Mice whose brains had lost a large number of neurons due to neurodegeneration regained long-term memories and the ability to learn after their surroundings were enriched with toys and other sensory stimuli, according to new studies by Howard Hughes Medical Institute researchers.
The scientists were able to achieve the same results when they treated the mice with a specific type of drug that encourages neuronal growth.
The new studies suggest two promising avenues for treatment that might alleviate learning deficits and memory loss in humans with Alzheimer’s disease or other neurodegenerative diseases.
The results of the experiments suggest that the term “memory loss” may be an inaccurate description of the kinds of mental deficits associated with neurodegenerative diseases. “The memories are still there, but they are rendered inaccessible by neural degeneration,” said the senior author Li-Huei Tsai, a Howard Hughes Medical Institute researcher at the Massachusetts Institute of Technology.
Tsai led the research group that published its findings on April 29, 2007, in an advance online publication in the journal Nature.
“I believe that these findings could have particular significance for treatment of people who already have advanced neurodegenerative disease,” said Tsai. “Most current treatments seem to be aimed at affecting the early stages of the disease. But our mouse model shows that even when there has been a significant loss of neurons, it is still possible to improve learning and memory.”
Over the last five plus years, Tsai’s research team has developed and refined a mouse model of Alzheimer’s disease. In earlier studies, Tsai’s group had shown that a protein called p25 contributes to neurodegeneration. Over time they developed a genetically engineered mouse in which they are able to turn on p25 gene expression at specific stages in development. In these animals, evidence of neuronal loss is first detected six weeks after the induction of p25. At this age, animals exhibit a profound impairment in learning and memory that is accompanied by synaptic loss and impaired long-term potentiation (LTP), a process involved in the storage of memories.