particularly abundant in nerve cells in a part of the brain that is critical for memory and is severely affected by Alzheimer's disease.