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Genetics, Vol. 182, 3-9, May 2009, Copyright © 2009
doi:10.1534/genetics.109.103341
The Szilard Hypothesis on the Nature of Aging Revisited
Henrik Zetterberg*,1,
Magnus Båth
,
,
Madeleine Zetterberg
,**,
Peter Bernhardt, and
Ola Hammarsten
* Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at University of Gothenburg, S-431 80 Mölndal, Sweden, Institute of Clinical Sciences, Department of Radiation Physics, The Sahlgrenska Academy at University of Gothenburg, S-413 45 Gothenburg, Sweden, Department of Medical Physics and Biomedical Engineering, The Sahlgrenska University Hospital, S-413 45 Gothenburg, Sweden, Institute of Biomedicine, Department of Medical Chemistry and Cell Biology, The Sahlgrenska Academy at University of Gothenburg, S-405 30 Gothenburg, Sweden, ** Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation, The Sahlgrenska Academy at University of Gothenburg, S-431 80 Mölndal, Sweden and Institute of Biomedicine, Department of Clinical Chemistry and Transfusion Medicine, The Sahlgrenska Academy at University of Gothenburg, S-413 45 Gothenburg, Sweden
1 Corresponding author: Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at University of Gothenburg, S-431 80 Mölndal, Sweden.
E-mail: henrik.zetterberg{at}clinchem.gu.se
This year marks the 50th anniversary of a nearly forgotten hypothesis on aging by Leo Szilard, best known for his pioneering work in nuclear physics, his participation in the Manhattan Project during World War II, his opposition to the nuclear arms race in the postwar era, and his pioneering ideas in biology. Given a specific set of assumptions, Szilard hypothesized that the major reason for the phenomenon of aging was aging hits, e.g., by ionizing radiation, to the gene-bearing chromosomes and presented a mathematical target-hit model enabling the calculation of the average and maximum life span of a species, as well as the influence of increased exposure to DNA-damaging factors on life expectancy. While many new findings have cast doubt on the specific features of the model, this was the first serious effort to posit accumulated genetic damage as a cause of senescence. Here, we review Szilard's assumptions in the light of current knowledge on aging and reassess his mathematical model in an attempt to reach a conclusion on the relevance of Szilard's aging hypothesis today.
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