Effects of Alzheimer’s disease can be partially reversed in mice

Memory pathology in older mice with Alzheimer’s disease can be reversed with treatment. Even animals with advanced pathology can be rescued with this molecule.

The researchers found an increased level of a receptor known as bradykinin B1 receptor (B1R) in the brain of mice with AD, a receptor involved in inflammation. “By administering a molecule that selectively blocks the action of this receptor, we observed important improvements in both cognitive and cerebrovascular function,” says Dr. Baptiste Lacoste, research fellow who conducted the study at The Neuro and now pursuing his training at Harvard Medical School in Boston. “Alzheimer’s disease destroys nerve cells and also compromises the function of blood vessels in the brain. Not only were there improvements in learning and memory, but also marked recovery in blood flow and vascular reactivity, i.e. the ability 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.

Journal of Neuroinflammation – Cognitive and cerebrovascular improvements following kinin B1 receptor blockade in Alzheimer’s disease mice

Recent evidence suggests that the inducible kinin B1 receptor (B1R) contributes to pathogenic neuroinflammation induced by amyloid-beta (Abeta) peptide. The present study aims at identifying the cellular distribution and potentially detrimental role of B1R on cognitive and cerebrovascular functions in a mouse model of Alzheimer’s disease (AD).

These findings show a selective upregulation of astroglial B1R in the APP mouse brain, and the capacity of the B1R antagonist to abrogate amyloidosis, cerebrovascular and memory deficits. Collectively, these findings provide convincing evidence for a role of B1R in AD pathogenesis.

SOURCES – Planetherald, Journal of Neuroinflammation

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