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Buck Institute Scientists Discover a Potential Way to Repair Synapses Damaged in Alzheimer’s Disease

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A new study proposes a strategy for reversing the memory problems that accompany Alzheimer’s disease and related dementias, exploring an alternative to the laser-focused approach of big pharma to target toxic tau proteins known to go hand in glove with these diseases.

Rather than remove the damaging compound, scientists at the Buck Institute for Research on Aging aimed to reverse the damage the compound caused using an innate protein found in the kidneys and the brain.

“While newly approved drugs for Alzheimer’s show some promise for slowing the memory-robbing disease, the current treatments fall far short of being effective at regaining memory. What is needed are more treatment options targeted to restore memory,” said Buck Assistant Professor Tara Tracy, PhD, the senior author of the study.

The protein in question is called KIBRA, named because it is found in the kidney and the brain. Along with being produced in the kidney, Tracy and her team identified its presence throughout brain synapses, which are the connections between neurons that allow memories to be formed and recalled.

They also found that KIBRA is deficient in the brains of people with Alzheimer’s and dementia.

“We wondered how the lower levels of KIBRA affected signaling at the synapse, and whether understanding that mechanism better could yield some insight into how to repair the synapses damaged during the course of Alzheimer’s disease,” said Buck Staff Scientist ​​Grant Kauwe, Ph.D., co-first author of the study.

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