As he works in the lab, Research Assistant Professor Jason Gerstner is kept company by hundreds of little companions on his bench. Tiny fruit flies bounce off the walls of small, clear vials standing up in cardboard containers.
The flies are the featured actors in research done by Gerstner’s team. They’re exploring the role that specific fatty acid binding proteins can play in improving the quality of life for Alzheimer’s patients.
So how do the fruit flies fit in? Years ago, scientists decoding the human genome found that the fly — known as Drosophila melanogaster — is remarkably similar genetically to human beings. And, Gerstner says, the fruit fly is an excellent model organism to study neurogenerative diseases such as Alzheimer’s, since they exhibit many of the hallmark traits as Alzheimer’s patients, making it a perfect – and relatively inexpensive – medium for experiments. Another benefit of working with the flies is that their life cycle is so short that scientists don’t have to wait long before they see results.
Gerstner says scientists have long known that it is common for Alzheimer’s patients to suffer from disrupted sleep. Relatively recently, however, researchers theorized that improving sleep can delay the onset of their disease. The culprit may be peptides known as beta-amyloid (or amyloid-B), which sometimes clump together in the brains of Alzheimer’s patients and play a role in the onset and advancement of the disease.
Gerstner and his team postulate that fatty acid binding proteins may nullify the effects of beta-amyloid, which could lead to better, uninterrupted sleep and greater quality of life for Alzheimer’s patients. So they’ve been working with Alzheimer’s disease models in flies to see how changing levels of fatty acid binding proteins counteract the sleep disruption induced by beta-amyloid. He and his team recently published these findings in the Journal of Neuroscience Research.
Next, they’ll test other Alzheimer’s models to see if they can recapitulate these observations and determine if molecules in their fatty acid binding protein pathways can improve negative outcomes of other toxic compounds associated with Alzheimer’s and other neurodegenerative diseases. Gerstner hopes these discoveries will lead to new therapeutic strategies that delay or arrest the progression of Alzheimer’s and other neurodegenerative diseases.