A team of neuroscientists from the University of Texas Medical School at Houston reversed memory loss in nerve cells of the California sea hare (Aplysia californica). They were able to help the cells compensate for memory loss by retraining them through the use of optimized training schedules.
The California sea hare, Aplysia californica
“Although much works remains to be done, we have demonstrated the feasibility of our new strategy to help overcome memory deficits,” said Dr John Byrne, senior author of a study published in the Journal of Neuroscience.
The current study builds on Dr Byrne’s 2012 investigation that pioneered this memory enhancement strategy. The 2012 study showed a significant increase in long-term memory in healthy A. californica, an animal that has a simple nervous system, but with cells having properties similar to other more advanced species including humans.
The team has developed a sophisticated mathematical model that can predict when the biochemical processes in the snail’s brain are primed for learning. The model is based on five training sessions scheduled at different time intervals ranging from 5 to 50 minutes. It can generate 10,000 different schedules and identify the schedule most attuned to optimum learning.
“The logical follow-up question was whether you could use the same strategy to overcome a deficit in memory. Memory is due to a change in the strength of the connections among neurons. In many diseases associated with memory deficits, the change is blocked,” Dr Byrne said.
To test whether their strategy would help with memory loss, the neuroscientists simulated a brain disorder in a cell culture by taking sensory cells from the sea snails and blocking the activity of a gene that produces a memory protein. This resulted in a significant impairment in the strength of the neurons’ connections, which is responsible for long-term memory.
To mimic training sessions, cells were administered a chemical at intervals prescribed by the mathematical model. After five training sessions, which like the earlier study were at irregular intervals, the strength of the connections returned to near normal in the impaired cells.
“This methodology may apply to humans if we can identify the same biochemical processes in humans. Our results suggest a new strategy for treatments of cognitive impairment. Mathematical models might help design therapies that optimize the combination of training protocols with traditional drug treatments,” Dr Byrne said.
“Combining these two could enhance the effectiveness of the latter while compensating at least in part for any limitations or undesirable side effects of drugs. These two approaches are likely to be more effective together than separately and may have broad generalities in treating individuals with learning and memory deficits.”
The study is a major step in efforts to help people with memory loss tied to brain disorders such as Alzheimer’s disease.
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Bibliographic information: Rong-Yu Liu et al. 2013. Deficit in Long-Term Synaptic Plasticity Is Rescued by a Computationally Predicted Stimulus Protocol. The Journal of Neuroscience, 33 (16): 6944-6949; doi: 10.1523/JNEUROSCI.0643-13.2013
