Researchers have found that Alzheimer’s patients’ failure to recognize family and friends results from a breakdown in the protective networks that surround nerve cells in the brain. Preventing the loss of these networks in laboratory mice protected the mice from losing their memories of previous social interactions.
The new study sheds important light on the development of the disease, and previous studies have revealed the importance of so-called networks surrounding neurons in the brain.
These mesh-like structures surround neurons and serve as a barrier that enables neurons to communicate properly. These connections enable neurons to form and store new memories.
The study was conducted by researchers from the University of Virginia in the United States, and its results were published in the Alzheimer’s Association magazine on October 22, and the Eurek Alert website wrote about it.
Researchers say these results represent an exciting target for developing new treatments that benefit Alzheimer’s patients.
Social memory failure
“Finding a structural change that explains specific memory loss in Alzheimer’s patients is very exciting,” said study co-author Harald Sontheimer, chair of the Department of Neuroscience at the University of Virginia and a member of the University of Virginia Brain Institute.
The researchers found that experimental mice whose networks were defective lost their ability to remember other mice – that is, their social memory – although they were still able to form new memories about things in their environment. This mimics what is observed in Alzheimer’s patients, where social memory often fails before memory of objects.
Sontheimer and his team then used a class of experimental drugs being tested for their potential to treat cancer and arthritis, to see if they could prevent the loss of surrounding neural networks. This method prevented deterioration of the networks and preserved the mice’s social memory.
The changes the scientists observed in the brains of mice are consistent with those observed in human Alzheimer’s patients, suggesting that targeting networks in humans could provide similar benefits.