Third Public Conference: Cellular Aging and Apoptosis
June 22, 2000

Introduction

In the 1990s, cellular aging and apoptosis gained prominence as two of the most exciting topics in biology. Today, science is on the cusp of appreciating how these processes are involved in human disease. This frontier was the focus of a one-day symposium at Harvard Medical School, where the Giovanni Armenise-Harvard Foundation brought together some of the world's leading researchers on cellular aging and apoptosis. Held on June 22, 2000, the program drew more than 250 enthusiastic researchers, clinicians, and students from HMS, other Boston-area medical and scientific institutions, and five Italian universities where the Foundation underwrites basic scientific research. The aging and apoptosis symposium capped a week of events that began with the naming of an HMS research building for Count Giovanni Auletta Armenise, whose generosity created the Foundation, and continued with the Foundation's 4th Annual Scientific Symposium.

Although aging cells stop dividing when senescence sets in, they remain metabolically active for a time. In apoptosis, however, healthy cells abruptly decide to kill themselves. "Although both phenomena have been investigated for years, only now are researchers gaining a molecular and biochemical understanding of how they work," said program chair Peter M. Howley, Fabian Professor of Pathology and head of the Department of Pathology at HMS. It is increasingly clear that some diseases are caused by the inappropriate engagement of these normal cellular processes. A dramatic example of aging gone wrong is Werner's disease, a syndrome that prematurely transforms children into wizened, debilitated versions of elderly adults. Apoptosis, on the other hand, has been associated with progressive neurological disorders including Alzheimer's disease and amyotrophic lateral sclerosis. Cancer researchers like Dr. Howley are also intrigued by new findings about cellular aging and apoptosis, because only cells that escape or overcome these processes turn into cancer cells. Ultimately, scientists hope that a better understanding of these basic events will open the door to novel therapies for diseases now considered difficult, or even impossible, to treat.


Contents of the Public Conference

  Introduction

  Cancer, Aging and the Double-edged Sword of Cellular Senescence

  A Link Between Silencing, Metabolism and Aging

  Regulation of the Oxidative Stress Response and Life Span by the Mammalian Shc Gene

  Integrating the Cell-Death Pathway

  The Proteases to Die For

  The Genetic Basis for Neurodegeneration in Alzheimer's Disease

 

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