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The early stages of Alzheimer's disease often involve a subtle decline in short-term memory, along with other growing challenges such as mood swings, disorientation, and difficulty concentrating.
As the disease progresses, these effects can take a toll on both patients and their families. In some cases, family and friends may begin to notice signs of a particularly cruel symptom: social memory loss, which robs patients of their ability to recognize loved ones.
A new study in mice by scientists at the University of Virginia School of Medicine and Virginia Tech has recently found that disruptions in specialized structures that support the junctions between neurons may play a critical role in this gradual memory loss.
"Finding a structural change that explains a specific memory loss in Alzheimer's disease is very exciting. It's a completely new target, and we already have suitable candidates for finding the right drugs ," says University of Virginia neuroscientist Harald Sontheimer.
In healthy adults, structures called the perineuronal reticulum form a mesh-like matrix around neurons in certain regions of the brain, where they regulate neural plasticity, protect against oxidative stress, and stabilize the synaptic contacts that connect neurons together.
These stabilizing networks enable proper communication between neurons in the brain, as Sontheimer and other experts have discovered in previous research, and this communication is important for the neurons' ability to record and store memories.
Suspecting that the failure of these networks may play a role in the progression of Alzheimer's disease, the study authors designed the new study to investigate this idea in mice.
When perineuronal networks were damaged in a part of the hippocampus known as CA2, the mice lost the ability to remember other mice, despite retaining the ability to form new memories about objects in their environment.
While studies in mice don't always translate to humans, the results resemble the common experiences of people with Alzheimer's, in which social memory often fades before object memory. Previous research has suggested that CA2 is essential for social memory.
"In Alzheimer's disease, people have difficulty remembering their family and friends, due to the loss of a memory known as social memory. We found that the mesh-like covering known as the perineuronal reticulum protects these social memories ," says lead author Lata Shaunsali, a graduate student in neuroscience at the University of Virginia.
Beyond uncovering a possible mechanism, the authors also tested whether they could prevent the loss of social memories in mice by disrupting it. They used matrix metalloproteinase (MMP) inhibitors, which are also being studied as potential anti-cancer drugs.
These drugs block the activity of MMPs, enzymes that can digest extracellular matrix proteins like those in perineuronal networks. If MMP inhibitors can preserve those networks, researchers hope that these compounds might also protect social memory.
Their experiments with a mouse model of Alzheimer's disease seem to confirm this hope. Mice given MMP inhibitors suffered less degradation of their perineuronal networks, the study found, and retained more social memory functions, despite having Alzheimer's disease.
"In our study with mice, when we kept these brain structures intact from early life, the mice suffering from this disease were better at remembering their social interactions," says Shaunsali.
" Our research will help us get closer to finding a new, non-traditional way to treat or even better, prevent Alzheimer's disease, something that is sorely needed today ," she adds.
Around 55 million people worldwide are currently living with dementia, with Alzheimer's disease accounting for more than 60 percent of cases. As populations continue to age, these numbers are expected to rise, potentially exceeding 80 million within the next decade.
The new findings are promising, the researchers say, but they are still preliminary. More research will be needed to confirm these results and explore their applicability to our own species.
"Although we have drugs that can delay the loss of perineuronal networks, and thus delay memory loss in the disease, more research needs to be done on the safety and effectiveness of our approach before it can be considered in humans ," says Sontheimer./ Adapted from "Sciencealert"
*The study was published in “Alzheimer & Dementia: The Journal of the Alzheimer's Association”.
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