Witten 1983, MAD,

Witten83MAD argues for a systems approach and argues that a 'local model' is need for mechanistic insights. 

Without loss of generality, let us consider a single cell as our system of interest. When a new cell comes into being, it must function in some "average normal" manner (we'll assume that we are examining normal cells). In order for a cell to function in this "average normal manner" it must have some idea of what functions it must perform. That is to say, if it is a pancreatic islet cell then it must do all those things a "normal" pancreatic islet cell must do. This knowledge must be abstractly embedded in the cell as programming an internal model/rules and laws - whatever you choose. In brief, the cell has a set of internal perceptions as to what its normal function in a normal environment must be. (page 71, Witten83MAD).

If, as clock time passes, the cell's external environment changes in some substantial
manner, then the deviation between the cell's programmed picture of the normal world environment and the real world environment becomes quite large. The consequence of this deviation could well be the development of reversible and non-reversible agerelated effects. In the following paragraphs, we investigate how these concepts may be formalized. This will lead us to a definition of senescence in terms of these deviations. (page 72).

Witten83 use $R_SYS$ as survival function, and $\lambda$ as mortality rate. Witten83 formulated the normal deviation $\alpha_N$ and aging devivation $\alpha_R(t)".

 Its aging model in linear form is:

Its threshold-like aging model is:

Witten83 then use mortality rate and survival function to find a probability density function, called a "general form of mortality" (page 75). Witten83 parametrized $\alpha_R(t)$ for detailed studies.