This very interesting paper reports that treatment with an antibody against the EFRH sequence of β amyloid increases neurogenesis in the brains of mice carrying a mutant gene for amyloid precursor protein found in some patients with familial Alzheimer disease (AD).

This finding is of interest because it suggests that immunotherapy for AD might not only mobilize and remove amyloid from the brain, but also stimulate the production of new neurons, which could contribute to brain repair.

An important caveat in interpreting these findings is that, although newborn neurons in the brains of antibody-treated mice showed evidence of being functional cells, there is no evidence as yet that this improved behavioral or cognitive deficits in the mouse model.

Another interesting aspect of the study is that neurogenesis induced by EFRH immunization was found throughout the brain, and was not restricted to the classic neuroproliferative zones of the adult brain—dentate gyrus and subventricular zone. This means that either that newborn neurons arising in these regions migrated...  Read more

This very interesting paper reports that treatment with an antibody against the EFRH sequence of β amyloid increases neurogenesis in the brains of mice carrying a mutant gene for amyloid precursor protein found in some patients with familial Alzheimer disease (AD).

This finding is of interest because it suggests that immunotherapy for AD might not only mobilize and remove amyloid from the brain, but also stimulate the production of new neurons, which could contribute to brain repair.

An important caveat in interpreting these findings is that, although newborn neurons in the brains of antibody-treated mice showed evidence of being functional cells, there is no evidence as yet that this improved behavioral or cognitive deficits in the mouse model.

Another interesting aspect of the study is that neurogenesis induced by EFRH immunization was found throughout the brain, and was not restricted to the classic neuroproliferative zones of the adult brain—dentate gyrus and subventricular zone. This means that either that newborn neurons arising in these regions migrated extensively in response to AD pathology, or that many more areas can give rise to new neurons in the diseased than in the normal brain.

Finally, the fact that clearing amyloid increased neurogenesis argues that amyloid itself may not be the trigger for the increased neurogenesis observed in some mouse models of AD. This would be consistent with the previous observation that the increase in neurogenesis in these animals precedes the onset of amyloid deposition.

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