An In Silico Model to Simulate the Evolution of Biological Aging

We examine the dynamics of an age-structured population model in which the life expectancy of an offspring may be mutated with respect to that of the parent. While the total population of the system always reaches a steady state, the fitness and age characteristics exhibit counter-intuitive behavior as a function of the mutational bias. By analytical and numerical study of the underlying rate equations, we show that if deleterious mutations are favored, the average fitness of...

In these lecture notes I describe some of the main theoretical ideas emerged to explain the aging dynamics. This is meant to be a very short introduction to aging dynamics and no previous knowledge is assumed. I will go through simple examples that allow one to grasp the main results and predictions.

We study the interplay of population growth and evolutionary dynamics using a stochastic model based on birth and death events. In contrast to the common assumption of an independent population size, evolution can be strongly affected by population dynamics in general. Especially for fast reproducing microbes which are subject to selection, both types of dynamics are often closely intertwined. We illustrate this by considering different growth scenarios. Depending on whether ...

A simple evolutionary model for biological ageing is modified such that it requires a minimum population for survival, like in human society. This social effect leads to a transition between extinction and survival of the species.

We have simulated demographic changes in the human population using the Penna microscopic model, based on the simple Monte Carlo method. The results of simulations have shown that during a few generations changes in the genetic pool of a population are negligible, while improving the methods of compensation of genetic defects or genetically determined proneness to many disorders drastically affects the average life span of organisms. Age distribution and mortality of the simu...

Mammalian cells are restricted from proliferating indefinitely. Telomeres at the end of each chromosome are shortened at cell division and, when they reach a critical length, the cell will enter permanent cell cycle arrest - a state known as senescence. This mechanism is thought to be tumor suppressing, as it helps prevent precancerous cells from dividing uncontrollably. Stem cells express the enzyme telomerase, which elongates the telomeres, thereby postponing senescence. ...

Modifying the Redfield model of sexual reproduction and the Penna model of biological aging, we compare reproduction with and without recombination in age-structured populations. In contrast to Redfield and in agreement with Bernardes we find sexual reproduction to be preferred to asexual one. In particular, the presence of old but still reproducing males helps the survival of younger females beyond their reproductive age.

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.

The gradual accumulation of damage and dysregulation during the aging of living organisms can be quantified. Even so, the aging process is complex and has multiple interacting physiological scales -- from the molecular to cellular to whole tissues. In the face of this complexity, we can significantly advance our understanding of aging with the use of computational models that simulate realistic individual trajectories of health as well as mortality. To do so, they must be sys...

Aging is thought to be a consequence of intrinsic breakdowns in how genetic information is processed. But mounting experimental evidence suggests that aging can be slowed. To help resolve this mystery, I derive a mortality equation which characterizes the dynamics of an evolving population with a given maximum age. Remarkably, while the spectrum of eigenvalues that govern the evolution depends on the fitness, how they change with the maximum age is independent of fitness. Thi...