summary: Increasing neurogenesis by deleting the Bax gene in a mouse model of Alzheimer’s improved the animals’ performance in tests measuring spatial recognition and contextual memory.
Source: Rockefeller University
Researchers at the University of Illinois at Chicago have discovered that increasing the production of new neurons in mice with Alzheimer’s disease (AD) protects the animals’ memory defects.
Study to be published August 19 Journal of Experimental Medicineshows that new neurons may be involved in neural circuits that store memories and restore their normal function, suggesting that boosting neuron production may be a viable strategy for treating AD patients.
New neurons are produced from neural stem cells through a process called 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 that is involved in memory acquisition and retrieval. is important.
“However, the role of newly formed neurons in memory formation, and whether defects in neurogenesis contribute to the cognitive impairment associated with AD, are unclear,” says Orly Lazarov, a professor in the Department of Anatomy and Cell Biology at the University of Illinois at Chicago College. of medicine.
In the new study, Lazarov and colleagues promoted neurogenesis in AD mice by genetically enhancing the survival of neuronal stem cells. The researchers removed Bax, a gene that plays a major role in neuronal stem cell death, eventually leading to the maturation of more new neurons.
Thus increasing the production of new neurons restored the animals’ performance in two separate tests measuring spatial recognition and contextual memory.
By fluorescently labeling neurons activated during memory acquisition and retrieval, the researchers determined that, in the brains of healthy mice, the neural circuit involved in storing memories consists of many newly formed neurons along with older, more mature neurons.
AD rats have fewer new neurons in these memory-storing circuits, but the integration of newly formed neurons was restored as neurogenesis progressed.
Further analysis of neurons that make up memory-storing circuits revealed that promoting neurogenesis also increases the number of dendritic spines, which are structures at synapses known to be important for memory formation, and neuronal genes. Restores a normal pattern of expression.
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Lazarov and his colleagues confirmed the importance of newly formed neurons for memory formation by specifically deactivating them in the brains of AD rats. This reversed the benefits of promoting neurogenesis, leaving no improvement in the animals’ memory.
“Our study is the first to show that impairment in hippocampal neurogenesis plays a role in memory deficits associated with AD by reducing the availability of immature neurons for memory formation,” says Lazarov.
“Taken together, our results suggest that increasing neurogenesis in AD patients may be of therapeutic value.”
About this Neurogenesis and Alzheimer’s disease research news
Author: Press Office
Source: rockefeller university press
contact: Press Office – Rockefeller University Press
image: Image credit is given to Mishra et al.
Basic Research: will appear in the conclusion Journal of Experimental Medicine
(This story has not been edited by seemayo staff and is published from a rss feed)