SEOUL, South Korea: A new study has identified a possible molecular mechanism that could help explain how Alzheimer’s disease damages connections between brain cells and eventually affects memory and thinking.
Researchers at South Korea’s Institute for Basic Science found that abnormal activity of a receptor molecule called ERBB4 in a specific type of excitatory neuron may trigger several changes associated with Alzheimer’s disease.
Amyloid plaques and tau tangles have long been considered major features of Alzheimer’s disease. However, scientists have increasingly focused on how these abnormalities contribute to excessive activity in neurons, loss of connections between brain cells and changes in supporting brain cells.
The new findings suggest ERBB4 may be an important link between these processes.
Researchers found that a specific group of excitatory neurons appeared during the early stages of Alzheimer’s-like disease and contained the ERBB4 receptor, which helps nerve cells respond to signals from other cells.
The scientists also examined astrocytes and microglia, two types of brain cells that support neurons and help remove damaged or unnecessary neural connections.
In mice showing Alzheimer’s-like symptoms, the researchers found that astrocytes and microglia increasingly removed connections between otherwise healthy excitatory neurons.
The findings suggest that Alzheimer’s disease may involve more than the weakening or loss of connections between neurons. The brain’s own maintenance system may also begin removing healthy connections, potentially contributing to cognitive decline.
The researchers said abnormal ERBB4 activity could play an important role in this process, offering a possible target for future research into Alzheimer’s disease.
The findings were based on experiments involving mice and do not establish that ERBB4 is the sole cause of Alzheimer’s disease in humans. Further research will be needed to determine whether the mechanism operates in people and whether targeting ERBB4 could lead to effective treatments.
