Inasmuch as one enjoys being alive, waiting longer until the signs of frailty and old age occur seems an appealing proposition, and so there is an entire field of research dedicated to understand the aging process. A recent summary for a popular audience is in David Sinclair's recent book Lifespan. But I wanted to provide a deeper and more concise explanation, plus communicating not only the results but also their robustness. There is also a previous Longevity FAQ from Laura Deming, but I thought something a bit longer that explains the field from the ground up should exist.
At first, reading about research regarding longevity can seem like magic: "We knocked out Sirt1 in mice, leading to reduced lifespan". That sentence is not only compressing a lot of information (What does it mean to knock out? What's Sirt1?) but also once we know that knocking out Sirt1 means to stop a gene from being expressed (i.e. stopping the cell from manufacturing the protein associated with that gene), we may want to know things like "Are there different ways of knocking out genes? How do different genes related in the genetics of aging relate to each other? If we do the same things in dogs, does it work?"
My goal here is to demystify what seems initially obscure, and to make available a summary of the current state of the art, the quality of the evidence available so far, and what promising avenues of research are being pursued at the moment.
If you disagree with anything said here, you can get in touch with me if you want to correct this FAQ (You may get paid if you do so!) or to suggest additions to it. To write this FAQ, I've reviewed over 100 papers, most of these literature reviews themselves. Everything I say is referenced, but you can find the sources, tagged by area here. As people comment and review the FAQ, I'll be making changes to make sure it stays up to date.
I will explain first some key concepts as this will make it easier to understand what is going on
From a structural perspective, DNA is a double-helix of two chains of nucleotides (adenine, thymine, guanine, cytosine, ATGC). If we take one of the strands of this double-helix, one can identify different sections that do different things, these are the genes. In turn, a given gene can be further broken down into codons, or triplets of nucleotides, e.g. the sequence A-T-G.
To go from the sequence of codons to something more interesting, the DNA is copied by the enzyme RNA polymerase into a strand of RNA (pre-mRNA) which is then modified to eventually become messenger RNA (mRNA). A single strand of pre-mRNA can yield many strands of mRNA. A strand of pre-mRNA can be thought of as a chain of "useful" sections (exons) and "separator" sections (introns). pre-mRNA is cut at the introns and joined back together by a spliceosome, a complex association of 80 proteins conforming a molecular machine. This process is not always the same! Depending on how this cutting and pasting happens, different mRNA sequences will result, in turn leading to different proteins being made out of the same gene.
mRNA is basically like one of the two strands of DNA but instead of using ATGC, it has uracil instead of thymine, so AUGC. The strand of mRNA is sent into the cytoplasm of the cell where they reach the ribosomes. There, yet another form of RNA, transfer RNA (tRNA) reads the mRNA and assembles a chain of amino acids in the order dictated by the codons. So if the mRNA says AUG-GCU-UAA we get methionine-alanine (The last codon is a stop codon, and stops the transcription right there).
But because there are so many of them, and because they have a few functional groups attached to them, they will interact with each other and end up curling up to conform a protein.
Occasionally more than a single chain will be required for a protein to be assembled. To recap, if we write down the DNA sequence, we can know what amino acids will be produced and how they will be stitched together. But knowing how the protein will assemble itself, and what final shape it will adopt is a very hard problem