UI neuroscientists discover mechanism crucial to memory storage

Neuroscientists at the University of Iowa have found a protein folding mechanism in mice that helps with memory storage and hope it will help treatment of human patients suffering from neurodegenerative diseases.

Contributed+of+Snehajyoti+Chatterjee

Contributed of Snehajyoti Chatterjee

Anthony Neri, News Reporter


A neuroscience research team at the University of Iowa has discovered a crucial biochemical mechanism that impacts memory storage. Its research article was published in the journal Science Advances on March 23.

Snehajyoti Chatterjee, a UI postdoctoral scholar in the Ted Abel Lab and lead researcher on the project, said mice with neurodegenerative diseases regained their long-term memory when his research team reactivated the mechanism.

While researchers have previously found ways to restore memory in rodents, this method is novel, Chatterjee said.

“We found that protein folding is a critical machinery that drives memory consolidation,” he said.

Chatterjee termed the mechanism a “multiprotein chaperone complex.” It folds proteins on the surface of cells and connects the neurons to a larger network of neurons.

“We also found that this machinery is downregulated [weakened] in diseases associated with memory impairment such as Alzheimer’s disease and related dementias,” he said.

Ted Abel, director of the Iowa Neuroscience Institute and chair and DEO of the UI department of neuroscience and pharmacology, said Chatterjee made the discovery after he took creative liberty with his microscope.

“That gave us this new class of memory molecules, and we then went on to show that it was linked to neurodegeneration,” he said.

Abel said once a protein is folded, it changes the function of connections between neurons.

“It’s particularly folding proteins that are on the cell membrane that are kind of the cell’s connection to the world,” Abel said. “We identified a particular protein that’s involved with that, and we’re working to identify more.”

Abel said the team hopes the discovery can eventually improve the treatment of human patients suffering from neurodegenerative diseases.

Although the application of this memory reversal is not yet proven to work and is “ways down the road,” Abel said the team’s findings in rodents are encouraging.

“You might imagine that as the pathology happens, you lose the ability to store memories and you can’t get it back,” he said. “So, the first thing that our research says is that you can, at least in rodents, but at least you can.”

Abel said the new mechanism might be used as a marker of the progression of Alzheimer’s Disease. Since a major challenge of neurodegenerative diseases is tracking the disease before the patient suffers memory deficits, these markers may be part of a future solution.

“We don’t really have the markers of the origin of the disease [right now],” he said. “So these molecular markers we’re studying we would predict would be more of an origin of disease.”