What inspired you to pursue aging research?
As a myelin biologist, I am very interested in understanding the factors that guide myelin dynamics throughout life. Much of the work related to myelination has focused on developmental myelination early in life and myelin plasticity in adulthood, with less focus on aging. We know that with normal aging, there is a decline in myelination potential, but the mechanisms driving this remain incompletely understood. I believe understanding these aging-associated myelin changes will garner a number of insights related to the role of myelin in normal cognitive processes, how its dysregulation will impact aging-associated cognitive decline, and consequently how this aging-associated myelin dysregulation may influence pathology in the aging brain.
In your view, what does AFAR mean to the field, and what does it mean, for you, to receive an AFAR grant now?
AFAR is instrumental in our understanding of what healthy aging means.
The AFAR-supported research is imperative to the growth of my lab, which is working at the intersection of myelination and sleep, given the known dysregulation of both of these processes with aging. I believe we learn the most about biological processes by studying what happens in both normative and aberrant states. Sleep disturbances are not only disruptive to cognition but also accelerate aging phenotypes. Thus, understanding how sleep is regulated normally and how it is disrupted in aging will allow us to find new therapeutic strategies to enhance sleep quality, which may minimize aging-associated cognitive decline.
What is exciting about your research’s potential impact?
Neuron-centric mechanisms have dominated sleep research, with the discovery of hypocretins/orexins revolutionizing sleep science. Despite this, nearly 70 million people suffer from sleep disorders in the United States, with increasing prevalence as we age. I posit that one reason for this is that sleep science has neglected the role of glia in sleep. One component underexplored in our understanding of glia in sleep regulation is the role of oligodendroglia in this process. Our work identifies a putative mechanism by which neurons and oligodendrocytes may interact during aging to regulate sleep and arousal, and subsequent cognition.
How would you describe your research to a non-scientist?
The brain consists of two main classes of cells—neurons and glia. Historically, the majority of neuroscience has focused on neurons despite glia being imperative to neural circuit dynamics. Glia comprise more than half of the cells in the brain and perform such diverse functions as maintaining structure and support between neurons, immune modulation within the nervous system, and myelination. Myelin, the multi-layered structure that encapsulates neuronal axons, facilitates essential communication between neurons. Myelin is produced by glial cells called oligodendrocytes. Our work focuses on understanding how these oligodendrocytes regulate sleep and cognition as we age and how disruptions in myelination may contribute to the known deficits in sleep and cognition with aging.
