Patients with Alzheimer's disease (AD) may recover lost memories and form new ones, a study from the Massachusetts Institute of Technology has found.
Scientists discovered that although people with early stage AD cannot remember recent events, they still have it in their brains. The problem is, they cannot easily access it.
So Near Yet So Far
While episodic memory decline in AD patients is well recognized by experts, it remains unclear whether this observed amnesia is due to disturbance in encoding and arrangement of episodic data or an impairment in retrieval of stored memory.
In the new study, MIT scientists were able to successfully stimulate those memories via artificial means using a method called optogenetics. Although this technique cannot be used in humans, this still provides valuable information that can help develop future treatments for memory decline in early-stage AD patients.
"The important point is, this a proof of concept," says study author Susumu Tonegawa. Such idea signifies that not being able to remember a memory does not mean it is entirely lost in the brain. The memory is still there, it's just a matter of how to access it again.
Losing Memories Fast
Tonegawa has identified specific cells in the brain's hippocampus that store specific memories. The team has found that they can manipulate these cells such that they can instill false memories, activate past memories or modify the emotional connection present in each memory.
During one of their investigations, they found that mice models that cannot remember the events that happened before a stress or injury, suffered from memory recall but can still form new memories. With this, the team thought about how this may also be true for patients with early stage AD, when plaques are not yet pronounced in the brain.
The researchers studied two groups of mice, one that was genetically engineered to have AD and another one that was generally healthy.
The mice were exposed to a foot shock inside a chamber. An hour later, the researchers placed the mice back to the same chamber and both groups showed fear. However, after a week, when the mice were put back inside the said chamber, only the healthy mice showed fear, signifying that the AD mice have already forgotten the foot shock experiment.
All About The Access
The scientists, however, were able to show that despite not being able to remember the foot shock experiment, the memory is still there. They demonstrated this by tagging a fearful event-associated cell linked with a light-sensitive protein technique which they developed back in 2012.
When the researchers activated the tagged cells with light, the normal mice recalled the memory. When they did this to the AD mice placed in a chamber they have never seen before, the animals showed immediate fear.
"Directly activating the cells that we believe are holding the memory gets them to retrieve it," says study author Dheeraj Roy. This means that the problem is not about losing the memory, it is about how to gain access to that memory again.
Rudolph Tanzi from Harvard Medical School says this study is remarkable and is the first to prove that the earliest memory problem in AD involves information retrieval issues. With this, the professor, who was not involved in the study, finds developing AD treatments that centers on boosting synapses or brain connections to be exciting.
The study was published on Wednesday in the journal Nature.