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Study: Boosting neuron formation may help restore memory in Alzheimer's disease

Posting time:2022-12-06 01:12:05

Study: Boosting neuron formation may help restore memory in Alzheimer's disease

Scientists have found that increasing the production of new neurons in mice with Alzheimer's disease (AD) rescues the animals' memory deficits. The study showed that the new neurons were able to integrate into the neural circuits that store memories and restore their normal function. This suggests that promoting neuronal production may be a viable strategy for treating AD patients. The study, published Aug. 19 in the Journal of Experimental Medicine, was done by researchers at the University of Illinois at Chicago. New neurons are generated from neural stem cells through a process called neurogenesis. Previous studies have shown that neurogenesis is impaired in both AD patients and in laboratory mice carrying genetic mutations linked to AD. The damage is particularly severe in a region of the brain called the hippocampus, which is critical for memory acquisition and retrieval. "However, the role of newly formed neurons in memory formation and whether deficits in neurogenesis contribute to the cognitive impairment associated with AD is currently unclear," said Professor Orly Lazarov from the Department of Anatomy and Cell Biology at the University of Illinois at Chicago School of Medicine. ." In the new JEM study, Lazarov and colleagues genetically enhanced the survival of neuronal stem cells to promote neurogenesis in AD mice. The scientists deleted the gene Bax, which plays a major role in neuronal stem cell death, and ultimately led to the maturation of more new neurons. Increasing the production of new neurons in this way restored the animals' cognitive abilities, as demonstrated in two different tests that measure spatial recognition and contextual memory. By fluorescently labeling neurons that activate during memory acquisition and retrieval, the scientists found that in the brains of healthy mice, the neural circuits involved in storing memories included many newly formed neurons and older, more mature neurons. In AD mice, these circuits that store memory contained fewer new neurons, but when neurogenesis increased, the integration of newly formed neurons was restored. Further analysis of the neurons that form memory storage circuits revealed that boosting neurogenesis also increased the number of dendritic spines. These are structures in synapses that are known to be critical for the formation of memories. In addition, promoting neurogenesis restores normal expression patterns of neuronal genes. Lazarov and colleagues demonstrated the importance of newly formed neurons for memory formation by deliberately inactivating them in the brains of AD mice. This reversed the benefits of boosting neurogenesis and prevented any improvement in the animals' memory. "Our study shows for the first time that impairments in hippocampal neurogenesis play a role in AD-related memory deficits by reducing the availability of immature neurons for memory formation," Lazarov said. Taken together, our results suggest that, Enhancing neurogenesis may have therapeutic value in AD patients."

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