We are getting more and more clarity on the pathology of Alzheimer’s.
We can start becoming optimistic that a solution can be found. It
does not appear to be as intractable as other diseases we could
mention and the labs are cranking out good stuff.
In fact, brain diseases appear to now be getting serious attention
that seems to be a little of better late than never. They were
almost ignored for far too long and one got the impression that our
outright ignorance of brain function discouraged interest.
In any case, it is looking much easier to be optimistic.
Blocking Overactive
Receptor in Alzheimer's Recovers Memory Loss
Jun 17, 2013 10:37
A new study shows that
memory pathology in older mice with Alzheimer’s disease can be
reversed with treatment. The study by researchers from the Montreal
Neurological Institute and Hospital - The Neuro, at McGill University
and at Université de Montréal found that blocking the activity of a
specific receptor in the brain of mice with advanced Alzheimer’s
disease (AD) recovers memory and cerebrovascular function. The
results, published in the Journal of Neuroinflammation in
May, also suggest an underlying mechanism of AD as a potential target
for new therapies.
“The exciting and
important aspect of this study is that even animals with advanced
pathology can be rescued with this molecule” says Dr. Edith Hamel,
neuroscientist at The Neuro and lead investigator on the paper in
collaboration with Dr Réjean Couture at the Department of Physiology
at Université de Montréal. “We have rarely seen this type of
reversal of AD symptoms before in our mouse model at this advanced
age – when mice have been developing AD for one year.”
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,”
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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