Memory loss is a condition that affects millions of people around the world, including those suffering from diseases like Alzheimer’s and dementia. However, despite a wealth of research conducted on the subject, the medical community is constantly finding new explanations to explain the disorder.
One of the latest comes from Dr. Carlos Saura at the Institut de Neurociències (Inc) in Barcelona. He believes that the loss of associative memory is the key factor in broader memory loss, and he has tracked it to a molecular mechanism that takes place in the hippocampus region of the brain.
In basic terms, Saura believes that a certain brain protein, called CRTC1, is disrupted in the brains of people with neurodegenerative disorders. This is important, he explains, because CRTC1 is responsible for regulating neuron function that allows for associative memories to be stored. Restoring CRTC1 function, he says, may reverse memory loss.
"The relevance of this discovery is that activation of specific neurons of the hippocampus reverses memory loss even at late stages of neurodegeneration," said Saura.
Potential therapeutic target
Associative memory is important for remembering much of the information that our brains process. It involves remembering people, situations and places for the long-term. However, previous research has shown that it is one of the first cognitive abilities to falter in patients who develop Alzheimer’s, dementia, and other neurodegenerative disorders.
Saura’s study used a gene therapy approach on mice models that had symptoms of neurodegeneration. Researchers inserted copies of CRTC1 into the hippocampus region of models’ brains and observed whether they could remember a negative experience.
Mice who were treated with the therapy were able to remember the negative experience and changed their behavior to avoid it, while mice who weren’t treated acted as they normally would. The findings give hope of possible therapeutic approaches to treating memory loss in the future.
"These results are exciting since provide strong support for potential translational applications in the clinic because this molecular mechanism could be a new target to reverse memory decline in dementia," Saura concluded.