Alzheimer’s disease is the sixth most common cause of death in the United States. Someone develops the disease every 67 seconds. Yet, there are no effective treatments for Alzheimer’s and no underlying cause has ever been identified. “It’s really astonishing,” said Dr. Kurt Lucin, assistant professor of biology at Eastern Connecticut State University. “There are certain genetic mutations that can severely increase your risk, but an estimated 95% of cases are sporadic. They just occur and no one knows why.”
Dr. Lucin is investigating what could be a key player in Alzheimer’s disease – the protein Beclin-1. “Traditionally it is thought that [Beclin-1] controls autophagy,” explained Dr. Lucin. “This is a process in the cell that allows for the elimination of material that isn’t needed anymore. Research I’ve done suggests Beclin-1 also has other roles, like regulating the movement of receptors. So if Beclin-1 is impaired, then [cells] may not be finding things they need in an appropriate way,” said Dr. Lucin. Interestingly, previous studies have found that Beclin-1 levels are reduced in the brains of Alzheimer’s patients.
Beclin-1 is found in all cells of the body. This includes astrocytes, which are a neuronal support cell and the most numerous cell type in the brain and spinal cord. While other studies have investigated the consequences of reduced Beclin-1 levels on neuronal function, the role of Beclin-1 in astrocytes is unclear. In addition to supporting neurons, astrocytes have been shown to eat amyloid beta, a protein that forms dense plaques in the brains of Alzheimer’s patients. “So, if the ability of astrocytes to eat is impaired, then maybe by increasing Beclin-1 they would be better at eating these plaques,” said Dr. Lucin.
Dr. Lucin and undergraduate student researchers will be investigating this possibly revolutionary hypothesis this summer and fall. “Students will be doing all the experiments. They’ll be culturing the cells, altering the levels of Beclin-1, and then culturing the astrocytes with the neurons,” said Dr. Lucin. Students will measure the astrocytes’ ability to eat particles via a process called “phagocytosis.” In phagocytosis, a cell engulfs and absorbs a solid particle. “We supply florescent beads and see how, or if, they get them. You wait 24 hours and you can use a microscope to see how many cells are filled with beads. I have movies of this happening – the cell approaching and moving and picking it up. They’ll eat twenty beads sometimes. They are hungry things.”
If Dr. Lucin’s hypothesis is correct, it would dramatically increase understanding of the mechanisms behind Alzheimer’s disease. It could even potentially lead to effective therapies. Potentially, a virus could be genetically engineered to infect astrocytes and boost their levels of Beclin-1.