Reversing memory loss

April 19, 2013
Aplysia_californica

Aplysia californica (credit: Nordelch/Wikimedia Commons)

Neuroscientists at The University of Texas Health Science Center at Houston (UTHealth) have reversed memory loss in sea-snail nerve cells by by retraining them on optimized training schedules.

This may be a major step in helping people with memory loss tied to brain disorders such as Alzheimer’s disease, the researchers suggest.

“Although much works remains to be done, we have demonstrated the feasibility of our new strategy to help overcome memory deficits,” said as well as

This latest study builds on a 2012 investigation by John “Jack” Byrne, Ph.D., the study’s senior author, that pioneered this memory enhancement strategy. He is also director of the W.M. Keck Center for the Neurobiology of Learning and Memory and chairman of the Department of Neurobiology and Anatomy at the UTHealth Medical School.

The 2012 study showed a significant increase in long-term memory in healthy sea snails called Aplysia californica, an animal that has a simple nervous system, but with cells having properties similar to other more advanced species including humans.

A mathematical model for prime-time learning

Yili Zhang, Ph.D., the study’s co-lead author and a research scientist at the UTHealth Medical School, developed a sophisticated mathematical model that can predict when the biochemical processes in the snail’s brain are primed for learning. Her 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,” Byrne said. “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.”

To test whether their strategy would help with memory loss, Rong-Yu Liu, Ph.D., co-lead author and senior research scientist at the UTHealth Medical School, 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,” Byrne said.

He added, “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.”