Neurogenesis and angiogenesis are sorely needed after a stroke so get those clinical trials going.
http://onlinelibrary.wiley.com/doi/10.1002/jnr.23147/abstract;jsessionid=C09C894321FDCAD70366819EABFC4CEA.d01t02?deniedAccessCustomisedMessage=&userIsAuthenticated=false
Abstract
Leptin is a potent AMP kinase
(AMPK) inhibitor that induces neuroprotection, neurogenesis, and
angiogenesis when administered immediately after stroke. To dissociate
these effects, we explored the effects of delayed administration of
leptin, at 10 days after stroke onset, on neurogenesis and angiogenesis
after stroke. Sabra mice underwent photothrombotic stroke and were
treated with vehicle or leptin given either as a single dose or in
triple dosing, 10 days later. Newborn cells were labeled with
bromodeoxyuridine. Functional outcome was studied with the neurological
severity score for 90 days poststroke, and the brains were then
evaluated via immunohistochemistry. Final infarct volumes did not differ
between the groups. Exogenous leptin led to significant increments in
the number of proliferating BrdU
+ cells in the subventricular
zone and in the cortex abutting the lesion (2.5-fold and 1.4-fold,
respectively). There were significant increments in the number of
newborn neurons and glia (4- and 3.4-fold, respectively) in
leptin-treated animals. Leptin also significantly increased the number
of blood vessels in the perilesioned cortex. However, animals treated
with leptin failed to demonstrate significantly better functional
states. In conclusion, leptin induces neurogenesis and angiogenesis even
when given late after stroke but does not lead to better functional
outcome in this delayed-treatment paradigm. These results suggest that
the main beneficial effects of leptin after stroke are associated with
its early neuroprotective role rather than with its proneurogenic or
proangiogenic effects.
No comments:
Post a Comment