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Blocking overactive receptor in Alzheimer's recovers memory loss and more
Date:6/17/2013

lity of cerebral vessels to dilate or constrict when necessary." Proper functioning of blood vessels in the brain is vital to providing nutrients and oxygen to nerve cells, and vascular diseases represent important risk factors for developing AD at an advanced age.

"Another interesting result that has not been seen before in our mouse model is a reduction by over 50% of toxic amyloid-beta peptide," adds Dr. Hamel. "In Alzheimer's disease, protein fragments called amyloid-beta have a deleterious effect on the blood and nervous systems. Normally, these protein fragments are broken down and removed. In Alzheimer's disease, the protein fragments clump together a factor believed to contribute to neuronal and vascular dysfunction. We are not sure if these decreases contribute to the functional recovery, but we hope that our findings will aid in clarifying this issue and identifying new targets for therapeutic approaches."

The results show that an increase in B1R is associated with amyloid-beta plaques in Alzheimer's disease mice with impaired memory, and that chronic blockade of B1R significantly improves learning, memory, cerebrovascular function, and several other pathological AD hallmarks in mice with a fully developed pathology. Together, these findings confirm a role of B1R in AD pathogenesis and the role of neuroinflammation as an underlying mechanism in AD. The next step would be to further investigate potential blockers of the bradykinin B1R as a potential treatment for AD in humans.


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Contact: Anita Kar
514-398-3376
McGill University
Source:Eurekalert

Page: 1 2

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