It is worth considering whether focusing on repairing damaged synapses in neurodegenerative conditions like Alzheimer’s disease, without addressing the causative mechanisms of the condition, will have a significant impact on patient outcomes. While synaptic repair may be beneficial in the early stages of cognitive impairment, it may have limited effectiveness as the condition progresses and underlying mechanisms like protein aggregation and neuroinflammation continue to cause damage. However, it is intriguing to contemplate the extent to which neural function could be maintained in the presence of damaging mechanisms, without directly addressing those mechanisms.
Although current treatments for Alzheimer’s are not particularly effective at regaining memory, new research is exploring the potential of synaptic repair as an alternative approach. This research focuses on a protein called KIBRA, which has been found to be deficient in the brains of individuals with Alzheimer’s disease. Studies have shown that KIBRA is essential for synaptic function and memory formation, and experiments in mice have demonstrated that enhancing KIBRA levels can reverse memory impairment associated with Alzheimer’s. This suggests that targeting synaptic repair, rather than directly addressing toxic protein accumulation, could provide a viable therapy for improving memory in Alzheimer’s patients.
