The molecular and cellular basis of the aging process is not well understood, particularly in humans, as the scientific community has yet to develop a reliable and predictive set of biomarkers that can be utilized to quantitate specific aspects of senescence within discrete regions and/or cell populations. The longevity of a given species depends on several parameters, including frailty (intrinsic vulnerability to death) and senescence (rate of change in frailty over time) [1, 2]. Actuarial rates and survival curves are not particularly useful for predicting aging rates in the brains of mammals. A general consensus is that using surrogate molecular and cellular markers to evaluate senescence throughout the lifespan of animal models is a plausible approach to gain greater insight into mechanisms that underlie aging in humans, with the hope of developing rational pharmacotherapeutic interventions to avoid the scourge of progressive late-onset neurodegenerative disorders and related phenomena that occur in the aging brain. It is unlikely that a single gene is responsible for aging. Rather, a complex pattern of genes probably influences a wide variety of critical parameters, including cellular defense, disease resistance, and generalized homeostasis. While an exact mosaic of gene products responsible for aging remains unknown, current research is beginning to identify candidate markers from a wide variety of transcript classes. Another obstacle using animal models in aging research has been the divergence of uniform genetic backgrounds in model systems, which has led to variable complexity in phenotypic expression. Moreover, from an experimental perspective, there still remains a relative lack of effective means to measure small, but potentially significant, changes in gene expression .
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