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Should we expect an approach focused on repair of synapses in neurodegenerative conditions like Alzheimer’s disease, while leaving the causative mechanisms of the condition operating intact, to have a large effect on patient outcomes? Given what is known of the underlying mechanisms of protein aggregation, neuroinflammation, and other problems that ultimately kill neurons, not just damage them, it seems possible that synaptic repair might do well in the early stages of cognitive impairment, but later do little to help as the condition progresses. Regardless, it is interesting to consider to degree to which neural function could in principle be maintained in the face of damaging mechanisms, without actually addressing those mechanisms.
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. Since most current research on potential treatments for Alzheimer’s focuses on reducing the toxic proteins, such as tau and amyloid beta, that accumulate in the brain as the disease progresses, researchers veered away from this route to explore an alternative. The work hinges on a protein called KIBRA, named because it is found in the kidney and the brain. In the brain, it is primarily localized at the synapses, which are the connections between neurons that allow memories to be formed and recalled. Research has shown that KIBRA is required for synapses to form memories, and the team has found that brains with Alzheimer’s disease are deficient in KIBRA.
The team first measured the levels of KIBRA in the cerebrospinal fluid of humans. They found that higher levels of KIBRA in the cerebrospinal fluid, but lower levels in the brain, corresponded to the severity of dementia. To figure out how KIBRA affects synapses, the team created a shortened functional version of the KIBRA protein. In laboratory mice that have a condition mimicking human Alzheimer’s disease, they found that this protein can reverse the memory impairment associated with this type of dementia. They found that KIBRA rescues mechanisms that promote the resilience of synapses. “Interestingly, KIBRA restored synaptic function and memory in mice, despite not fixing the problem of toxic tau protein accumulation. 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.”
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