"Brain Bursts" Improve Learning and Memory
Neuroscientists offer new clues on Alzheimer's and reversing memory loss.
Posted Apr 19, 2013
Although the genetic link to Alzheimer's disease is strong, neuroscientists published studies this week showing that daily lifestyle choices that stimulate "Brain Bursts" may help protect against Alzheimer’s and that it is possible to reverse memory loss.
Researchers have known for years that mental workouts like crossword puzzles and exposure to enriched environments alter the brain’s neural circuits and improve learning and memory. This week scientists made major advances in confirming that Alzheimer’s is not just driven by genetic mutations, but by physiological mechanisms as well.
“High-frequency bursts” of brain activity improve memory encoding, information processing, and neuroplasticity. For more on how to create these brain bursts you can check out my Psychology Today blogs "The Brain Drain of Inactivity" and "Enriched Environments Build Better Brains".
“Brain Bursts” May Help Protect Against Alzheimer’s
Scientists are beginning to better understand the specific mechanisms of how patterns of electrical pulses (called “spikes”) trigger a cascade of changes in neural circuits linked to learning and memory.
In a report published on April 18, 2013 in the journal Nature Neuroscience researchers from Tel Aviv University suggest that ‘stimulant-rich’ environments and problem solving puzzles could be a contributing factor in preventing or delaying the onset of Alzheimer’s disease in some people.
The accumulation of amyloid-beta proteins is linked to the development of Alzheimer's disease. The disease is triggered by an imbalance in two different amyloid proteins—which form a plaque found in the brains of Alzheimer's patients. A reduction in the relative level of healthy amyloid-beta 40 compared to 42 is linked to Alzheimer’s. Dr. Inna Slutsky of Tel Aviv University's Sackler Faculty of Medicine and colleagues have uncovered two main features of the brain circuits that impact this crucial balance.
The researchers found that spikes in the patterns of electrical pulses in the form of high-frequency bursts combined with the filtering properties of synapses are crucial to the regulation of the amyloid-beta 40/42 ratio. Synapses that transfer information in spike bursts improve the amyloid-beta 40/42 ratio. This research represents a major advance in understanding how brain circuits regulate the composition of amyloid-beta proteins.
According to Dr. Slutsky, different kinds of environmental changes—as well as sensory and emotional experience—can modify the properties of synapses and change the spiking patterns in the brain.
Previous research has suggested that a stimulant-rich environment could contribute to preventing the development of Alzheimer's disease. Crossword and similar puzzles appear to stimulate 'brain bursts' that may protect against Alzheimer's disease. In this recent study, the researchers discovered that changes in sensory experiences also regulate synaptic properties—triggering an increase in amyloid-beta 40.
Reversing Memory Loss
On April 17, 2013 Neuroscientists at the University of Texas Health Science Center at Houston published an article in the Journal of Neuroscience claiming to have successfully reversed memory loss in animal brain cells. "Although much works remains to be done, we have demonstrated the feasibility of our new strategy to help overcome memory deficits," said John "Jack" Byrne, Ph.D., the study's senior author.
The researchers simulated a brain disorder by blocking proteins associated with memory and were able to create a loss of long-term memory. Then, by using a complex mathematical model the researchers were able to determine when the brain cells of a sea snail were primed for learning. The scientists were able to help the cells compensate for memory loss by retraining them through the use of optimized training schedules.
After just five perfectly timed sessions, the impaired neuron connections linked to long-term memory in the healthy sea snails called Aplysia californica returned to near-normal levels. Although sea snails have a simple nervous system, their brain cells have properties similar to humans and other more advanced species.
The study was designed to serve more as a proof of principle, but holds promise for research in fighting the effects of Alzheimer’s disease. "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."
"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."
Conclusion: More Research Needs to Be Done
It is encouraging to see that lifestyle choices can kickstart high-frequency brain bursts that may protect against Alzheimer’s disease and that scientists are discovering ways to reverse memory loss through properly timed training protocols. But, more research needs to be done.
Another study released by Duke Medicine on April 18, 2013 confirmed that the genetic link to Alzheimer's disease is strong. According to the study, close family members of people with Alzheimer’s disease are more than twice as likely as those without a family history to develop silent buildup of brain plaques associated with Alzheimer’s disease. The Duke study raises more questions about genetic factors involved in the disease that have yet to be identified.