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Alzheimer's: Discovery of a protein that rebuilds synapses and restores memory |  WH3 – System 103 – Radio Rayo de Luz – Radio Leader

Alzheimer's: Discovery of a protein that rebuilds synapses and restores memory | WH3 – System 103 – Radio Rayo de Luz – Radio Leader

Hope against Alzheimer's disease may lie in a protein that scientists have discovered is able to rebuild synapses, the connections between nerve cells that allow memory formation and retrieval. The alternative approach differs from most current research on treatments for the disease.

The key lies in the protein KIBRA, which is found in the kidneys and brain, in so-called synapses.

“Instead of trying to reduce toxic proteins in the brain, we are trying to reverse the damage caused by Alzheimer's disease to restore memory,” explained Grant Kao, co-author of the study and a scientist at the Buck Institute in the US.

New treatment

When studying the protein, the group found something incredible.

“What we have identified is a mechanism that can be targeted to repair synaptic function, and we are now trying to develop a treatment based on this work,” Grant said.

The higher the level of KIBRA in the cerebrospinal fluid and the lower the level of KIBRA in the brain, the more severe the dementia.

“Our work supports the possibility of using KIBRA as a treatment to improve memory after the onset of amnesia, even if the toxic protein that caused the damage remains,” Christine said.

Traditional treatments

Today, much of the scientific research on Alzheimer's disease focuses on reducing toxic proteins such as tau and beta-amyloid.

These, in turn, accumulate in the brain as the disease progresses, leading many scientists to believe that the key to reversing the disease may lie there.

“We wondered how low levels of KIBRA affect signaling at the synapse and whether a better understanding of this mechanism could provide some insights into how damaged synapses are repaired during Alzheimer's disease.”

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How to rebuild synapses

To learn how KIBRA affects synapses, they created a shortened, functional version of the protein in laboratory mice.

The animals had a disease that mimicked human Alzheimer's disease.

Thus, the protein was able to rescue the mechanisms that promote synaptic plasticity.

“Interestingly, KIBRA restored synaptic function and memory in mice, although the problem of toxic tau accumulation was not resolved,” said study co-author Christine Pareja-Navarro.

Promising future

Now, with the discovery of a new frontier of study, the future is promising.

The team also highlighted the importance of continuing research that helps reduce toxic proteins, but KIBRA could be a valuable addition to science.

“Reducing toxic proteins is clearly important, but repairing synapses and improving their function is another crucial factor that can help,” Tracy concluded.