As a fourth-grader, Sarah L. Simmons kept a lab notebook detailing dissections of mussels, clams, and sea urchins. Once in college at Angelo State University in San Angelo, Texas, Simmons began doing research with the professor who taught her introductory biology class, an experience that left her with a keen desire to combine research and teaching. Just as she finished a PhD in botany at the University of Texas at Austin, a job came up that she couldn’t resist. Among other things, Simmons administers UT’s Freshman Research Initiative, a program that allows students to work in a lab during their first year. She writes about the value and feasibility of such programs in this month’s Critic at Large column.
John Morris (far left) didn’t know anything about research when he began his neurology residency, but an opportunity to study a rare familial dementia soon changed his outlook. By 1984 he’d joined a new effort at Washington University in Saint Louis to study Alzheimer’s disease (AD). Within a year, the effort turned into a full-fledged research center, which Morris now directs. He was instrumental in a collaboration that demonstrated that morphological changes occur years before AD symptoms emerge. “I’m honored to work with such a deeply committed group, including [study] volunteers,” who don’t expect to see AD therapies in their lifetimes, Morris says. He was approached by the Alliance for Aging Research to organize a white paper, discussing the use of biomarkers in Alzheimer’s clinical trials, with Dennis Selkoe, who’s known Morris for 25 years, and has similarly devoted his career to elucidating the complexities of AD. Part of the team that isolated the snarled tau fibrils that are AD’s hallmark, Selkoe also helped devise the amyloid hypothesis, which proposes that overproduction of certain amyloid peptides begins the cascade that leads to plaque formation and cognitive impairment. In this issue’s Thought Experiment, Selkoe and Morris advocate that it is time to use well-studied AD biomarkers to inform clinical trials.
Ole Petersen published his first paper on the pancreas in 1973. Unlike many researchers, Petersen wasn’t interested in diabetes; he wanted to understand how eating controlled secretion of enzymes important for digesting food. “It was a black box,” says Petersen. He had initially intended to become a clinician, but an early job teaching younger med students encouraged him to gain a deeper understanding of the systems he lectured on. Petersen was hooked on research after his first study—which he initiated with a friend in an empty lab space while still in medical school. “No supervisor, no grants. It was pretty crazy,” he remembers. After starting with salivary glands, Petersen quickly jumped to the pancreas, and spent the next 20 years elucidating the function of calcium signaling in normal pancreatic functions. By the mid-90s, only the details remained unresolved, and he decided to avoid “the law of diminishing returns” and find a new angle. Reasoning that pancreatitis, where the enzymes digest the gland itself instead of food, was unmined territory, Petersen has spent the last decade trying to understand what goes wrong molecularly speaking.Accompanying him have been husband and wife Julia and Oleg Gerasimenko, who arrived from Kiev, Ukraine, almost 20 years ago when Julia began her thesis work in Petersen’s lab. Oleg remembers his jump from neurophysiology to an array of new approaches with sanguinity. “Science is always challenging,” he says, “but it’s always stimulating.” In their feature article, “The War Within," the trio discusses how advances in the understanding of pancreatitis illuminate avenues to possible therapies. “Textbooks are no longer silent” about how the pancreas works, Petersen says. Perhaps soon they will also describe new treatments for pancreatic disease.