Humans are born with the about same number of neurons that we die with, meaning that a neuron can live for 100 years or more. Over the decades of our lives, we show signs of aging – our skin becomes wrinkled, our hair turns gray. Our neurons likewise show signs of aging. This is problematic for health: first, aging is often accompanied by cognitive decline, and second, aging is by far the primary risk factor for dementia and neurodegenerative disease.
Our lab asks, what causes neuronal aging, and can it be prevented?
The nematode Caenorhabditis elegans has evolved the remarkable ability to de-couple the symptoms of aging from chronological age. Normally, C. elegans age and die in two weeks. However, in the alternate organismal state called “dauer,” animals pause all growth and development programs and survive for months. Neurons remain functional, but features of neuronal aging are likewise stalled. We exploit this phenotypic plasticity to investigate how neuron aging can be stalled.
We are particularly interested in the interplay between neuronal aging and endosomes. Aberrant endosome morphology and function is associated with neurodegenerative diseases. We hypothesize that there is a conserved role for the endocytic pathway in promoting the pathologies associated with neuronal aging.
Synaptic vesicles are a highly specialized type of endosome used for the rapid communication of firing activity between connected neurons in a circuit. We are interested in the regulation of synaptic vesicle homeostasis in development versus adulthood, and what causes synaptic vesicle homeostasis to decline in aging.
