Aging involves a set of functional declines that occur at timescales several orders of magnitude slower than most physiologic mechanisms in cell biology and metabolism. At such slow aging timescales, the consequences of molecular events anywhere in an individual have sufficient time to propagate broadly across cells, tissues, and organs to influence potentially any aspect of physiology. New methods are needed to measure, model, and understand the complex causal structure of these long-distance, many-to-many interactions.

In this talk I'll discuss a new approach called "Asynch-Seq" that leverages the natural asynchrony in individual aging rates across a population to map organismal-scale mechanistic interactions. I'll explore what this map tells us about where and how inter-individual variation arises during aging.