StemCell Therapy

This article is about the ageing of living things. For ageing specifically in humans, see ageing. For the study of ageing in humans, see gerontology. For the science of the care of the elderly, see geriatrics. For experimental gerontology, see life extension. For premature ageing disorders, see Progeroid syndromes.

Senescence () (from Latin: senescere, meaning "to grow old", from senex) or biological aging (also spelled biological ageing) is the gradual deterioration of function characteristic of most complex lifeforms, arguably found in all biological kingdoms, that on the level of the organism increases mortality after maturation. The word "senescence" can refer either to cellular senescence or to senescence of the whole organism. It is commonly believed that cellular senescence underlies organismal senescence. The science of biological aging is biogerontology.

Senescence is not the inevitable fate of all organisms. Organisms of some taxonomic groups (taxa), including some animals, even experience chronological decrease in mortality, for all or part of their life cycle.[1] On the other extreme are accelerated aging diseases, rare in humans. There is also the extremely rare and poorly understood "Syndrome X", whereby a person remains physically and mentally an infant or child throughout one's life.[2][3]

Even if environmental factors do not cause aging, they may affect it; in such a way, for example, overexposure to ultraviolet radiation accelerates skin aging. Different parts of the body may age at different rates. Two organisms of the same species can also age at different rates, so that biological aging and chronological aging are quite distinct concepts.

Albeit indirectly, senescence is by far the leading cause of death (other than in the trivially accurate sense that cerebral hypoxia, i.e., lack of oxygen to the brain, is the immediate cause of all human death). Of the roughly 150,000 people who die each day across the globe, about two thirds100,000 per daydie of age-related causes; in industrialized nations, moreover, the proportion is much higher, reaching 90%.[4]

There are a number of hypotheses as to why senescence occurs; for example, some posit it is programmed by gene expression changes, others that it is the cumulative damage caused by biological processes. Whether senescence as a biological process itself can be slowed down, halted or even reversed, is a subject of current scientific speculation and research.[5]

Cellular senescence is the phenomenon by which normal diploid cells cease to divide. In cell culture, fibroblasts can reach a maximum of 50 cell divisions before becoming senescent. This phenomenon is known as "replicative senescence", or the Hayflick limit in honour of Dr.Leonard Hayflick, co-author with Paul Moorhead, of the first paper describing it in 1961.[6] Replicative senescence is the result of telomere shortening that ultimately triggers a DNA damage response. Cells can also be induced to senesce via DNA damage in response to elevated reactive oxygen species (ROS), activation of oncogenes and cell-cell fusion, independent of telomere length. As such, cellular senescence represents a change in "cell state" rather than a cell becoming "aged" as the name confusingly suggests. Although senescent cells can no longer replicate, they remain metabolically active and commonly adopt an immunogenic phenotype consisting of a pro-inflammatory secretome, the up-regulation of immune ligands, a pro-survival response, promiscuous gene expression (pGE) and stain positive for senescence-associated -galactosidase activity.[7] The nucleus of senescent cells is characterized by senescence-associated heterochromatin foci (SAHF) and DNA segments with chromatin alterations reinforcing senescence (DNA-SCARS).[8] Senescent cells are known to play important physiological functions in tumour suppression, wound healing and possibly embryonic/placental development and paradoxically play a pathological role in age-related diseases.[9] The elimination of senescent cells using a transgenic mouse model led to greater resistance against aging-associated diseases,[10] suggesting that cellular senescence is a major driving force of ageing and its associated diseases.

Organismal senescence is the aging of whole organisms. In general, aging is characterized by the declining ability to respond to stress, increased homeostatic imbalance, and increased risk of aging-associated diseases. Death is the ultimate consequence of aging, though "old age" is not a scientifically recognized cause of death because there is always a specific proximal cause, such as cancer, heart disease, or liver failure. Aging of whole organisms is therefore a complex process that can be defined as "a progressive deterioration of physiological function, an intrinsic age-related process of loss of viability and increase in vulnerability".[11]

Differences in maximum life span among species correspond to different "rates of aging". For example, inherited differences in the rate of aging make a mouse elderly at 3 years and a human elderly at 80 years.[12] These genetic differences affect a variety of physiological processes, including the efficiency of DNA repair, antioxidant enzymes, and rates of free radical production.

Senescence of the organism gives rise to the GompertzMakeham law of mortality, which says that mortality rate accelerates rapidly with age.

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Senescence - Wikipedia, the free encyclopedia

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