The early-onset memory loss in Alzheimer's disease is the result of impaired memory retrieval ability, not the loss of information coding ability. This study of an early mouse model of Alzheimer's disease shows that by activating specific cells in the hippocampus, forgotten memories can be preserved.
Alzheimer's disease, also known as Alzheimer's disease, is a neurodegenerative disease. From a pathological point of view, it mainly damages neurons and synapses in the brain and certain subcortical areas, leading to severe brain atrophy and patient weakness. The exact cause is still unknown. Many studies have shown that the inability to recall the events observed by patients with Alzheimer's disease (event memory) is the result of invalid coding of new information. However, because cognitive testing relies on memory retrieval, scientists have not yet figured out whether memory impairment is caused by insufficient information coding or insufficient information retrieval capabilities.
This time, Tonegawa Jin of the Massachusetts Institute of Technology and his research team tried to solve this problem by studying three different genetically modified mice. These mice suffer from amnesia and cannot complete long-term memory tests. The researchers found that the optogenetic method of stimulating the imprinted cells of the hippocampal dentate gyrus can restore the memory of early Alzheimer’s disease mice, and the function in the contextual fear memory experiment is similar to that of controlling mice. I found that I can do To.
The research team reported that in the early stages of Alzheimer’s disease, the density of dendritic spines in imprinted cells of the dentate gyrus is related to memory loss. Without these units, long-term memory cannot be restored. They need further research to understand whether the storage capacity for maintaining long-term memory will decrease with the development of Alzheimer's disease, and the mechanism behind the cognitive impairment of non-intermittent memory also needs further research.