(CN) — While most current research on treating Alzheimer’s disease focuses on stopping the condition’s advancement, researchers from the Buck Institute for Research on Aging suggest a way to return what Alzheimer’s stole.
According to their study published Thursday in the Journal of Clinical Investigation, newly approved drugs attempt to reduce toxic proteins such as tau and amyloid beta that accumulate in the brain as the disease progresses. Although the Buck Institute researchers believe that this type of work is important to help Alzheimer's patients, they also believe that a protein called KIBRA is up to the equally important task of restoring the lost memories.
KIBRA’s name comes from its location in the kidney and in the brain. When located in the latter, KIBRA is in the synapses that connect the neurons that allow the brain to form and recall memories. Other research reported that KIBRA is necessary for synapses to form memories, and the team found that brains with Alzheimer’s are deficient in KIBRA.
That gave the researchers the idea to test if they could target KIBRA to repair the synaptic function that Alzheimer’s damaged.
According to senior author of the study and Buck Institute assistant professor Tara Tracy, the researchers first measured the KIBRA levels found in human cerebrospinal fluid. They found the presence of higher levels of KIBRA in cerebrospinal fluid and lower levels in the brain, which Tracy said corresponded to the severity of dementia.
“We also found this amazing correlation between increased tau levels and increased KIBRA levels in the cerebrospinal fluid,” said Tracy. “It was very surprising how strong the relationship was, which really points to the role of KIBRA being affected by tau in the brain.”
With these findings, the team then decided to test the correlation on laboratory mice.
The researchers created a shortened functional version of the KIBRA protein before injecting it into lab mice, which the study said had a condition that mimicked human Alzheimer’s disease. Upon studying the mice, the researchers said they found that the artificial protein could reverse the memory impairment associated with this type of dementia.
Furthermore, the researchers said that KIBRA rescues mechanisms that could make synapses more resilient.
“Interestingly, KIBRA restored synaptic function and memory in mice, despite not fixing the problem of toxic tau protein accumulation,” said Kristeen Pareja-Navarro, co-first author of the study. “Our work supports the possibility that KIBRA could be used as a therapy to improve memory after the onset of memory loss, even though the toxic protein that caused the damage remains.”
Intent on studying KIBRA further, the team said that they wanted to see if they could use the protein as a biomarker of synaptic dysfunction and cognitive decline. That way, it could be useful for diagnosis, treatment planning, tracking disease progression and response to therapy.
“There are different strategies that could be effective in developing treatments for Alzheimer’s disease,” said Tracy. “Our strategy to repair plasticity in the brain could be useful in combination with other therapies to reduce toxicity in Alzheimer’s disease.”
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