Fight Aging!

Reliability theory is, put very simply, a way of modeling and predicting the failure modes and mean time to failure of complex systems with many redundant parts subject to wear and tear. Reliability theory has seen a great deal of use in the electronics industry, amongst many others, but the human body is also a complex system that can be considered in these terms. Looking at our life spans and age-related illnesses in the context of reliability theory and the accumulating failure of redundant systems can add a great deal to our understanding of aging and our expectations for longevity science.

In recent years there has been more interest in this topic amongst aging researchers. I'm sure that Leonid Gavrilov and Natalia Gavrilova, who produced some of the important papers in this space, will be pleased to see that more researchers are now rigorously applying reliability theory to aging and longevity:

Aging in mouse brain is a cell/tissue-level phenomenon exacerbated by proteasome loss

Biological aging is often described by its phenotypic effect on individuals. Still, its causes are more likely found on the molecular level. Biological organisms can be considered as reliability-engineered, robust systems and applying reliability theory to their basic non-aging components, proteins, could provide insight into the aging mechanism.

Reliability theory suggests that aging is an obligatory trade-off in a fault-tolerant system such as the cell which is constructed based on redundancy design. Aging is the inevitable redundancy loss of functional system components, that is proteins, over time. In our study we investigated mouse brain development, adulthood and aging from embryonic day 10 to 100 weeks. We determined redundancy loss of different protein categories with age using reliability theory. We observed a near-linear decrease of protein redundancy during aging.

Aging may therefore be a phenotypic manifestation of redundancy loss caused by non-functional protein accumulation. This is supported by a loss of proteasome system components faster than dictated by reliability theory. This loss is highly detrimental to biological self-renewal and seems to be a key contributor to aging and therefore could represent a major target for therapies for aging and age-related diseases.

Proteins are the cogs, building blocks, and tools of your cells and the machines inside your cells. Without all the specific proteins needed, cells and cellular components become dysfunctional, fail, or die. If you look through the contributions to aging outlined in the Strategies for Engineered Negligible Senescence, you'll see numerous ways in which malformed or damaged proteins can increase greatly in number across a life span - often indirectly as an end result of a chain of other forms of failure and damage in cellular machinery.

Mao L, Roemer I, Nebrich G, Klein O, Koppelstaetter A, Hin SC, Hartl D, & Zabel C (2010). Aging in mouse brain is a cell/tissue-level phenomenon exacerbated by proteasome loss. Journal of proteome research PMID: 20469937