Biogerontology

From Wikipedia, the free encyclopedia
Jump to navigation Jump to search
The hand of an older adult

Biogerontology is the sub-field of gerontology concerned with the biological aging process, its evolutionary origins, and potential means to intervene in the process. It involves interdisciplinary research on biological aging's causes, effects, and mechanisms. Biogerontologist Leonard Hayflick said that the natural average lifespan for human is around 92 years and, if we do not invent new approaches for treating aging, we get stuck there.[1] While James Vaupel have predicted that in industrialized countries life expectancies will reach 100 for children born after the year 2000.[2] Many surveyed biogerontologists have predicted life expectancies of more than three centuries for a person born in the year 2100.[3] And some scientists say about naturally unlimited lifespan for already living people. For example, Aubrey de Grey offers the "tentative timeframe" that with adequate funding of research to develop interventions in aging such as Strategies for Engineered Negligible Senescence, "we have a 50/50 chance of developing technology within about 25 to 30 years from now that will, under reasonable assumptions about the rate of subsequent improvements in that technology, allow us to stop people from dying of aging at any age".[4] His idea is to repair in an organism what can be repaired using present technology, allowing humans to live until the time when technology progress will allow to cure the remained deeper damage. This concept got the name "longevity escape velocity".

Biomedical gerontology, also known as experimental gerontology and life extension, is a sub-discipline of biogerontology that endeavors to slow, prevent, and even reverse aging in both humans and animals. Most "life extensionists" believe the human life span can be multiplied for already living persons.

Biogerontologists vary in the degree to which they focus on the study of the aging process as a means of mitigating the diseases of aging or extending lifespan. Some say that it is enough only to make aging healthy and prolong healthspan - duration of life when person lives without serious illnesses. In this direction recently new interdisciplinary field was formulated called geroscience, that is focused on preventing diseases of aging.[5][6][7] Some argue that maximum life span cannot be altered or that it is undesirable to do due to some moral considerations. Other biogerontologists, in contrast, consider that aging is disease per se and should be treated directly. If an organism is in youth condition, it only with small probability get age-related diseases, and those are easily cured.[8][9][10] They don't agree that life, unlimited by certain age, have moral problems.

In contrast with biogerontology, which aims to prevent age-related disease by intervening in aging processes, geriatrics is a field of medicine that studies the treatment of existing disease in aging people.

There are numerous theories of aging, and no one theory has been accepted. There is a wide spectrum of the types of theories for the causes of aging with programmed theories on one extreme and error theories on the other.[11] Regardless of the theory, a commonality is that as humans age, functions of the body decline.[12]

Stochastic theories[edit]

Stochastic theories of aging are theories suggesting that aging is caused by small changes in the body over time and the body's failure to restore the system and mend the damages to the body. The cells and tissues are eventually injured due to the damage gathered over time. This causes the diminishes in an organ's function related to age. The notion of accumulated damage was first introduced by biologist Dr. August Weismann as the "wear and tear" theory in 1882.[13][14]

Wear and tear theory[edit]

Wear and tear theories of aging suggest that as an individual ages, body parts such as cells and organs wear out from continued use. Wearing of the body can be attributable to internal or external causes that eventually lead to an accumulation of insults which surpasses the capacity for repair. Due to these internal and external insults, cells lose their ability to regenerate, which ultimately leads to mechanical and chemical exhaustion. Some insults include chemicals in the air, food, or smoke. Other insults may be things such as viruses, trauma, free radicals, cross-linking, and high body temperature.[12]

Accumulation[edit]

Accumulation theories of aging suggest that aging is bodily decline that results from an accumulation of elements, whether introduced to the body from the environment or resulting from cell metabolism.[12] An example of an accumulation theory is the Free Radical Theory of Aging.

Free radical theory[edit]

Free radicals are reactive molecules produced by cellular and environmental processes, and can damage the elements of the cell such as the cell membrane and DNA and cause irreversible damage. The free-radical theory of aging proposes that this damage cumulatively degrades the biological function of cells and impacts the process of aging.[15] The idea that free radicals are toxic agents was first proposed by Rebeca Gerschman and colleagues in 1945,[16] but came to prominence in 1956, when Denham Harman proposed the free-radical theory of aging and even demonstrated that free radical reactions contribute to the degradation of biological systems.[17] Oxidative damage of many types accumulate with age, such as oxidative stress that oxygen-free radicals,[18] because the free radical theory of aging argues that aging results from the damage generated by reactive oxygen species (ROS).[19] ROS are small, highly reactive, oxygen-containing molecules that can damage a complex of cellular components such as fat, proteins, or from DNA; they are naturally generated in small amounts during the body's metabolic reactions. These conditions become more common as humans grow older and include diseases related to aging, such as dementia, cancer and heart disease.

DNA damage theory[edit]

DNA damage has been one of the many causes in diseases related to aging. The stability of the genome is defined by the cells machinery of repair, damage tolerance, and checkpoint pathways that counteracts DNA damage. One hypothesis proposed by Gioacchino Failla in 1958[20] is that damage accumulation to the DNA causes aging. The hypothesis was developed soon by physicist Leó Szilárd.[21] This theory has changed over the years as new research has discovered new types of DNA damage and mutations, and several theories of aging argue that DNA damage with or without mutations causes aging.[22]

Cross-linking theory[edit]

The cross-linking theory proposes that advanced glycation end-products (stable bonds formed by the binding of glucose to proteins) and other aberrant cross-links accumulating in aging tissues is the cause of aging. The crosslinking of proteins disables their biological functions. The hardening of the connective tissue, kidney diseases, and enlargement of the heart are connected to the cross-linking of proteins. Crosslinking of DNA can induce replication errors, and this leads to deformed cells and increases the risk of cancer.[13]

Genetic[edit]

Genetic theories of aging propose that aging is programmed within each individual's genes. According to this theory, genes dictate cellular longevity. Programmed cell death, or apoptosis, is determined by a "biological clock" via genetic information in the nucleus of the cell. Genes responsible for apoptosis provide an explanation for cell death, but are less applicable to death of an entire organism. An increase in cellular apoptosis may correlate to aging, but is not a 'cause of death'. Environmental factors and genetic mutations can influence gene expression and accelerate aging. More recently epigenetics have been explored as a contributing factor. The epigenetic clock, which objectively measures the biological age of cells and tissues, may become useful for testing different biological aging theories.[23]

General imbalance[edit]

General imbalance theories of aging suggest that body systems, such as the endocrine, nervous, and immune systems, gradually decline and ultimately fail to function. The rate of failure varies system by system.[12]

Immunological theory[edit]

The immunological theory of aging suggests that the immune system weakens as an organism ages. This makes the organism unable to fight infections and less able to destroy old and neoplastic cells. This leads to aging and will eventually lead to death. This theory of aging was developed by Ray Walford, an American gerontologist. According to Walford, incorrect immunological procedures are the cause of the process of aging.[15]

See also[edit]

References[edit]

  1. ^ Geoff Watts (June 2011). "Leonard Hayflick and the limits of aging". The Lancet. 377 (9783): 2075. doi:10.1016/S0140-6736(11)60908-2. PMID 21684371. S2CID 205963134.
  2. ^ Christensen, L; Doblhammer, K; Rau, G; Vaupel, JW (2009). "Aging populations: the challenges ahead". The Lancet. 374 (9696): 1196–1208. doi:10.1016/s0140-6736(09)61460-4. PMC 2810516. PMID 19801098.
  3. ^ Richel, Theo (December 2003). "Will human life expectancy quadruple in the next hundred years? Sixty gerontologists say public debate on life extension is necessary". Journal of Anti-Aging Medicine. 6 (4): 309–314. doi:10.1089/109454503323028902. PMID 15142432.
  4. ^ de Grey, Aubrey D. N. J.; Rae, Michael (October 14, 2008). Ending Aging. St. Martin's Griffin. p. 15. ISBN 978-0312367077.
  5. ^ Lithgow, Gordon J. (1 September 2013). "Origins of Geroscience". Public Policy & Aging Report. 4 (1): 10–11. doi:10.1093/ppar/23.4.10.
  6. ^ Burch, John B.; et al. (2014-05-08). "Advances in Geroscience: Impact on Healthspan and Chronic Disease". The Journals of Gerontology: Series A. 69 (Suppl_1): S1–S3. doi:10.1093/gerona/glu041. PMID 24833579.
  7. ^ Seals, Douglas R.; Justice, Jamie N.; LaRocca, Thomas J. (2015-01-29). "Physiological geroscience: targeting function to increase healthspan and achieve optimal longevity". The Journal of Physiology. 594 (8): 2001–2024. doi:10.1113/jphysiol.2014.282665. PMID 25639909.
  8. ^ Stambler, Ilia (2017-10-01). "Recognizing Degenerative Aging as a Treatable Medical Condition: Methodology and Policy". Aging and Disease. 8 (5): 583–589. doi:10.14336/AD.2017.0130. PMID 28966803.
  9. ^ "Opening the door to treating ageing as a disease". The Lancet Diabetes & Endocrinology. 6 (8): 587. 2018-08-01. doi:10.1016/S2213-8587(18)30214-6. PMID 30053981.
  10. ^ Khaltourina, Daria; Matveyev, Yuri; Alekseev, Aleksey; Cortese, Franco; Ioviţă, Anca (July 2020). "Aging Fits the Disease Criteria of the International Classification of Diseases". ScienceDirect. 189. doi:10.1016/j.mad.2020.111230. PMID 32251691.
  11. ^ Carlos López-Otín, Maria A. Blasco, Linda Partridge, Manuel Serrano, Guido Kroemer (2013-06-06). "The Hallmarks of Aging". Cell. 153 (6): 1194–1217. doi:10.1016/j.cell.2013.05.039. PMC 3836174. PMID 23746838.CS1 maint: uses authors parameter (link)
  12. ^ a b c d Taylor, Albert W.; Johnson, Michel J. (2008). Physiology of Exercise and Healthy Aging. Human Kinetics. ISBN 978-0-7360-5838-4.
  13. ^ a b Lipsky, Martin S.; King, Mitch (2015). "Biological theories of aging". Disease-a-Month. 61 (11): 460–466. doi:10.1016/j.disamonth.2015.09.005. PMID 26490576.
  14. ^ Jessica Kelly. "Wear-and-Tear Theory". Lumen Learning.
  15. ^ a b Boniewska-Bernacka, Ewa (2016). "Selected Theories of Aging" (PDF). Higher School's Pulse. 10: 36–39.
  16. ^ Gerschman, Rebecca; Gilbert, DL, Nye, SW, Dwyer, P, and Fenn WO; Nye, Sylvanus W.; Dwyer, Peter; Fenn, Wallace O. (7 May 1954). "Oxygen poisoning and x-irradiation: a mechanism in common". Science. 119 (3097): 623–626. Bibcode:1954Sci...119..623G. doi:10.1126/science.119.3097.623. PMID 13156638. S2CID 27600003.CS1 maint: multiple names: authors list (link)
  17. ^ Harman, D (November 1981). "The aging process". Proc. Natl. Acad. Sci. U.S.A. 78 (11): 7124–7128. Bibcode:1981PNAS...78.7124H. doi:10.1073/pnas.78.11.7124. PMC 349208. PMID 6947277.
  18. ^ Hagen, Bruce N; MK Shigenaga; TM Hagen (September 1993). "Oxidants, antioxidants, and the degenerative diseases of aging". Proc. Natl. Acad. Sci. U.S.A. 90 (17): 7915–7922. Bibcode:1993PNAS...90.7915A. doi:10.1073/pnas.90.17.7915. PMC 47258. PMID 8367443.
  19. ^ Beckman, KB; Ames BN (April 1998). "The free radial theory of aging matures". Physiol Rev. 78 (2): 547–581. doi:10.1152/physrev.1998.78.2.547. PMID 9562038. S2CID 1774858.
  20. ^ Failla, G (30 September 1958). "The aging process and cancerogenesis". Annals of the New York Academy of Sciences. 71 (6): 1124–1140. Bibcode:1958NYASA..71.1124F. doi:10.1111/j.1749-6632.1958.tb46828.x. PMID 13583876.
  21. ^ Szilard, Leo (January 1959). "On the nature of the aging process". Proc. Natl. Acad. Sci. U.S.A. 45 (1): 30–45. Bibcode:1959PNAS...45...30S. doi:10.1073/pnas.45.1.30. PMC 222509. PMID 16590351.
  22. ^ Freitas, AA; de Magalhaes, JP (Jul–Oct 2011). "A review and appraisal of the DNA damage theory of aging". Mutat Res. 728 (1–2): 12–22. doi:10.1016/j.mrrev.2011.05.001. PMID 21600302.
  23. ^ Horvath S (2013). "DNA methylation age of human tissues and cell types". Genome Biology. 14 (10): R115. doi:10.1186/gb-2013-14-10-r115. PMC 4015143. PMID 24138928.

attribution contains material copied from Gerontology.