S Senescence

One of the greatest mysteries in the life of almost every living organism is the fact that most organisms, as they age, experience deterioration in their functional status. (Lemaître et.al. 2014; It is due to this then that these organisms can be said to have a continually decreasing fitness as their survival and reproductive performance decline as they age. This effect on their fitness is why selection should act against senescence persisting in organisms. This then has led scientists to ask the reason behind senescence evolving and actually becoming prevalent. Several theories have been raised to address this question. Three of which, namely the mutation accumulation theory, the antagonistic pleiotropy theory, and the disposable soma theory, will be discussed below.

Functional Ecology, 2020

Senescence—the decline in age‐specific contribution to fitness with increasing age—has been widely investigated in evolutionary ecology. A tremendous amount of detailed empirical analyses have now revealed the widespread occurrence of demographic senescence (i.e. both actuarial and reproductive senescence) and have started to identify factors (e.g. environmental conditions) that modulate its timing and intensity, both within and across species. In this special feature, we have built on this flourishing work to highlight several axes of research that would benefit from more integrative and multidisciplinary approaches. Several contributions compiled in this special feature emphasize that our understanding of senescence remains taxonomically limited, mostly focused on birds and mammals, and is therefore not representative of the biological diversity displayed across the tree of life. In line with this observation, the influence of some peculiar lifestyles (e.g. involving sociality or ...

2019

The American Journal of Human Genetics, 1998

The Phenomenon of Cellular Aging Human aging is a highly complex process, resulting from a number of small changes that differ from tissue to tissue. Several major obstacles have interfered with the study of aging in whole organisms. These include the genetic heterogeneity between individuals and the difficulty in distinguishing the consequences of normal aging from the effects of diseases that occur throughout life (see Schä chter 1998 [in this issue]). For these reasons, human cells grown in culture offer a simplified and attractive model with which to study cellular processes involved in aging. More than 30 years ago, Hayflick and Moorhead reported that diploid fibroblasts undergo a finite number of cell divisions, after which they stop proliferating. This phenomenon was equated with normal cellular aging and was termed "replicative senescence" (Hayflick 1965). Various other cell types have since been found to undergo replicative senescence, including epidermal keratinocytes, smooth-muscle cells, lens epithelial cells, glial cells, endothelial cells, melanocytes, T lymphocytes (see Effros 1998 [in this issue]), and adrenocortical cells. What defines replicative senescence? Cells having completed a finite number of divisions in culture become irreversibly growth arrested in the G1 stage of the cell cycle. A distinctive feature of senescent cells is that they persist in this state from months to as long as several years, remaining metabolically active but incapable of DNA synthesis (Matsumura et al. 1979). This block in cell-cycle progression in senescent cells is irreversible and is not associated with programmed cell death. Senescent cells also undergo morphological changes that include enlargement and flattening of the cells and an unexplained expression of a b-galactosidase activity at pH 6 (Dimri et al. 1995). These criteria are few, in part because many changes that occur in senescence are also seen in

Frontiers in Genetics, 2016

Frontiers in genetics, 2024

2024

There is a main difference between theories explaining aging as a genetically determined and modulated adaptive phenomenon and theories explaining aging as a non-adaptive phenomenon caused by the accumulation of random degenerative events. In fact, for adaptive theories a genetically determined and modulated program determining aging is indispensable, while for non-adaptive theories such a program cannot exist. However, the evidence supporting the existence of this program appears strong according to the mechanism of the subtelomere-telomere theory of aging with the action of TERRA sequences. This theory was developed in four successive phases: 1) Aging simply caused by limitations in cell duplication; 2) Aging caused by progressive telomere shortening; 3) Aging caused by progressive inhibition of particular hypothetical regulatory sequences in subtelomeric position (r-sequences) determined by progressive telomere shortening; 4) Identification of the r-sequences in the TERRA sequences whose effects are well known and documented. The theories 1 and 2 were untenable because their predictions were contradicted by the evidence. Theory 3 was based, among other things, on the hypothesis of sequences that had to be confirmed by evidence. Phase 4 overcame this difficulty. The mechanism proposed by theory 4 describes a determined and regulated genetically pivotal mechanism of aging, and therefore confirms the hypothesis of aging as an adaptive phenomenon and invalidates the opposite thesis. Among other things, for the validity of the hypothesis of aging as a non-adaptive phenomenon, it would be essential to justify in evolutionary terms: (i) the position of regulatory sequences of great importance for cellular functions in a position where they are inhibited by telomere shortening; (ii) cell senescence which is an oncogenic factor and cannot be explained as a defense against cancer; and (iii) gradual cell senescence which cannot be hypothesized as an anti-cancer defense. Furthermore, the phenomena referred to in points (ii) and (iii) and TERRA sequences inhibition are reversible with appropriate manipulations and this is incompatible with their possible interpretation as a consequence of random degenerative phenomena. Conference Presentation at SIBE / ISBE Congress, Naples 2024, Spetember 8-11

… of the Royal …, 1991

International Journal of Molecular Sciences

This Special Issue aims to address the impact of cellular senescence on human biology, looking at both physiological and pathological processes [...]

Ecology Letters, 2008

Comparative analyses of survival senescence by using life tables have identified generalizations including the observation that mammals senesce faster than similar-sized birds. These generalizations have been challenged because of limitations of life-table approaches and the growing appreciation that senescence is more than an increasing probability of death. Without using life tables, we examine senescence rates in annual individual fitness using 20 individual-based data sets of terrestrial vertebrates with contrasting life histories and body size. We find that senescence is widespread in the wild and equally likely to occur in survival and reproduction. Additionally, mammals senesce faster than birds because they have a faster life history for a given body size. By allowing us to disentangle the effects of two major fitness components our methods allow an assessment of the robustness of the prevalent life-table approach. Focusing on one aspect of life history – survival or recruitment – can provide reliable information on overall senescence.