Alzheimer’s disease is a devastating condition that affects millions of people worldwide. It causes progressive memory loss, cognitive decline, and behavioral changes that impair the quality of life of patients and their caregivers. While some drugs can slow down the disease progression, there is no cure or effective treatment to reverse the memory impairment caused by Alzheimer’s.
However, a new study published in The Journal of Clinical Investigation suggests a novel way to repair the synapses, the connections between neurons that are essential for memory formation and recall, that are damaged by Alzheimer’s disease. The study focuses on a protein called KIBRA, which is involved in synaptic plasticity and memory. The researchers found that KIBRA levels are reduced in the brains of Alzheimer’s patients, and that restoring KIBRA function can reverse the memory problems in mice with Alzheimer’s-like symptoms.
The study was led by Tara Tracy, an assistant professor at Buck Institute for Research on Aging, and co-authored by Grant Kauwe, a staff scientist at Buck. They measured the levels of KIBRA in the cerebrospinal fluid of humans and found that higher levels of KIBRA in the fluid, but lower levels in the brain, correlated with the severity of dementia. They also found a strong relationship between increased levels of tau, a toxic protein that accumulates in the brain during Alzheimer’s disease, and increased levels of KIBRA in the cerebrospinal fluid.
To understand how KIBRA affects synapses, the team created a shortened functional version of the protein and tested it in mice that had a condition mimicking human Alzheimer’s disease. They found that this protein could restore the synaptic function and reverse the memory impairment associated with this type of dementia.
The study suggests that KIBRA could be a potential target for developing new therapies to repair synaptic damage and restore memory in Alzheimer’s patients. The team is now working on developing a drug based on this work.