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home:diseases:aging [12.06.2018] – [Aging (senescence)] sallieqhome:diseases:aging [01.26.2019] – [summary of Olmesartan research on aging] sallieq
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   * **Cellular theory** – According to this theory, the normal body has a finite potential to replicate and maintain functional capacity (Hayflick limit).   * **Cellular theory** – According to this theory, the normal body has a finite potential to replicate and maintain functional capacity (Hayflick limit).
  
 +==== Breaking up defunct cells ====
  
 +[[https://www.ebiomedicine.com/article/S2352-3964(18)30629-7/fulltext|Article in Press
 +Senolytics in idiopathic pulmonary fibrosis]]  
 +<blockquote>
 + Selectively ablating senescent cells using dasatinib plus quercetin (DQ) alleviates IPF-related dysfunction in bleomycin-administered mice.
 +
 +Our first-in-humans open-label pilot supports study feasibility and provides initial evidence that senolytics may alleviate physical dysfunction in IPF  (({{pubmed>long:30616998}})).</blockquote>
 ===== Diseases of the aging are chronic diseases ===== ===== Diseases of the aging are chronic diseases =====
  
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 Aging deeply affects (or is affected by!) the human microbiota's homeostasis with the host's immune system:(({{pubmed>long: 20498852}})) (({{pubmed>long:22283774}})) Aging deeply affects (or is affected by!) the human microbiota's homeostasis with the host's immune system:(({{pubmed>long: 20498852}})) (({{pubmed>long:22283774}}))
-  * **macrophage function** – Macrophages, which act as "pathogen sensors", lose the ability to initiate an inflammatory response as people age.(({{pubmed>long:15268749}})) Microbes use a variety of methods to infect macrophages. For example, //Neisseria meningitidis// prevents macrophage apoptosis via genes encoding nitric oxide detoxification and a porin, PorB.(({{pubmed>long:16369030}}))+
   * **autoimmune** – As people age, their risk for developing an "autoimmune" condition also increases.(({{pubmed>long:1822969}})) The article on [[home:alternate:autoimmunity|autoimmune conditions]] discusses why so-called “autoantibodies” are merely antibodies generated in response to pathogenic bacterial cells that have been destroyed as a result of an active immune response.   * **autoimmune** – As people age, their risk for developing an "autoimmune" condition also increases.(({{pubmed>long:1822969}})) The article on [[home:alternate:autoimmunity|autoimmune conditions]] discusses why so-called “autoantibodies” are merely antibodies generated in response to pathogenic bacterial cells that have been destroyed as a result of an active immune response.
 +  * **macrophage function** – Macrophages, which act as "pathogen sensors", lose the ability to initiate an inflammatory response as people age.(({{pubmed>long:15268749}})) Microbes use a variety of methods to infect macrophages. For example, //Neisseria meningitidis// prevents macrophage apoptosis via genes encoding nitric oxide detoxification and a porin, PorB.(({{pubmed>long:16369030}}))
 +
 +
 +<blockquote>This theory is based on the fact that genes affecting host organism longevity are represented by subpopulations: genes of host eukaryotic cells, commensal microbiota, and non-living genetic elements. ........... we propose that lifespan and aging are defined by the accumulation of alterations over all genes of macroorganism and microbiome and the non-living genetic elements associated with them. (({{pubmed>long:29978435}}))  </blockquote>
 +
  
 Could the chronic inflammation associated with aging be caused by pathogens? Given the crudeness of tools now used to measure microbes and the ubiquity of the human microbiota, this seems like a reasonable if not inevitable conclusion as the early studies have begun to suggest.  Could the chronic inflammation associated with aging be caused by pathogens? Given the crudeness of tools now used to measure microbes and the ubiquity of the human microbiota, this seems like a reasonable if not inevitable conclusion as the early studies have begun to suggest. 
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 //**E. Cevenini**//(({{pubmed>long:20388071}}))</blockquote> //**E. Cevenini**//(({{pubmed>long:20388071}}))</blockquote>
 +
 +
  
  
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 +===== Recent research =====
 +
 +Cell membranes are primarily made up of two types of lipids — phospholipids and glycolipids. Inside cells, these lipids bind to a molecule called CD1d that transports them to the surface. Once there, phospholipids stimulate phospholipid-reactive T cells, and glycolipids stimulate a different type of T cell called iNKTs.
 +
 +On their way to the cell’s surface, phospholipids more easily attach themselves to CD1d molecules, making it more difficult for glycolipids to attach to CD1d. Because of this, it is harder for glycolipids to make it to the surface of the cell. This means that iNKTs cannot be as easily stimulated by glycolipids.
  
 +Scientists believe iNKT cells are necessary because they appear to protect cells against the progression of certain cancers and autoimmune diseases. However, iNKT cells are extremely active and can cause alcoholic hepatitis or other types of liver diseases if they are overstimulated. The phospholipid’s ability to more easily bind to CD1d molecules than glycolipids keeps a balance between the two cell types and maintains homeostasis in the immune system.   (({{pubmed>long:30508304}})) 
 ===== Read more ===== ===== Read more =====
  
   * **Declining testosterone levels in men not part of normal aging, study finds** – A [[http://www.eurekalert.org/pub_releases/2012-06/tes-dtl062212.php|2012 study]] found that declining testosterone levels are not an inevitable part of the aging process, as many people think. Men who had declines in testosterone were more likely to be those who became obese, had stopped smoking or were depressed at either clinic visit.   * **Declining testosterone levels in men not part of normal aging, study finds** – A [[http://www.eurekalert.org/pub_releases/2012-06/tes-dtl062212.php|2012 study]] found that declining testosterone levels are not an inevitable part of the aging process, as many people think. Men who had declines in testosterone were more likely to be those who became obese, had stopped smoking or were depressed at either clinic visit.
 +  * [[https://immunityageing.biomedcentral.com/articles/10.1186/1742-4933-3-12/comments|We have a lot to learn about 'diseases of the aging']]
  
  
-==== summary of Olmesartan research on aging ====+==== summary of research into effects of Olmesartan ====
  
  
-[[home:food:aim_health:aging|Geriatric protective effects of Olmesartan]]+[[home:food:aim_health:aging|Protective effects of Olmesartan]]
  
  
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 ===== Notes and comments ===== ===== Notes and comments =====
    
 +//Lee// " I am 70 now (not 65) when we started this conversation ...lolDr's were amazed that I was in such good shape and all fractures were closed and healed well. I would like to say I may not bicycle ride now ..but it's a family thing and I probably will "
  
 +  (({{pubmed>long:000}})) 
 +  
 <DiseaseHierarchy> <DiseaseHierarchy>
  
home/diseases/aging.txt · Last modified: 09.14.2022 by 127.0.0.1
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