September 3, 1997
We present a model for biological aging that considers the number of individuals whose (inherited) genetic charge determines the maximum age for death: each individual may die before that age due to some external factor, but never after that limit. The genetic charge of the offspring is inherited from the parent with some mutations, described by a transition matrix. The model can describe different strategies of reproduction and it is exactly soluble. We applied our method to the bit-string model for aging and the results are in perfect agreement with numerical simulations.
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March 17, 1995
We present a simple model for biological aging. We studied it through computer simulations and we have found this model to reflect some features of real populations.
September 29, 1995
We succeeded in obtaining exact results of the bit-string model of biological aging for populations whose individuals breed only once. These results are in excellent agreement with those obtained through computer simulations. In addition, we obtain an expression for the minimum birth needed to avoid mutational meltdown.
July 25, 1995
The bit-string model of biological aging is used to simulate the catastrophic senescence of Pacific Salmon. We have shown that reproduction occuring only once and at a fixed age is the only ingredient needed to explain the catastrophic senescence according the mutation accumulation theory. Several results are presented, some of them with up to $10^8$ fishes, showing how the survival rates in catastrophic senescence are affected by changes in the parameters of the model.
February 1, 2016
Biological aging is characterized by an age-dependent increase in the probability of death and by a decrease in the reproductive capacity. Individual age-dependent rates of survival and reproduction have a strong impact on population dynamics, and the genetic elements determining survival and reproduction are under different selective forces throughout an organism lifespan. Here we develop a highly versatile numerical model of genome evolution --- both asexual and sexual --- ...
July 28, 2000
A stochastic genetic model for biological aging is introduced bridging the gap between the bit-string Penna model and the Pletcher-Neuhauser approach. The phenomenon of exponentially increasing mortality function at intermediate ages and its deceleration at advanced ages is reproduced for both the evolutionary steady-state population and the genetically homogeneous individuals.
November 30, 2000
The sexual version of the Penna model of biological ageing, simulated since 1996, is compared here with alternative forms of reproduction as well as with models not involving ageing. In particular we want to check how sexual forms of life could have evolved and won over earlier asexual forms hundreds of million years ago. This computer model is based on the mutation-accumulation theory of ageing, using bits-strings to represent the genome. Its population dynamics is studied b...
September 29, 2023
The chronological age used in demography describes the linear evolution of the life of a living being. The chronological age cannot give precise information about the exact developmental stage or aging processes an organism has reached. On the contrary, the biological age (or epigenetic age) represents the true evolution of the tissues and organs of the living being. Biological age is not always linear and sometimes proceeds by discontinuous jumps. These jumps can be positive...
February 9, 2001
We generalize the standard Penna bit-string model of biological ageing by assuming that each deleterious mutation diminishes the survival probability in every time interval by a small percentage. This effect is added to the usual lethal but age-dependent effect of the same mutation. We then find strong advantages or disadvantages of sexual reproduction (with males and females) compared to asexual cloning, depending on parameters.
August 28, 2003
We removed from the Penna model for biological ageing any random killing Verhulst factor. Deaths are due only to genetic diseases and the population size is fixed, instead of fluctuating around some constant value. We show that these modifications give qualitatively the same results obtained in an earlier paper, where the random killings (used to avoid an exponential increase of the population) were applied only to newborns.
October 13, 2011
Lifespan distributions of populations of quite diverse species such as humans and yeast seem to surprisingly well follow the same empirical Gompertz-Makeham law, which basically predicts an exponential increase of mortality rate with age. This empirical law can for example be grounded in reliability theory when individuals age through the random failure of a number of redundant essential functional units. However, ageing and subsequent death can also be caused by the accumula...