The Human Diseasome
Mapping the genetic links among all diseases
Albert-László Barabási, Distinguished Professor of Physics

One of the world’s foremost network scientists, Barabási is leading an interdisciplinary team of researchers on a quest to construct the human “diseasome”—the sum of all human diseases and the ways they relate to one another.

This map of human diseases would revolutionize medicine on all levels, says Barabási, enabling researchers to understand the molecular and genetic linkages between one disease, like asthma, and other respiratory diseases.

The team has already developed a map of 70 of the most common diseases based on their protein and metabolite interactions. As the pool of knowledge about those molecular interactions expands, so will the map.

Once the diseasome is more fully mapped, Barabási says, physicians could use individual genetic mutations as a predictor of future health. And pharmaceutical researchers would have a powerful tool to design drugs with greater precision and effectiveness.

Brain Chemistry
Understanding how the brain works at the chemical level
Heather Clark, associate professor of pharmaceutical sciences

Clark is a leading researcher in the field of nanosensors, and she is applying her expertise to reveal what has eluded generations of scientists: How, exactly, do the chemicals in our brains interact to generate emotions, thoughts, memories, and actions?

More precisely, how do neurotransmitters like glutamate, dopamine, or serotonin behave differently in a patient with Alzheimer’s or schizophrenia versus someone with a healthy brain? Without that knowledge, neuroscience researchers and clinicians are practically working in the dark.

To unlock the brain’s chemical secrets, Clark and her team are in the early stages of developing nanoparticles containing a particular menu of molecules.

These nanosensors will react with different chemicals, producing a detectable signal of brain chemistry in real time and allowing her team to map the brain in greater detail than ever before. This more nuanced understanding of how the brain works will enable an entirely new, and targeted, line of therapies to treat neurological conditions.

Identifying a sleeping cause of chronic infection
Kim Lewis, University Distinguished Professor of Biology

Lewis’s original work on persister cells could refocus the direction of antibiotic drug development by demonstrating that bacterial resistance to antibiotics is not the only cause of chronic infections.

He has discovered that another culprit—persister cells that survive antibiotic treatment by going dormant—are largely responsible for recalcitrance of chronic infections. Once an antibiotic leaves a person’s system, those sleeper cells reawaken and begin their work anew.

Lewis and his team, who have defined the field of persister-cell research, are pursuing two parallel approaches to dealing with these stubborn bacteria. In one, the team examines antibiotic compounds produced by other bacterial cells, which work against persisters; in another, they look for ways to identify synthetic drugs that can kill dormant cells.