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Aging-associated diseases

An aging-associated disease (commonly termed age-related disease, ARD) is a disease that is most often seen with increasing frequency with increasing senescence. They are essentially complications of senescence, distinguished from the aging process itself because all adult animals age (with rare exceptions) but not all adult animals experience all age-associated diseases. The term does not refer to age-specific diseases, such as the childhood diseases chicken pox and measles, only diseases of the elderly. They are also not accelerated aging diseases, all of which are genetic disorders.

Age-specific SEER incidence rates, 2003–2007

Examples of aging-associated diseases are atherosclerosis and cardiovascular disease, cancer, arthritis, cataracts, osteoporosis, type 2 diabetes, hypertension and Alzheimer's disease. The incidence of all of these diseases increases exponentially with age.[1]

Of the roughly 150,000 people who die each day across the globe, about two thirds—100,000 per day—die of age-related causes.[2] In industrialized nations, the proportion is higher, reaching 90%.[2]

Patterns of differences edit

By age 3, about 30% of rats have had cancer, whereas by age 85 about 30% of humans have had cancer. Humans, dogs and rabbits get Alzheimer's disease, but rodents do not. Elderly rodents typically die of cancer or kidney disease, but not of cardiovascular disease. In humans, the relative incidence of cancer increases exponentially with age for most cancers, but levels off or may even decline by age 60–75 [3](although colon/rectal cancer continues to increase).[4]

People with the so-called segmental progerias are vulnerable to different sets of diseases. Those with Werner's syndrome experience osteoporosis, cataracts, and, cardiovascular disease, but not neurodegeneration or Alzheimer's disease; those with Down syndrome have type 2 diabetes and Alzheimer's disease, but not high blood pressure, osteoporosis or cataracts. In Bloom syndrome, those affected most often die of cancer.

Research edit

Aging (senescence) increases vulnerability to age-associated diseases, whereas genetics determines vulnerability or resistance between species and individuals within species. Some age-related changes (like graying hair) are said to be unrelated to an increase in mortality. But some biogerontologists believe that the same underlying changes that cause graying hair also increase mortality in other organ systems and that understanding the incidence of age-associated disease will advance knowledge of the biology of senescence just as knowledge of childhood diseases advanced knowledge of human development.[5]

Strategies for engineered negligible senescence (SENS) is an emerging research strategy that aims to repair "root causes" for age-related illness and degeneration, as well as develop medical procedures to periodically repair all such damage in the human body, thereby maintaining a youth-like state indefinitely.[6] The SENS programme has identified seven types of aging-related damage, and feasible solutions have been outlined for each. Some critics argue that the SENS agenda is optimistic at best, and that the aging process is too complex and little-understood for SENS to be scientific or implementable in the foreseeable future.[7][8][9] It has been proposed that age-related diseases are mediated by vicious cycles.[10]

On the basis of extensive research, DNA damage has emerged a major culprit in cancer and numerous other diseases related to ageing.[11] DNA damage can initiate the development of cancer or other aging related diseases depending on several factors. These include the type, amount, and location of the DNA damage in the body, the type of cell experiencing the damage and its stage in the cell cycle, and the specific DNA repair processes available to react to the damage.[11]

Types edit

Macular degeneration edit

Age-related macular degeneration (AMD) is a disease that affects the eyes and can lead to vision loss through break down of the central part of the retina called the macula. Degeneration can occur in one eye or both and can be classified as either wet (neovascular) or dry (atrophic). Wet AMD commonly is caused by blood vessels near the retina that lead to swelling of the macula.[12] The cause of dry AMD is less clear, but it is thought to be partly caused by breakdown of light-sensitive cells and tissue surrounding the macula. A major risk factor for AMD is age over the age of 60.[13]

Alzheimer's edit

Alzheimer's disease is classified as a "protein misfolding" disease. Aging causes mutations in protein folding, and as a result causes deposits of abnormal modified proteins to accumulate in specific areas of the brain. In Alzheimer's, deposits of Beta-amyloid and hyperphosphorylated tau protein form extracellular plaques and extracellular tangles.[14] These deposits are shown to be neurotoxic and cause cognitive impairment due to their initiation of destructive biochemical pathways.[15]

Atherosclerosis edit

Atherosclerosis is categorized as an aging disease and is brought about by vascular remodeling, the accumulation of plaque, and the loss of arterial elasticity. Over time, these processes can stiffen the vasculature. For these reasons, older age is listed as a major risk factor for atherosclerosis.[16] Specifically, the risk of atherosclerosis increases for men above 45 years of age and women above 55 years of age.[17]

Benign prostatic hyperplasia edit

Benign prostatic hyperplasia (BPH) is a noncancerous enlargement of the prostate gland due to increased growth.[18] An enlarged prostate can result in incomplete or complete blockage of the bladder and interferes with a man's ability to urinate properly. Symptoms include overactive bladder, decreased stream of urine, hesitancy urinating, and incomplete emptying of the bladder.[19][20] By age 40, 10% of men will have signs of BPH and by age 60, this percentage increases by 5 fold. Men over the age of 80 have over a 90% chance of developing BPH and almost 80% of men will develop BPH in their lifetime.[18][21]

Cancer edit

Although it is possible for cancer to strike at any age, most patients with invasive cancer are over 65,[22] and the most significant risk factor for developing cancer is age.[22] According to cancer researcher Robert A. Weinberg, "If we lived long enough, sooner or later we all would get cancer."[23] Some of the association between aging and cancer is attributed to immunosenescence,[24] errors accumulated in DNA over a lifetime[25] and age-related changes in the endocrine system.[26] Aging's effect on cancer is complicated by factors such as DNA damage and inflammation promoting it and factors such as vascular aging and endocrine changes inhibiting it.[27]

Parkinson's edit

Parkinson's disease, or simply Parkinson's,[28] is a long-term degenerative disorder of the central nervous system that mainly affects the motor system. The disease has many complications, including Dementia, depression, anxiety.[29] Parkinson's disease typically occurs in people over the age of 60, of whom about one percent are affected.[30][31] The prevalence of Parkinson's disease dementia also increases with age, and to a lesser degree, duration of the disease.[32] Exercise in middle age may reduce the risk of PD later in life.[33]

Stroke edit

Stroke was the second most frequent cause of death worldwide in 2011, accounting for 6.2 million deaths (~11% of the total).[34] Stroke could occur at any age, including in childhood, the risk of stroke increases exponentially from 30 years of age, and the cause varies by age.[35] Advanced age is one of the most significant stroke risk factors. 95% of strokes occur in people age 45 and older, and two-thirds of strokes occur in those over the age of 65.[36][37] A person's risk of dying if he or she does have a stroke also increases with age.

Endocrine diseases edit

Studies in animal models show that clearance of senescent cells improves multiple age related endocrine disorders.[38]

Osteoporosis edit

Bone density declines with age. By the age of 85 years, ~70% of women and 30% of men have a osteoporosis defined as a bone density less than or equal to 2.5 standard deviations lower than young adults.[39]

Metabolic syndrome edit

The metabolic syndrome is the co-occurrence of metabolic risk factors for type 2 diabetes and cardiovascular disease (abdominal obesity, hyperglycemia, dyslipidemia, and hypertension). The prevalence of the metabolic syndrome increases with age reaching close to 50% of people over 60 years old in the USA.[40] as

See also edit

References edit

  1. ^ Belikov AV (January 2019). "Age-related diseases as vicious cycles". Ageing Research Reviews. 49: 11–26. doi:10.1016/j.arr.2018.11.002. PMID 30458244. S2CID 53567141.
  2. ^ a b de Grey A (2007). (PDF). Studies in Ethics, Law, and Technology. 1 (1, Article 5). CiteSeerX 10.1.1.395.745. doi:10.2202/1941-6008.1011. S2CID 201101995. Archived from the original (PDF) on October 13, 2016. Retrieved August 7, 2011.
  3. ^ Belikov AV (September 2017). "The number of key carcinogenic events can be predicted from cancer incidence". Scientific Reports. 7 (1): 12170. Bibcode:2017NatSR...712170B. doi:10.1038/s41598-017-12448-7. PMC 5610194. PMID 28939880.
  4. ^ (PDF). Surveillance Epidemiology and End Results (SEER). National Cancer Institute. Archived from the original (PDF) on 2006-09-25. Retrieved 2006-11-20.
  5. ^ Hayflick L (June 2004). "The not-so-close relationship between biological aging and age-associated pathologies in humans". The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences. 59 (6): B547–B550. doi:10.1093/gerona/59.6.B547. PMID 15215261.
  6. ^ "The SENS Platform: An Engineering Approach to Curing Aging 2008-08-31 at the Wayback Machine". Methuselah Foundation. Retrieved on June 28, 2008.
  7. ^ Warner H, Anderson J, Austad S, Bergamini E, Bredesen D, Butler R, et al. (November 2005). "Science fact and the SENS agenda. What can we reasonably expect from ageing research?". EMBO Reports. 6 (11): 1006–1008. doi:10.1038/sj.embor.7400555. PMC 1371037. PMID 16264422.
  8. ^ de Grey AD (November 2005). "Like it or not, life-extension research extends beyond biogerontology". EMBO Reports. 6 (11): 1000. doi:10.1038/sj.embor.7400565. PMC 1371043. PMID 16264420.
  9. ^ de Grey, Aubrey. "The biogerontology research community's evolving view of SENS". Methuselah Foundation. Retrieved on July 1, 2008.
  10. ^ Belikov AV (January 2019). "Age-related diseases as vicious cycles". Ageing Research Reviews. 49: 11–26. doi:10.1016/j.arr.2018.11.002. PMID 30458244. S2CID 53567141.
  11. ^ a b Hoeijmakers JH (October 2009). "DNA damage, aging, and cancer". The New England Journal of Medicine. 361 (15): 1475–1485. doi:10.1056/NEJMra0804615. PMID 19812404.
  12. ^ Zarbin MA (April 2004). "Current concepts in the pathogenesis of age-related macular degeneration". Archives of Ophthalmology. 122 (4): 598–614. doi:10.1001/archopht.122.4.598. PMID 15078679.
  13. ^ "Facts About Age-Related Macular Degeneration | National Eye Institute". nei.nih.gov. Retrieved 2019-08-06.
  14. ^ Franceschi C, Garagnani P, Morsiani C, Conte M, Santoro A, Grignolio A, et al. (2018-03-12). "The Continuum of Aging and Age-Related Diseases: Common Mechanisms but Different Rates". Frontiers in Medicine. 5: 61. doi:10.3389/fmed.2018.00061. PMC 5890129. PMID 29662881.
  15. ^ Bloom GS (April 2014). "Amyloid-β and tau: the trigger and bullet in Alzheimer disease pathogenesis". JAMA Neurology. 71 (4): 505–508. doi:10.1001/jamaneurol.2013.5847. PMID 24493463.
  16. ^ Wang JC, Bennett M (July 2012). "Aging and atherosclerosis: mechanisms, functional consequences, and potential therapeutics for cellular senescence". Circulation Research. 111 (2): 245–259. doi:10.1161/CIRCRESAHA.111.261388. PMID 22773427.
  17. ^ "Atherosclerosis | National Heart, Lung, and Blood Institute (NHLBI)". www.nhlbi.nih.gov. Retrieved 2019-08-05.
  18. ^ a b "Prostate Enlargement (Benign Prostatic Hyperplasia) | NIDDK". National Institute of Diabetes and Digestive and Kidney Diseases. Retrieved 2019-08-06.
  19. ^ "What is Benign Prostatic Hyperplasia (BPH)? – Urology Care Foundation". www.urologyhealth.org. Retrieved 2019-08-06.
  20. ^ "Benign Prostatic Hyperplasia (BPH) Guideline – American Urological Association". www.auanet.org. Retrieved 2019-08-06.
  21. ^ "Medical Student Curriculum: Benign Prostatic Hypertrophy (BPH) – American Urological Association". www.auanet.org. Retrieved 2019-08-06.
  22. ^ a b Coleman WB, Rubinas TC (2009). "4". In Tsongalis GJ, Coleman WL (eds.). Molecular Pathology: The Molecular Basis of Human Disease. Amsterdam: Elsevier Academic Press. p. 66. ISBN 978-0-12-374419-7.[permanent dead link]
  23. ^ Johnson G (28 December 2010). "Unearthing Prehistoric Tumors, and Debate". The New York Times. from the original on 24 June 2017.
  24. ^ Pawelec G, Derhovanessian E, Larbi A (August 2010). "Immunosenescence and cancer". Critical Reviews in Oncology/Hematology. 75 (2): 165–172. doi:10.1016/j.critrevonc.2010.06.012. PMID 20656212.
  25. ^ Alberts B, Johnson A, Lewis J, et al. (2002). "The Preventable Causes of Cancer". Molecular biology of the cell (4th ed.). New York: Garland Science. ISBN 978-0-8153-4072-0. from the original on 2 January 2016. A certain irreducible background incidence of cancer is to be expected regardless of circumstances: mutations can never be absolutely avoided, because they are an inescapable consequence of fundamental limitations on the accuracy of DNA replication, as discussed in Chapter 5. If a human could live long enough, it is inevitable that at least one of his or her cells would eventually accumulate a set of mutations sufficient for cancer to develop.
  26. ^ Anisimov VN, Sikora E, Pawelec G (August 2009). "Relationships between cancer and aging: a multilevel approach". Biogerontology. 10 (4): 323–338. doi:10.1007/s10522-008-9209-8. PMID 19156531. S2CID 17412298.
  27. ^ de Magalhães JP (May 2013). "How ageing processes influence cancer". Nature Reviews. Cancer. 13 (5): 357–365. doi:10.1038/nrc3497. PMID 23612461. S2CID 5726826.
  28. ^ "Understanding Parkinson's". Parkinson's Foundation. Retrieved 12 August 2020.
  29. ^ Sveinbjornsdottir S (October 2016). "The clinical symptoms of Parkinson's disease". Journal of Neurochemistry. 139 (Suppl 1): 318–324. doi:10.1111/jnc.13691. PMID 27401947.
  30. ^ "Parkinson's Disease Information Page". NINDS. 30 June 2016. Retrieved 18 July 2016.
  31. ^ Carroll WM (2016). International Neurology. John Wiley & Sons. p. 188. ISBN 978-1118777367. from the original on 8 September 2017.
  32. ^ Garcia-Ptacek S, Kramberger MG (September 2016). "Parkinson Disease and Dementia". Journal of Geriatric Psychiatry and Neurology. 29 (5): 261–270. doi:10.1177/0891988716654985. PMID 27502301. S2CID 21279235.
  33. ^ Ahlskog JE (July 2011). "Does vigorous exercise have a neuroprotective effect in Parkinson disease?". Neurology. 77 (3): 288–294. doi:10.1212/wnl.0b013e318225ab66. PMC 3136051. PMID 21768599.
  34. ^ "The top 10 causes of death". WHO. from the original on 2013-12-02.
  35. ^ Ellekjaer H, Holmen J, Indredavik B, Terent A (November 1997). "Epidemiology of stroke in Innherred, Norway, 1994 to 1996. Incidence and 30-day case-fatality rate". Stroke. 28 (11): 2180–2184. doi:10.1161/01.STR.28.11.2180. PMID 9368561. from the original on February 28, 2008.
  36. ^ National Institute of Neurological Disorders and Stroke (NINDS) (1999). "Stroke: Hope Through Research". National Institutes of Health. from the original on 2015-10-04.
  37. ^ Senelick RC, Rossi PW, Dougherty K (1994). Living with Stroke: A Guide for Families. Contemporary Books, Chicago. ISBN 978-0-8092-2607-8. OCLC 40856888.
  38. ^ Stokar J (May 2023). "Targeting senescent cells in ageing-related endocrine diseases". Nature Reviews. Endocrinology. 19 (7): 382. doi:10.1038/s41574-023-00848-x. PMID 37173439. S2CID 258663551.
  39. ^ Trajanoska K, Schoufour JD, de Jonge EA, Kieboom BC, Mulder M, Stricker BH, et al. (September 2018). "Fracture incidence and secular trends between 1989 and 2013 in a population based cohort: The Rotterdam Study". Bone. 114: 116–124. doi:10.1016/j.bone.2018.06.004. PMID 29885926. S2CID 47016339.
  40. ^ Hirode G, Wong RJ (June 2020). "Trends in the Prevalence of Metabolic Syndrome in the United States, 2011-2016". JAMA. 323 (24): 2526–2528. doi:10.1001/jama.2020.4501. PMC 7312413. PMID 32573660.

External links edit

  • Segmental Progeria

aging, associated, diseases, aging, associated, disease, commonly, termed, related, disease, disease, that, most, often, seen, with, increasing, frequency, with, increasing, senescence, they, essentially, complications, senescence, distinguished, from, aging, . An aging associated disease commonly termed age related disease ARD is a disease that is most often seen with increasing frequency with increasing senescence They are essentially complications of senescence distinguished from the aging process itself because all adult animals age with rare exceptions but not all adult animals experience all age associated diseases The term does not refer to age specific diseases such as the childhood diseases chicken pox and measles only diseases of the elderly They are also not accelerated aging diseases all of which are genetic disorders Age specific SEER incidence rates 2003 2007Examples of aging associated diseases are atherosclerosis and cardiovascular disease cancer arthritis cataracts osteoporosis type 2 diabetes hypertension and Alzheimer s disease The incidence of all of these diseases increases exponentially with age 1 Of the roughly 150 000 people who die each day across the globe about two thirds 100 000 per day die of age related causes 2 In industrialized nations the proportion is higher reaching 90 2 Contents 1 Patterns of differences 2 Research 3 Types 3 1 Macular degeneration 3 2 Alzheimer s 3 3 Atherosclerosis 3 4 Benign prostatic hyperplasia 3 5 Cancer 3 6 Parkinson s 3 7 Stroke 3 8 Endocrine diseases 3 8 1 Osteoporosis 3 8 2 Metabolic syndrome 4 See also 5 References 6 External linksPatterns of differences editBy age 3 about 30 of rats have had cancer whereas by age 85 about 30 of humans have had cancer Humans dogs and rabbits get Alzheimer s disease but rodents do not Elderly rodents typically die of cancer or kidney disease but not of cardiovascular disease In humans the relative incidence of cancer increases exponentially with age for most cancers but levels off or may even decline by age 60 75 3 although colon rectal cancer continues to increase 4 People with the so called segmental progerias are vulnerable to different sets of diseases Those with Werner s syndrome experience osteoporosis cataracts and cardiovascular disease but not neurodegeneration or Alzheimer s disease those with Down syndrome have type 2 diabetes and Alzheimer s disease but not high blood pressure osteoporosis or cataracts In Bloom syndrome those affected most often die of cancer Research editAging senescence increases vulnerability to age associated diseases whereas genetics determines vulnerability or resistance between species and individuals within species Some age related changes like graying hair are said to be unrelated to an increase in mortality But some biogerontologists believe that the same underlying changes that cause graying hair also increase mortality in other organ systems and that understanding the incidence of age associated disease will advance knowledge of the biology of senescence just as knowledge of childhood diseases advanced knowledge of human development 5 Strategies for engineered negligible senescence SENS is an emerging research strategy that aims to repair root causes for age related illness and degeneration as well as develop medical procedures to periodically repair all such damage in the human body thereby maintaining a youth like state indefinitely 6 The SENS programme has identified seven types of aging related damage and feasible solutions have been outlined for each Some critics argue that the SENS agenda is optimistic at best and that the aging process is too complex and little understood for SENS to be scientific or implementable in the foreseeable future 7 8 9 It has been proposed that age related diseases are mediated by vicious cycles 10 On the basis of extensive research DNA damage has emerged a major culprit in cancer and numerous other diseases related to ageing 11 DNA damage can initiate the development of cancer or other aging related diseases depending on several factors These include the type amount and location of the DNA damage in the body the type of cell experiencing the damage and its stage in the cell cycle and the specific DNA repair processes available to react to the damage 11 Types editMacular degeneration edit Age related macular degeneration AMD is a disease that affects the eyes and can lead to vision loss through break down of the central part of the retina called the macula Degeneration can occur in one eye or both and can be classified as either wet neovascular or dry atrophic Wet AMD commonly is caused by blood vessels near the retina that lead to swelling of the macula 12 The cause of dry AMD is less clear but it is thought to be partly caused by breakdown of light sensitive cells and tissue surrounding the macula A major risk factor for AMD is age over the age of 60 13 Alzheimer s edit Alzheimer s disease is classified as a protein misfolding disease Aging causes mutations in protein folding and as a result causes deposits of abnormal modified proteins to accumulate in specific areas of the brain In Alzheimer s deposits of Beta amyloid and hyperphosphorylated tau protein form extracellular plaques and extracellular tangles 14 These deposits are shown to be neurotoxic and cause cognitive impairment due to their initiation of destructive biochemical pathways 15 Atherosclerosis edit Atherosclerosis is categorized as an aging disease and is brought about by vascular remodeling the accumulation of plaque and the loss of arterial elasticity Over time these processes can stiffen the vasculature For these reasons older age is listed as a major risk factor for atherosclerosis 16 Specifically the risk of atherosclerosis increases for men above 45 years of age and women above 55 years of age 17 Benign prostatic hyperplasia edit Benign prostatic hyperplasia BPH is a noncancerous enlargement of the prostate gland due to increased growth 18 An enlarged prostate can result in incomplete or complete blockage of the bladder and interferes with a man s ability to urinate properly Symptoms include overactive bladder decreased stream of urine hesitancy urinating and incomplete emptying of the bladder 19 20 By age 40 10 of men will have signs of BPH and by age 60 this percentage increases by 5 fold Men over the age of 80 have over a 90 chance of developing BPH and almost 80 of men will develop BPH in their lifetime 18 21 Cancer edit Although it is possible for cancer to strike at any age most patients with invasive cancer are over 65 22 and the most significant risk factor for developing cancer is age 22 According to cancer researcher Robert A Weinberg If we lived long enough sooner or later we all would get cancer 23 Some of the association between aging and cancer is attributed to immunosenescence 24 errors accumulated in DNA over a lifetime 25 and age related changes in the endocrine system 26 Aging s effect on cancer is complicated by factors such as DNA damage and inflammation promoting it and factors such as vascular aging and endocrine changes inhibiting it 27 Parkinson s edit Parkinson s disease or simply Parkinson s 28 is a long term degenerative disorder of the central nervous system that mainly affects the motor system The disease has many complications including Dementia depression anxiety 29 Parkinson s disease typically occurs in people over the age of 60 of whom about one percent are affected 30 31 The prevalence of Parkinson s disease dementia also increases with age and to a lesser degree duration of the disease 32 Exercise in middle age may reduce the risk of PD later in life 33 Stroke edit Stroke was the second most frequent cause of death worldwide in 2011 accounting for 6 2 million deaths 11 of the total 34 Stroke could occur at any age including in childhood the risk of stroke increases exponentially from 30 years of age and the cause varies by age 35 Advanced age is one of the most significant stroke risk factors 95 of strokes occur in people age 45 and older and two thirds of strokes occur in those over the age of 65 36 37 A person s risk of dying if he or she does have a stroke also increases with age Endocrine diseases edit Studies in animal models show that clearance of senescent cells improves multiple age related endocrine disorders 38 Osteoporosis edit Bone density declines with age By the age of 85 years 70 of women and 30 of men have a osteoporosis defined as a bone density less than or equal to 2 5 standard deviations lower than young adults 39 Metabolic syndrome edit The metabolic syndrome is the co occurrence of metabolic risk factors for type 2 diabetes and cardiovascular disease abdominal obesity hyperglycemia dyslipidemia and hypertension The prevalence of the metabolic syndrome increases with age reaching close to 50 of people over 60 years old in the USA 40 asSee also editAccelerated aging disease Alliance for Aging Research Gerontology SenescenceReferences edit Belikov AV January 2019 Age related diseases as vicious cycles Ageing Research Reviews 49 11 26 doi 10 1016 j arr 2018 11 002 PMID 30458244 S2CID 53567141 a b de Grey A 2007 Life Span Extension Research and Public Debate Societal Considerations PDF Studies in Ethics Law and Technology 1 1 Article 5 CiteSeerX 10 1 1 395 745 doi 10 2202 1941 6008 1011 S2CID 201101995 Archived from the original PDF on October 13 2016 Retrieved August 7 2011 Belikov AV September 2017 The number of key carcinogenic events can be predicted from cancer incidence Scientific Reports 7 1 12170 Bibcode 2017NatSR 712170B doi 10 1038 s41598 017 12448 7 PMC 5610194 PMID 28939880 SEER Cancer Statistics Review 1975 2003 PDF Surveillance Epidemiology and End Results SEER National Cancer Institute Archived from the original PDF on 2006 09 25 Retrieved 2006 11 20 Hayflick L June 2004 The not so close relationship between biological aging and age associated pathologies in humans The Journals of Gerontology Series A Biological Sciences and Medical Sciences 59 6 B547 B550 doi 10 1093 gerona 59 6 B547 PMID 15215261 The SENS Platform An Engineering Approach to Curing Aging Archived 2008 08 31 at the Wayback Machine Methuselah Foundation Retrieved on June 28 2008 Warner H Anderson J Austad S Bergamini E Bredesen D Butler R et al November 2005 Science fact and the SENS agenda What can we reasonably expect from ageing research EMBO Reports 6 11 1006 1008 doi 10 1038 sj embor 7400555 PMC 1371037 PMID 16264422 de Grey AD November 2005 Like it or not life extension research extends beyond biogerontology EMBO Reports 6 11 1000 doi 10 1038 sj embor 7400565 PMC 1371043 PMID 16264420 de Grey Aubrey The biogerontology research community s evolving view of SENS Methuselah Foundation Retrieved on July 1 2008 Belikov AV January 2019 Age related diseases as vicious cycles Ageing Research Reviews 49 11 26 doi 10 1016 j arr 2018 11 002 PMID 30458244 S2CID 53567141 a b Hoeijmakers JH October 2009 DNA damage aging and cancer The New England Journal of Medicine 361 15 1475 1485 doi 10 1056 NEJMra0804615 PMID 19812404 Zarbin MA April 2004 Current concepts in the pathogenesis of age related macular degeneration Archives of Ophthalmology 122 4 598 614 doi 10 1001 archopht 122 4 598 PMID 15078679 Facts About Age Related Macular Degeneration National Eye Institute nei nih gov Retrieved 2019 08 06 Franceschi C Garagnani P Morsiani C Conte M Santoro A Grignolio A et al 2018 03 12 The Continuum of Aging and Age Related Diseases Common Mechanisms but Different Rates Frontiers in Medicine 5 61 doi 10 3389 fmed 2018 00061 PMC 5890129 PMID 29662881 Bloom GS April 2014 Amyloid b and tau the trigger and bullet in Alzheimer disease pathogenesis JAMA Neurology 71 4 505 508 doi 10 1001 jamaneurol 2013 5847 PMID 24493463 Wang JC Bennett M July 2012 Aging and atherosclerosis mechanisms functional consequences and potential therapeutics for cellular senescence Circulation Research 111 2 245 259 doi 10 1161 CIRCRESAHA 111 261388 PMID 22773427 Atherosclerosis National Heart Lung and Blood Institute NHLBI www nhlbi nih gov Retrieved 2019 08 05 a b Prostate Enlargement Benign Prostatic Hyperplasia NIDDK National Institute of Diabetes and Digestive and Kidney Diseases Retrieved 2019 08 06 What is Benign Prostatic Hyperplasia BPH Urology Care Foundation www urologyhealth org Retrieved 2019 08 06 Benign Prostatic Hyperplasia BPH Guideline American Urological Association www auanet org Retrieved 2019 08 06 Medical Student Curriculum Benign Prostatic Hypertrophy BPH American Urological Association www auanet org Retrieved 2019 08 06 a b Coleman WB Rubinas TC 2009 4 In Tsongalis GJ Coleman WL eds Molecular Pathology The Molecular Basis of Human Disease Amsterdam Elsevier Academic Press p 66 ISBN 978 0 12 374419 7 permanent dead link Johnson G 28 December 2010 Unearthing Prehistoric Tumors and Debate The New York Times Archived from the original on 24 June 2017 Pawelec G Derhovanessian E Larbi A August 2010 Immunosenescence and cancer Critical Reviews in Oncology Hematology 75 2 165 172 doi 10 1016 j critrevonc 2010 06 012 PMID 20656212 Alberts B Johnson A Lewis J et al 2002 The Preventable Causes of Cancer Molecular biology of the cell 4th ed New York Garland Science ISBN 978 0 8153 4072 0 Archived from the original on 2 January 2016 A certain irreducible background incidence of cancer is to be expected regardless of circumstances mutations can never be absolutely avoided because they are an inescapable consequence of fundamental limitations on the accuracy of DNA replication as discussed in Chapter 5 If a human could live long enough it is inevitable that at least one of his or her cells would eventually accumulate a set of mutations sufficient for cancer to develop Anisimov VN Sikora E Pawelec G August 2009 Relationships between cancer and aging a multilevel approach Biogerontology 10 4 323 338 doi 10 1007 s10522 008 9209 8 PMID 19156531 S2CID 17412298 de Magalhaes JP May 2013 How ageing processes influence cancer Nature Reviews Cancer 13 5 357 365 doi 10 1038 nrc3497 PMID 23612461 S2CID 5726826 Understanding Parkinson s Parkinson s Foundation Retrieved 12 August 2020 Sveinbjornsdottir S October 2016 The clinical symptoms of Parkinson s disease Journal of Neurochemistry 139 Suppl 1 318 324 doi 10 1111 jnc 13691 PMID 27401947 Parkinson s Disease Information Page NINDS 30 June 2016 Retrieved 18 July 2016 Carroll WM 2016 International Neurology John Wiley amp Sons p 188 ISBN 978 1118777367 Archived from the original on 8 September 2017 Garcia Ptacek S Kramberger MG September 2016 Parkinson Disease and Dementia Journal of Geriatric Psychiatry and Neurology 29 5 261 270 doi 10 1177 0891988716654985 PMID 27502301 S2CID 21279235 Ahlskog JE July 2011 Does vigorous exercise have a neuroprotective effect in Parkinson disease Neurology 77 3 288 294 doi 10 1212 wnl 0b013e318225ab66 PMC 3136051 PMID 21768599 The top 10 causes of death WHO Archived from the original on 2013 12 02 Ellekjaer H Holmen J Indredavik B Terent A November 1997 Epidemiology of stroke in Innherred Norway 1994 to 1996 Incidence and 30 day case fatality rate Stroke 28 11 2180 2184 doi 10 1161 01 STR 28 11 2180 PMID 9368561 Archived from the original on February 28 2008 National Institute of Neurological Disorders and Stroke NINDS 1999 Stroke Hope Through Research National Institutes of Health Archived from the original on 2015 10 04 Senelick RC Rossi PW Dougherty K 1994 Living with Stroke A Guide for Families Contemporary Books Chicago ISBN 978 0 8092 2607 8 OCLC 40856888 Stokar J May 2023 Targeting senescent cells in ageing related endocrine diseases Nature Reviews Endocrinology 19 7 382 doi 10 1038 s41574 023 00848 x PMID 37173439 S2CID 258663551 Trajanoska K Schoufour JD de Jonge EA Kieboom BC Mulder M Stricker BH et al September 2018 Fracture incidence and secular trends between 1989 and 2013 in a population based cohort The Rotterdam Study Bone 114 116 124 doi 10 1016 j bone 2018 06 004 PMID 29885926 S2CID 47016339 Hirode G Wong RJ June 2020 Trends in the Prevalence of Metabolic Syndrome in the United States 2011 2016 JAMA 323 24 2526 2528 doi 10 1001 jama 2020 4501 PMC 7312413 PMID 32573660 External links editSegmental Progeria nbsp Wikimedia Commons has media related to Aging associated diseases Retrieved from https en wikipedia org w index php title Aging associated diseases amp oldid 1208453029, wikipedia, wiki, book, books, library,

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