In a significant stride toward combatting Alzheimer’s disease, scientists at the Buck Institute have unearthed a potential method to repair damaged synapses, a key aspect of memory loss in Alzheimer’s patients.
While current treatments focus largely on slowing the disease’s progression, this new approach offers hope for restoring lost memories.
The study, led by Buck Assistant Professor Tara Tracy, PhD, adopts a different strategy from traditional methods targeting toxic proteins like tau and amyloid beta.
Instead, the team delved into understanding the role of a protein called KIBRA, crucial for synapse formation and memory retention. Their findings, published in The Journal of Clinical Investigation, suggest that enhancing KIBRA levels could reverse synaptic damage caused by Alzheimer’s.
Dr. Tracy explained, “Rather than trying to reduce toxic proteins in the brain, we are trying to reverse the damage caused by Alzheimer’s disease to restore memory.” The team discovered that brains affected by Alzheimer’s exhibit lower levels of KIBRA, indicating a potential link between KIBRA deficiency and synaptic dysfunction.
The study unveiled a correlation between higher KIBRA levels in cerebrospinal fluid and increased dementia severity, as well as a surprising connection between KIBRA and tau protein levels. This insight could pave the way for KIBRA to serve as a biomarker for synaptic dysfunction, aiding in diagnosis and treatment planning.
To test their theory, researchers engineered a functional version of the KIBRA protein and administered it to mice with Alzheimer’s-like conditions. Remarkably, the modified KIBRA protein reversed memory impairment in these mice, showcasing its potential as a therapeutic agent for memory restoration.
Kristeen Pareja-Navarro, co-first author of the study, highlighted, “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.”
The implications of this discovery are profound, offering a new avenue for Alzheimer’s treatment. Dr. Tracy emphasized, “Reducing toxic proteins is important, but repairing synapses and improving their function is another critical factor that could help.” This breakthrough holds promise for the future of Alzheimer’s research and treatment.
The study was funded by various organizations including the National Institutes of Health, the Alzheimer’s Association, and the Larry L. Hillblom Foundation, among others. The authors declared no conflicts of interest.
The citation for the study is: “KIBRA repairs synaptic plasticity and promotes resilience to tauopathy-related memory loss” (DOI: /10.1172/JCI169064). Researchers Lei Yao, Jackson H. Chen, Ivy Wong, Helen Cifuentes, Samah Shah, and Birgit Schilling were also integral to the study.
As Alzheimer’s continues to challenge the medical community, breakthroughs like this offer renewed hope for millions affected by the disease.