The brains of birds could reveal how human brains malfunction in diseases like Parkinson's and Alzheimer's. Duke Neurobiology's Erich Jarvis, Ph.D. and Richard D. Mooney, Ph.D. use zebra finches to research neurodegeneration. Their work is featured in a recent article in The Scientist.
Richard Mooney’s grandfather, a mechanical engineer, couldn’t imagine why birds would be useful for understanding the human brain. “The same way that taking apart a one-cylinder lawn mower can prepare you for how a supercharged V8 in a Formula One racer works,” explained Mooney, a neurobiologist at Duke University Medical Center. In fact, striking similarities between songbird and human brains are now driving bird neurobiology research in a new direction: the study of human neurodegenerative diseases.
Songbirds and people share the rare ability to learn vocal patterns through imitation, a skill driven by similar brain areas that have functionally converged over evolutionary time. This is true even at the genetic level, as Mooney’s Duke neurobiology colleague Erich Jarvis demonstrated in 2014. Songbird gene expression in these brain regions more closely resembled that of humans’ than that of chickens’, and human gene expression was closer to that of songbirds than to that of a fellow primate, the macaque.
One of these regions, known as Area X in birds, is a basal ganglia subarea dedicated to song learning. In the most common laboratory songbird, the zebra finch (Taeniopygia guttata), Jarvis and others have shown that dopamine sent to Area X from the midbrain plays a key role in song variability. When not in the presence of females, male finches sing “undirected songs,” perhaps to practice, that are more variable than the songs they use to attract mates. The less variable, female-directed songs are accompanied by an influx of the neurotransmitter dopamine into male basal ganglia neurons. That finding is intriguing for researchers interested in speech defects associated with the neurodegenerative disorder Parkinson’s disease, which is marked by both a loss of dopaminergic neurons and basal ganglia damage.