An MIT neuroscientist has made a breakthrough discovery that researchers say will open countless doors for future treatments: memories obscured by the devastating illness have the potential to be restored.
“The big message is that there is a way to strengthen these memory cells,” said Dheeraj Roy, doctoral student at MIT and lead author on the study. “If we had a way of restoring the memory of patients, we think this could have a huge impact on society.”
A paper published today online in the science journal “Nature” outlines the study by Roy and his colleagues, which found genetically engineered mice with early-stage Alzheimer’s could recall seemingly “lost” events when memory cells in the brain were stimulated.
The study involved both healthy and memory-impaired mice that were put in boxes and given a shock. Those that did not suffer from memory-loss froze out of fear when placed back in the box. The Alzheimer’s mice were not afraid.
The researchers used a technique known as optogenetics on the mice with memory loss: They injected the memory cells, called “engram cells,” with a light-sensitive protein and activated them using blue light.
The mice immediately showed fear.
The MIT researchers noted that the engram cells of Alzheimer’s mice were missing tiny buds called dendritic spines, which allow neurons to communicate with each other.
The study’s revelations have sent a ripple through the Alzheimer’s research community, and have effectively “shattered a 20-year paradigm of how we’re thinking about the disease,” said Rudy Tanzi, a Harvard neurology professor, who is not involved in the research.
“Since the mid-’80s, it’s been thought that these memories just weren’t getting stored,” Tanzi said. “This paper shows that the information is getting stored — we just can’t access it.”
He added that, while the research is still in the very early stages, it will likely inspire a slew of follow-up studies and pave the way for a new approach to tackling the disease.
“I think we’ll see lots of studies now where people use different techniques and attempts to activate those cells,” Tanzi said. “I can already think of experiments I would try to make that happen.”
The finding is especially important given bumped-up efforts to find new treatments for the age-related illness that is killing more people each year as life spans become longer, according to Dr. Lee Schwamm, executive vice chair of neurology at Massachusetts General Hospital, who is also not involved in the study.
“Nothing could be more important in thinking about the diseases that will plague modern Western society in the next 50 years,” Schwamm said. “It’s not just that there’s no cure, there’s not even a very good treatment.”
Roy’s study was funded by the non-profit Howard Hughes Medical Institute and Japan’s RIKEN Brain Science Institute.
According to Roy, the researchers will conduct further research that studies the various stages of Alzheimer’s.
“Maybe if we tease it apart, it may be more manageable,” he said. “With these neurogenetic tools, the future for me is exciting.”
Roy was motivated to do the research by the loss of his own grandmother to Alzheimer’s disease.
“I watched a person who knew everything about me from Day One become someone who could not remember who I was,” he said. The new research, he said, is “still early, but this gives some hope for the future.”