Ageing - Wikipedia. Ageing or aging (see spelling differences), is the process of becoming older. The term refers especially to human beings, many animals, and fungi, whereas for example bacteria, perennial plants and some simple animals are potentially immortal. In the broader sense, ageing can refer to single cells within an organism which have ceased dividing (cellular senescence) or to the population of a species (population ageing). In humans, ageing represents the accumulation of changes in a human being over time. Reaction time, for example, may slow with age, while knowledge of world events and wisdom may expand. Ageing is among the greatest known risk factors for most human diseases. Programmed ageing should not be confused with programmed cell death (apoptosis). The discovery, in 1. Ageing versus immortality. Immortal Hydra, a relative of the jellyfish. Human beings and members of other species, especially animals, necessarily experience ageing and mortality. Fungi, too, can age. Such organisms (prokaryotes, protozoans, algae) multiply by fissioning into daughter cells; thus do not age and are innately immortal. The sexual organism could henceforth pass on some of its genetic material to produce new individuals and could itself become disposable with respect to the survival of its species. Furthermore, many types of memory may decline with ageing, but not semantic memory or general knowledge such as vocabulary definitions, which typically increases or remains steady until late adulthood. Intelligence may decline with age, though the rate may vary depending on the type and may in fact remain steady throughout most of the lifespan, dropping suddenly only as people near the end of their lives. Individual variations in rate of cognitive decline may therefore be explained in terms of people having different lengths of life. Macular degeneration causes vision loss and increases with age, affecting nearly 1. In industrialised nations, the proportion is higher, reaching 9. A model organism for studying of ageing is the nematode. C. Programmed factors follow a biological timetable, perhaps one that might be a continuation of the one that regulates childhood growth and development. Sean July 12, 2012. Peter, do you think a low-carbohydrate diet becomes more effective (i.e., exponential) at reducing risk-factors the longer someone adheres to the. This regulation would depend on changes in gene expression that affect the systems responsible for maintenance, repair and defence responses. Damage- related factors include internal and environmental assaults to living organisms that induce cumulative damage at various levels. For example, numerous perennial plants ranging from strawberries and potatoes to willow trees typically produce clones of themselves by vegetative reproduction and are thus potentially immortal, while annual plants such as wheat and watermelons die each year and reproduce by sexual reproduction. In 2. 00. 8 it was discovered that inactivation of only two genes in the annual plant Arabidopsis thaliana leads to its conversion into a potentially immortal perennial plant. Some of the targeted genes have homologues across species and in some cases have been associated with human longevity. DNA methylation age of blood predicts all- cause mortality in later life. This resetting into a juvenile state was experimentally achieved by activating the four Yamanaka DNA transcription factors – Sox. Oct. 4, Klf. 4 and c- Myc (which have previously been routinely used for producing young animals from cloned adult skin cells). Sirtuin in turn inhibits m. TOR. When organisms restrict their diet, m. TOR activity is reduced, which allows an increased level of autophagy. This recycles old or damaged cell parts, which increases longevity and decreases the chances of being obese. This is thought to prevent spikes of glucose concentration in the blood, leading to reduced insulin signalling. This has been linked to less m. TOR activation as well. Therefore, longevity has been connected to caloric restriction and insulin sensitivity inhibiting m. Background Type 2 diabetes affects approximately 8 percent of adults in the United States. Some risk factors — elevated plasma glucose concentrations in the fasting.
TOR, which in turns allows autophagy to occur more frequently. It may be that m. TOR inhibition and autophagy reduce the effects of reactive oxygen species on the body, which damage DNA and other organic material, so longevity would be increased. The precise mechanism by which decreased GH/IGF- 1 signalling increases longevity is unknown, but various mouse strains with decreased GH and/or IGF- 1 induced signalling share a similar phenotype which includes increased insulin sensitivity, enhanced stress resistance and protection from carcinogenesis. The studied mouse strains with decreased GH signalling showed between 2. IGF- 1 induced signalling revealed a 1. Traits that benefit early survival and reproduction will be selected for even if they contribute to an earlier death. Such a genetic effect is called the antagonistic pleiotropy effect when referring to a gene (pleiotropy signifying the gene has a double function – enabling reproduction at a young age but costing the organism life expectancy in old age) and is called the disposable soma effect when referring to an entire genetic programme (the organism diverting limited resources from maintenance to reproduction). Also, it has been suggested that some of the genetic variants that increase fertility in the young increase cancer risk in the old. Such variants occur in genes p. Moreover, the hormones that regulate reproduction also regulate cellular metabolism, explaining the increases in fat deposition during pregnancy through to the deposition of centralised adiposity with the dysregulation of the HPG axis following menopause and during andropause (Atwood and Bowen, 2. This theory, which introduced a new definition of ageing, has facilitated the conceptualisation of why and how ageing occurs at the evolutionary, physiological and molecular levels. A number of diseases associated with ageing, such as atrophic gastritis and Hashimoto's thyroiditis, are probably autoimmune in this way. However, while inflammation is very much evident in old mammals, even completely immunodeficient mice raised in pathogen- free laboratory conditions still experience senescence. In 2. 01. 1, it was demonstrated that acetylation levels of AMP- activated protein kinase change with age in yeast and that preventing this change slows yeast ageing. DNA damage causes the cells to stop dividing or induces apoptosis, often affecting stem cell pools and hence hindering regeneration. However, lifelong studies of mice suggest that most mutations happen during embryonic and childhood development, when cells divide often, as each cell division is a chance for errors in DNA replication. These numbers are close to the ratio of the maximum longevities of the two species (1. The comparative percentage is also similar between the dog and human for yearly DNA loss in the brain and lymphocytes. As stated by lead author, Bernard L. For example, a waste product called lipofuscin is formed by a complex reaction in cells that binds fat to proteins. This waste accumulates in the cells as small granules, which increase in size as a person ages. The situation, however, has been complicated by the identification that autophagy up- regulation can also occur during ageing. The authors propose that mt. DNA mutations lead to respiratory- chain- deficient cells and thence to apoptosis and cell loss. They cast doubt experimentally however on the common assumption that mitochondrial mutations and dysfunction lead to increased generation of reactive oxygen species (ROS). Notwithstanding the similarly low calorie intake, the diet composition differed between the two studies (notably a high sucrose content in the Wisconsin study), and the monkeys have different origins (India, China), initially suggesting that genetics and dietary composition, not merely a decrease in calories, are factors in longevity. Once these factors are accounted for, the optimal body weight above age 6. People who live the longest report sleeping for six to seven hours each night. A chronically high cortisol level compromises the immune system, causes cardiac damage/arterosclerosis and is associated with facial ageing, and the latter in turn is a marker for increased morbidity and mortality. Of particular note, the treatment began in mice aged 2. De. Pinho and his colleagues published research in mice where telomerase activity was first genetically removed. Then, after the mice had prematurely aged, they restored telomerase activity by reactivating the telomerase gene. As a result, the mice were rejuvenated: Shrivelled testes grew back to normal and the animals regained their fertility. Other organs, such as the spleen, liver, intestines and brain, recuperated from their degenerated state. However, activating telomerase in humans could potentially encourage the growth of tumours. However, the benefits may not be proportional; longevity gains are typically greater in C. One explanation for this is that mammals, being much longer- lived, already have many traits which promote lifespan. The Methuselah Foundation offers the Mprize. Recently, the $1 Million Palo Alto Longevity Prize was launched. It is a research incentive prize to encourage teams from all over the world to compete in an all- out effort to . It was founded by Joon Yun. The age of an adult human is commonly measured in whole years since the day of birth. Arbitrary divisions set to mark periods of life may include: juvenile (via infancy, childhood, preadolescence, adolescence), early adulthood, middle adulthood, and late adulthood. More casual terms may include . These age specifications include voting age, drinking age, age of consent, age of majority, age of criminal responsibility, marriageable age, age of candidacy, and mandatory retirement age. Admission to a movie for instance, may depend on age according to a motion picture rating system. A bus fare might be discounted for the young or old. Each nation, government and non- governmental organisation has different ways of classifying age. In other words, chronological ageing may be distinguished from .
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