Cells Across the Body Talk to Each Other About Aging (Quanta)

Biologists discovered that mitochondria in different tissues talk to each other to repair injured cells. When their signal fails, the biological clock starts winding down.

Recently, a set of papers documented a new biochemical pathway that regulates aging, one based on signals passed between mitochondria, the organelles best known as the powerhouse of the cell. Working with worms, the researchers found that damage to mitochondria in brain cells triggered a repair response that was then amplified, setting off similar reactions in mitochondria throughout the worm’s body. The effect of this repair activity was to extend the organism’s life span: The worms with repaired mitochondrial damage lived 50% longer.

What’s more, cells in the germline — the cells that produce eggs and sperm — were central to this anti-aging communication system. It’s a finding that adds new dimensions to the fertility concerns implied when people talk about aging and their “biological clock.” Some of the findings were reported in Science Advances and others were posted on the scientific preprint server biorxiv.org in the fall.

The research builds on a recent body of work that suggests that mitochondria are social organelles that can talk to one another even when they are in different tissues. In essence, the mitochondria function as cellular walkie-talkies, sending messages throughout the body that influence the survival and life span of the entire organism.

Full article:

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the mitochondria in stressed neurons were using vesicles — bubblelike containers that move materials around the cell or between cells — to carry a signal called Wnt beyond the nerve cells to other cells in the body

The germline receives these signals:

As long as the germ cells are healthy, they send pro-survival signals to ensure that their host organism survives to reproduce

This turns on its head the dogma that longevity and reproduction are, loosely speaking, inversely related both evolutionarily and for the individual. It might even indicate that keeping the germ lines healthy, such as rapamycin seems to do with ovaries, preserves this signalling and enhances longevity.

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This is very cool! The closest thing to it I ever read was many years ago about how bacterial colonies colonizing different non-contiguous regions of the skin could communicate with each other, using our immune system as a carrier / vehicle. It was mind blowing.

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It does make me wonder though, that women have higher lifespan than men even though they run out of germ cells altogether whereas men don’t.

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Men don’t have estrogen protecting them from plaque accumulation until their late 40s :wink:

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This would also explain why aging in women seems to accelerate with menopause, and how pausing menopause may increase lifespan and healthspan in women.

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I don’t see any way to pause menopause though, only slow it down. Ovarian reserve keeps dwindling and only the rate can be slowed down. If you know anything otherwise in this field I’m all ears.

Just the work that Yusin Sun at Colombia U. is doing with rapamycin, and Oviva… perhaps combined they may provide some temporary pausing of menopause or revitalization of the ovary… The Biggest Breakthrough in Longevity May Start With Menopause

I don’t think women run out of eggs, they just quit maturing.

They do run out not because they “lay” them during ovulation but because the eggs get resorbed by the body. They do disappear though.

Ok, thanks … I didn’t know that.

All the other eggs present in that cycle’s group that haven’t been selected as the dominant follicle undergo atresia, which means that they die. This happens every month. You ovulate one egg, and the rest of the growing cohort or group die.

Yeah, I wonder what my reserve is as I’ve stopped ovulating at 25 from my first pregnancy and had 4 kids in total roughly two years apart, with over a year of breastfeeding in between for each of them, which also halts ovulation. All things equal based on these factors I should have a higher ovarian reserve now that I’m 37 compared to a 37 yo woman who never had kids. But it’s hard to quantify.

Men on rapamycin also have changes to fertility.

The post goes on to support the idea that these negatives reverse once rapamycin is discontinued, but I wonder if those negatives aren’t actually a result of preservation of the male germ lines. Any thoughts?

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So, you’re suggesting that (like in women with eggs) you’re just pausing spermatogenesis, and therefore maintaining fertility for longer. That seems like an entirely plausible explanation for the temporary fertility decrease during rapamycin use, very similar to what is seen with caloric restriction. Basically the body is pausing sexual reproduction during “fasting” times, and prioritizing survival and autophagy/maintenance, for better times.

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Yes, and you said it so much better than I could. This is just speculation, and I haven’t seen any possible research on this.

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Very interesting. Perhaps it’s not a (Dawkins) selfish gene thing but a mitochondria using our genome to help its own genome to survive indefinitely.

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Love that idea :heart:, maybe that’s why the age at menarche has fallen in industrialized countries, could it be due to an abundance of nutrients ?