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Blood flow in Alzheimer's disease
Date:7/27/2009

al for memory and is severely affected by Alzheimer's disease.

The increase in ECE-2 in Alzheimer's disease is not simply a by-product of nerve cell damage. When the researchers looked at brain tissue from patients with a different type of dementia (vascular dementia), ECE-2 levels were normal no different from the levels in brain tissue from elderly people without dementia. Further studies showed that the increase seen in Alzheimer's disease of ECE-2 could not be explained by differences in age, gender or time to brain removal after death between the various groups of patients that were studied.

To investigate why ECE-2 might be specifically elevated in Alzheimer's disease, the researchers then examined nerve cells that were grown in a laboratory. They showed that addition of Aβ caused these nerve cells to increase their production of ECE-2. The findings indicate that nerve cells produce more ECE-2 when they are exposed to Aβ.

In the normal brain, blood flow responds to nerve cell activity. If nerve cell activity in a particular part of the brain increases, so does the supply of blood that is needed to meet the extra demand for nutrients such as glucose and oxygen. If this demand is not met, as can happen in Alzheimer's disease, the nerve cells may not function normally and may even sicken and die.

Although the elevated ECE-2 in Alzheimer's disease may help to break down amyloid beta, it may also cause the decrease in blood flow in the brain, through the production of too much endothelin-1. This may have important implications for treatment. Drugs are available that can block the actions of endothelin-1 and which have been shown to treat some other diseases in which excess endothelin-1 reduces blood flow. The findings raise the possibility that these drugs may also be of benefit for the treatment of Alzheimer's disease.


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Contact: Joanne Fryer
joanne.fryer@bristol.ac.uk
44-117-331-7276
University of Bristol
Source:Eurekalert

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