BY KRISTA CONGER

Add this to your list of things to worry about: Even if you avoid heart disease and cancer as you grow older, you still may have to contend with degenerative brain disorders.

That's according to Nobel laureate Stanley Prusiner, who participated in the first Stanford Symposium on Aging: Biology, Disease and Economics. The March 13 event brought together experts in the fields of biology, neurology and economics of aging. Participating scientists described current advances in the understanding and treatment of age-related diseases and discussed how the advances may affect public policy decisions, including health care for the elderly and saving for retirement.

The symposium was organized by Helen Blau, PhD, chair of the molecular pharmacology department and director of gene therapy technology; Alan Garber, MD, PhD, professor of primary care and outcomes research; and William Mobley, MD, PhD, professor of neurology. It was supported in part by a grant from the Ellison Medical Foundation.

Prusiner, MD, professor of neurology and biochemistry at UC-San Francisco, delivered the Sterling Drug/Maurice L. Tainter Lecture at the symposium. He received the 1997 Nobel Prize in medicine for his discovery of prions, infectious protein particles that cause bovine spongiform encephalopathy (also known as mad cow disease) and its human counterpart, Creutzfeldt-Jakob disease.

Prusiner summarized recent findings in the field of prion research and compared prion diseases to such diseases as Parkinson's, Alzheimer's and amyotrophic lateral sclerosis, also known as Lou Gehrig's disease.

"What I really want to do is to try to put prion disease in perspective with other neurodegenerative diseases," said Prusiner, who directs the Gladstone Institute for Neurodegenerative Disease at UCSF.

The prion protein can assume different conformations. In its normal state, no disease occurs. But when alternatively folded prion proteins accumulate in the brain, the result is neurodegeneration and death. Brain sections from humans and animals who have died from prion disease are pockmarked with vacuoles, giving them a spongy appearance.

A common factor in prion diseases and disorders such as Alzheimer's and Parkinson's is the age at which symptoms first appear, said Prusiner.

"The major risk factor for most of these diseases is aging and there's no way to get around it," Prusiner said. He speculated that as time goes by, the rate of formation of the misfolded protein eventually exceeds the capability of the brain to remove it.

And like the other neurodegenerative diseases, prion disease can be caused by a genetic mutation or it may occur sporadically.

"If you live long enough and aren't killed by cancer or heart disease and you carry the genetic mutation, you will eventually get prion disease," Prusiner said.

Blau, in addition to help organize the symposium, also delivered a talk about her recent research. She and members of her lab discovered that adult bone marrow cells can travel to the brain and assume neuronal characteristics. The work may one day lead to new treatments for neurodegenerative diseases of aging.

Other speakers at the symposium included Eric Olson, University of Texas Southwestern Medical Center; Cynthia Kenyon, UCSF; Leonard Guarente, MIT; Donald Price, Johns Hopkins School of Medicine; Mahlon DeLong, Emory University School of Medicine; David Wise, Harvard University; James Poterba, MIT; and Victor Fuchs, PhD, Stanford.

The Sterling Drug/Maurice L. Tainter lectureship was established in 1986 in the department of molecular pharmacology in honor of Maurice L. Tainter, MD, a graduate of the School of Medicine and former faculty member in the department who subsequently became vice president of Sterling Drug, Inc.