SAN FRANCISCO, CAA new study from the Gladstone Institutes has revealed a way to alleviate the learning and memory deficits caused by apoE4, the most important genetic risk factor for Alzheimer's disease, improving cognition to normal levels in aged mice.
In the study, which was conducted in collaboration with researchers at UC San Francisco and published today in the Journal of Neuroscience, scientists transplanted inhibitory neuron progenitorsearly-stage brain cells that have the capacity to develop into mature inhibitory neuronsinto two mouse models of Alzheimer's disease, apoE4 or apoE4 with accumulation of amyloid beta, another major contributor to Alzheimer's. The transplants helped to replenish the brain by replacing cells lost due to apoE4, regulating brain activity and improving learning and memory abilities.
"This is the first time transplantation of inhibitory neuron progenitors has been used in aged Alzheimer's disease models," said first author Leslie Tong, a graduate student at the Gladstone Institutes and UCSF. "Working with older animals can be challenging from a technical standpoint, and it was amazing to see that the cells not only survived but affected activity and behavior."
The success of the treatment in older mice, which corresponded to late adulthood in humans, is particularly important, as this would be the age that would be targeted were this method ever to be used therapeutically in people.
"This is a very important proof of concept study," said senior author Yadong Huang, MD, PhD, an associate investigator at Gladstone Institutes and associate professor of neurology and pathology at UCSF. "The fact that we see a functional integration of these cells into the hippocampal circuitry and a complete rescue of learning and memory deficits in an aged model of Alzheimer's disease is very exciting."
A balance of excitatory and inhibitory activity in the brain is essential for normal func
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