My family and I have been sick for the past week or so, and during that time this topic popped into my head as I watched the difference between onset and recovery of symptoms between each family member.
Every cell in our bodies have an innate immune response to various insults, for example interferon pressure in the case of viral insult. Specialized cells extend these responses innate at the cellular level, and it got me thinking about how “memory T” and “memory B” (or “helper”) adaptively control immune response (not unlike astrocytes).
Along the same conceit, if aging is indeed a type of “cellular dementia”, we should be able to see this systemically, including response to microbial insult. This steady stripping of memory may reduce the precision of response, resulting in more severe downstream effects as we age.
What I keep coming back to is that loss of epigenetic information may not induce aging, but rather reduces protection against external insult. And external insult is unavoidable.
The most significant problem with the conceit is that for the most part, we aren’t born with the epigenetic information we lose in this process, and the process of maturity is specially a gathering process.
The conceit would require that individuals who develop on different timescales also have different “epigentic ages” as well. We often lose this conceit, that individuals mature at different rates, and sometimes significantly different, and this difference should be detectable in the lifespans of a population.
Could this conceit be driven by lab animals experiencing retarded development, thus extending their lifespans?
Is there any evidence that supports “fully developed” organisms starting these treatments and exhibiting extended life spans?
Notably missing from the work around this topic is work with aged or fully mature animals.
Rather than using this “epigenetic age” construct, which seems a little dicey, could we use “immunologic age” as an equivalent?
Neurologic Adverse Events of Immune Checkpoint Inhibitors – Do developmental checkpoints drive response to immunologic insult?
MicroRNA-mediated regulation of reactive astrocytes in central nervous system diseases – Relationship between metabolic insult response adaptivity and onset of “disease” itself.
Edit: Okay, apparently this is already a thing and described as the “immunological theory of aging”.
The interplay between immunosenescence and age-related diseases
My previous thought about this was that maximum age is a genetically derviable metabolic equation, this max is reduced by insults. We have continued to make amazing strides at reducing the impact of the most significant insults (specifically, control of pathology inducing organisms), increasing total lifespan maximum.
That “average age” has increased isn’t a sign that we’ve modified the maximum, it’s an indication that we’ve removed metabolic insults that subtracted from that maximum. We’re still hard capped at ~90 years with outliers achieving up to 50% on top of that. Outlier epigenomes are locked to the local environment, a family that lives on average 100 years in one environment may may only live 60 in another environment for instance. There’s no universal “extending” environment (metabolically).