David Sinclair· PhD
A loss of cell identity with age is a key feature of the ITOA, first described in the book Lifespan, and in this paper https://t.co/PHbmJSdikt
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The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
A loss of cell identity with age is a key feature of the ITOA, first described in the book Lifespan, and in this paper https://t.co/PHbmJSdikt
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how all of this makes up the "Information Theory of Aging"
Also, a groundbreaking new theory also suggests ageing is driven by the loss of vital regulatory information within our cells — rather than primarily accumulating damage over time, as previously thought
Exactly what The Information Theory of Aging (ITOA) predicts: 1. DNA damage -> 2. Epigenetic noise -> 3. Loss of cell identity -> 4. Aging -> 5. Frailty & disease
The Information Theory of Aging says aging is the deregulation of genes later in life, especially developmental genes.
If most cells maintain essentially the same DNA sequence throughout life, why do they progressively lose function? Why do young cells know how to repair themselves and maintain their identity, while old cells gradually lose those abilities?
The ITOA theory proposes that aging is caused, at least in part, by the progressive loss of epigenetic information. Cells retain the digital information encoded in their DNA, but over time lose access to the analog instructions that tell them how to read that information correctly.
What is the Information Theory of Aging (ITOA)? 1. Embryo cell identity is established by the epigenome 2. Epigenome erodes 3. Cells lose identity 4. Tissues malfunction 5. A back-up copy exists 6. Cells can be reset to regain identity
This is exactly what the Information Theory of Aging (ITOA) predicts: epigenetic information drifts first, and mitochondrial dysfunction follows as a downstream consequence. Loss of control causes loss of efficiency and compensatory overproduction...
In short, mitochondrial changes in aging aren’t random. They’re part of a predictable cascade triggered by epigenetic noise. And this new paper adds another piece of evidence that aging begins upstream, in the information layer
Aging isn't a hardware failure, it is a software corruption issue.
That idea eventually evolved into what I call the Information Theory of Aging (ITOA): DNA breaks force the cell to reshuffle chromatin regulators to repair the genome. Over time the epigenetic landscape becomes disorganized
And in fact, is now, I would say, the leading theory of why we age.
I came to the I wouldn't say conclusion but very strong gut feeling as a scientist that it's a loss of information that causes up probably all of those hallmarks of aging and and aging itself
i came to the i wouldn't say conclusion but very strong gut feeling as a scientist that it's a loss of information that causes uh probably all of those hallmarks of aging and and aging itself and so that this could be the very upstream uh part of the river
it's a loss of information that causes uh probably all of those hallmarks of aging
I think that the problem with what I'm calling the information theory of aging which is what I wrote about in my book is that we do lose information every cell does experience mutations it's not perfect though
the problem with what I'm calling the information theory of aging which is what I wrote about in my book is that we do lose information every cell does experience mutations
Right. This is all part of my idea, my hypothesis called the information theory of aging, is that we're really losing the information regulation over time and all of these other things that occur such as telomere loss, and mitochondria loss, and loss of proteostasis, as Andy would call it, loss of protein folding mechanisms, this could be upstream of all of that, that our cells lose their identity and don't turn on the right genes the way they did when we were young.