(1)<\/a>\u00a0Figure 6, \u201cFunctional Interconnections between the Hallmarks of Aging.\u201d<\/i><\/p>\nThere will be a number articles that cover the research paper, each focusing on a different group of hallmarks. We start with the first one:<\/p>\n
Genomic Instability<\/h2>\n
As we get older, our genes get attacked and more mutations occur.\u00a0<\/i><\/p>\n
The DNA that sits in each and every one of our cells is an encyclopaedia. It gives instructions in code, using the four bases A, T, G and C instead of the binary code of our computers or the 26 letters of English. Put three of these bases in a row and you have a\u00a0codon<\/b>. A codon is essentially a word, saying the name of a single building block of a protein. These building blocks are individual molecules called\u00a0amino acids<\/b>, and a string of amino acids is what makes up a protein. The whole list of codons that creates one protein from start to finish is called a gene.<\/p>\n
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Proteins can be a string up to 2000 amino acids long. In order to turn from a string of building blocks into a proper protein, the string needs to fold up in a very specific way. If there is a wrong amino acid in the string, or something stops the string folding up properly, then the end protein will not work. Proteins are a marvelously diverse and wide ranging group, able to be anything from signalling molecule to muscle fibre or catalyst. The function it takes on is dependent on its shape,\u00a0 in the same way that a chair or a table\u2019s function is derived from the shape of the wood used. The extensive functions of proteins is how DNA is able to act as a control manual for the cell, as by determining which parts of the DNA are read and translated into proteins, we create cells with different functions\u00a0(2).<\/p>\n
DNA is constantly under some form of attack, from physical and chemical dangers on the outside (like cigarette smoke and the sun\u2019s UV rays) to internal errors when the DNA copying method doesn\u2019t work as perfectly as it should.<\/p>\n
The attacks leave things like mutations. Not every mutation is dangerous, and DNA has strong repair mechanisms to minimise the harm, but if enough time goes by then the damage builds up. Eventually there are enough bad mutations that it leads to proteins not being made correctly, which in turn leads to dysfunctional cells that don\u2019t work like they once did. It is these repercussions that become what we see and experience as aging.<\/p>\n
Conclusion<\/h2>\n
This is only an introduction to the reasons why we age. Genomic instability is probably the hardest hallmark to understand if you come from a non-biomedical science background, but the other processes are just as intriguing. An article covering the rest of the primary damage causing hallmarks will come shortly. For further reading in the mean time, the papers referenced in this article are below.<\/p>\n
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![\"Grace](\"https:\/\/nem.health\/wp-content\/uploads\/2022\/11\/Grace-Marshall.jpeg\")
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Grace Marshall MSc<\/h4>\n
Bioentrepreneurship
\nNordic Executive Medicine<\/p>\n
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