Overview: Increasing neurogenesis by deleting the Bax gene in mouse models of Alzheimer’s disease improved the animals’ performance in tests measuring spatial recognition and contextual memory.
Source: Rockefeller University
Researchers at the University of Illinois Chicago have found that increasing the production of new neurons in mice with Alzheimer’s disease (AD) rescues the animals’ memory deficits.
The study, to be published Aug. 19 in the Journal of Experimental Medicineshows that new neurons can be incorporated into the neural circuits that store memories and restore their normal function, suggesting that boosting neuron production could be a viable strategy to treat AD patients.
New neurons are produced from neural stem cells through a process known as neurogenesis. Previous studies have shown that neurogenesis is impaired in both AD patients and laboratory mice that carry genetic mutations associated with AD, particularly in an area of the brain called the hippocampus, which is crucial for memory acquisition and retrieval.
“However, the role of newly formed neurons in memory formation, and whether defects in neurogenesis contribute to the cognitive impairments associated with AD, is unclear,” said Professor Orly Lazarov of the Department of Anatomy and Cell Biology at the University of Illinois Chicago College of Medicine.
In the new study, Lazarov and colleagues boosted neurogenesis in AD mice by genetically improving neuronal stem cell survival. The researchers removed Bax, a gene that plays an important role in the death of neuronal stem cells, ultimately leading to the maturation of more new neurons.
Increasing the production of new neurons in this way restored the animals’ performance in two different tests measuring spatial recognition and contextual memory.
By fluorescent labeling neurons that are activated during memory acquisition and retrieval, the researchers determined that, in the brains of healthy mice, the neural circuitry involved in storing memories includes many newly formed neurons in addition to older, more mature neurons. mature neurons.
These memory storage circuits contained fewer new neurons in AD mice, but the integration of newly formed neurons was restored when neurogenesis was increased.
Further analyzes of the neurons that make up the memory storage circuits revealed that stimulating neurogenesis also increases the number of dendritic spines, structures in synapses known to be crucial for memory formation, and restores a normal pattern of neuronal gene expression.
Lazarov and colleagues confirmed the importance of newly formed neurons for memory formation by specifically inactivating them in the brains of AD mice. This negated the benefits of stimulating neurogenesis, preventing any improvement in the animals’ memory.
“Our study is the first to show that disorders in hippocampal neurogenesis play a role in the memory deficits associated with AD by reducing the availability of immature neurons for memory formation,” Lazarov says.
Taken together, our results suggest that enhancing neurogenesis may be of therapeutic value in AD patients.
About this news about neurogenesis and Alzheimer’s disease
Author: press office
Source: Rockefeller University Press
Contact: Press Agency – Rockefeller University Press
Image: The image is attributed to Mishra et al
Original research: The findings appear in Journal of Experimental Medicine
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