Dr. Shermali Gunawardena, University at Buffalo - Neuronal Blockages and Alzheimers
In today’s Academic Minute, Dr. Shermali Gunawardena of the University of Buffalo explains how traffic moves along the neuronal highways in the brain.
Shermali Gunawardena is an assistant professor of biological sciences at the University at Buffalo. Her research seeks to determine if the degeneration of neurons in Alzheimer’s disease and Huntington’s disease is related to a defect in neuronal transport systems.
Dr. Shermali Gunawardena - Neuronal Blockages and Alzheimers
Imagine if you could open up your brain and look inside. What you would see is a network of brain cells called neurons, each one shaped like a cable. If you could go a level deeper and peer inside these cells, you would discover that each cable resembles a highway, housing tiny, microtubule tracks for moving materials between different parts of the cell.
When these roadways are operating smoothly, tiny vehicles called motor proteins carry precious cargo along microtubule tracks. This allows the cell to receive information, make repairs and send instructions to the body. But when a track gets blocked, cells die and serious health problems can occur, like Alzheimer’s disease. Understanding blockages — and how traffic should flow in healthy cells — could offer hope to patients with neurodegenerative disorders.
My latest research shows that a protein called “presenilin” plays an important role in controlling traffic on neuronal highways. In our study, presenilin helped to control the speed at which molecular vehicles called kinesins and dyneins moved. When we cut the amount of presenilin present by half, the motors moved faster. They paused fewer times and their pauses were shorter. Given our data, it’s possible that tweaking presenilin levels could help prevent traffic jams on the neuronal highway. The results were particularly interesting because we know presenilin is involved in Alzheimer’s disease: When the function of presenilin is defective, it helps create harmful build-ups called amyloid plaques that can damage cells.
By showing that presenilin also controls the movement of motor proteins along neuronal roadways, we show that presenilin may play multiple roles in causing disease. In Alzheimer’s patients, transport defects occur well before other symptoms. As a result, developing drugs that prevent these defects would be a useful way to attack the problem early.