Switching Off One Crucial Protein Appears to Reverse Brain Aging in Mice (sciencealert.com) 25
A research team just discovered older mice have more of the protein FTL1 in their hippocampus, reports ScienceAlert.
The hippocampus is the region of the brain involved in memory and learning. And the researchers' paper says their new data raises "the exciting possibility that the beneficial effects of targeting neuronal ferritin light chain 1 (FTL1) at old age may extend more broadly, beyond cognitive aging, to neurodegenerative disease conditions in older people."
FTL1 is known to be related to storing iron in the body, but hasn't come up in relation to brain aging before... To test its involvement after their initial findings, the researchers used genetic editing to overexpress the protein in young mice, and reduce its level in old mice. The results were clear: the younger mice showed signs of impaired memory and learning abilities, as if they were getting old before their time, while in the older mice there were signs of restored cognitive function — some of the brain aging was effectively reversed...
"It is truly a reversal of impairments," says biomedical scientist Saul Villeda, from the University of California, San Francisco. "It's much more than merely delaying or preventing symptoms." Further tests on cells in petri dishes showed how FTL1 stopped neurons from growing properly, with neural wires lacking the branching structures that typically provide links between nerve cells and improve brain connectivity...
"We're seeing more opportunities to alleviate the worst consequences of old age," says Villeda. "It's a hopeful time to be working on the biology of aging."
The research was led by a team from the University of California, San Francisco — and published in Nature Aging..
"It is truly a reversal of impairments," says biomedical scientist Saul Villeda, from the University of California, San Francisco. "It's much more than merely delaying or preventing symptoms." Further tests on cells in petri dishes showed how FTL1 stopped neurons from growing properly, with neural wires lacking the branching structures that typically provide links between nerve cells and improve brain connectivity...
"We're seeing more opportunities to alleviate the worst consequences of old age," says Villeda. "It's a hopeful time to be working on the biology of aging."
The research was led by a team from the University of California, San Francisco — and published in Nature Aging..
Different (Score:2)
TFA notes that there is a question of whether the Protein and the aging relationship is picking apart which changes in the body are the result of aging, and which changes might be driving it, while the scientist is quoted "It is truly a reversal of impairments"
My money is on the results of aging. But we can expect people to start claiming that cast iron cookware causes dem
Re:Different (Score:5, Insightful)
In the shorter term, it doesn't matter if suppressing this gene is correcting an age-related overexpression or if it is forcing an underexpression to correct for some other age-related failure.
Even if the machinery keeps falling apart and it doesn't offer a single extra day of life, it's one less symptom of a failing body you'd have to deal with when you're older.
Re: Different (Score:1)
Re: Different (Score:5, Interesting)
Completely agree! It's better if you can fix the ultimate cause, but if all we do is play whack a mole on the faults or outcomes it's still progress...
My point was that the author of the FA noted that this suppression of FTL1 protein may not mean a thing. while the scientist claims it actually rolls back aging. Read TFA, then tell me who has what outlook. Who do you agree with? Here's what he is quoted: "It is truly a reversal of impairments, it's much more than merely delaying or preventing symptoms."
Not a lick of ambiguity there, the problem is solved according to him.
I get these contradictory responses that really have nothing to do with my point. Are you telling me that the quoted scientist is right - we can roll back aging in this case, the problem of dementia is now solved by the suppression of FTL1 protein?
I know that it would be awesome to erase all dementia, no doubt, investigate FTL1, perhaps suppressing or eliminating it's effects will be a great thing, perhaps it has no other use than to cause dementia, we can maybe genetically engineer humanity to eliminate it altogether, and no one will suffer dementia ever again. But sometimes there is a lot of wishful thinking. We've had a lot of that wishfulness over the years. Things that do something in Petri dishes and lab mice always translate to humans?
There is an old southern saying "Wish in one hand, and shit in the other, and see which one fills up fastest".
Re: Different (Score:1)
Itâ(TM)s a bad study. Lacked an obvious control.
Re: (Score:2)
Re: Different (Score:1)
Re: (Score:2)
I'm agreeing with Baron. But also with you in general. It's incomplete reporting.
In terms of the article I'd like to be kind and suspect the scientist was quoted slightly out of context. Because such a black and white statement from a researcher lacks credibility (in the statement or the researcher).
A few things.
1. I am with you on the possibility of misquoting.
2. Or quoting being made up even. - I had some people in my organization make up a quote for me to say this past year. Anyone that knew me could figure that it was fake because I don't talk like what they had me "say". When I told them they had to strike the quote or use one I could give them, they told me that people have others make up quotes for people all the time. I told them not in the world I come from, and not on my watch. note: I
Re: (Score:2)
Do you want immortality ?
Terrible idea, mortality is not a bug, it's a feature
If you don't die you don't evolve, so when do you want to stop ?
Maybe we could have been since a long time immortal worms, that would be, nice, I guess...
I look around, see monkeys with incredibly stupid beliefs and terrifying weapons everywhere...
I don't think it's time to stop evolving just yet
Re: (Score:2)
"Reading TFA,"
We don't do that, you must be new here, welcome.
Yeah, "exciting" (Score:5, Funny)
Re:Yeah, "exciting" (Score:5, Interesting)
Re: (Score:3)
The only reason why this research is even being conducted is those aging billionaires. Otherwise nobody would pay for marginal results as this one.
Re: (Score:3)
Shirley if you're studying the Hippocampus, do the research on Seahorses.
I don't think this research is being conducted on the continent hosting hippos, so not on that campus. And don't call me Shirley!
Immortal Mice? (Score:3)
This could lead to immortal mice. Imagine the plague risk with immortal mice. We've got to put a stop to this research now!
Re: (Score:2)
more importantly, what happens to the cats that eat these mice?
No distinction between neurotypical and neurodiver (Score:1)
Neurodivergent brains have about 2-3 times the synaptic connections that neurotypical brains do. They are physically different, distinctly. It is not some deficiency in a neurotypical brain.
This basic fact makes neurological research that doesnâ(TM)t control for the known-different kinds of brains unreliable. They have failed to create a scientifically-valid experiment because they didnâ(TM)t control for an obvious physical difference. Mixed the apples in with the oranges and tried to draw a valid
Re: No distinction between neurotypical and neurod (Score:1)
Honestly itâ(TM)s the fault of the IRB involved.
Re: (Score:2)
Are you really asking scientists to create neurodivergent mice??? I presume you're neurodivergent and feeling underrepresented in the population of...mice test subjects? ;)
Re:No distinction between neurotypical and neurodi (Score:4, Informative)
Re: (Score:3)
Last I heard, the mouse models of Alzheimer's were really bad models.
Of Mice & Men (Score:2)
Keep in mind something about animal models, and rodents in particular; most of these single-gene aging related studies end up finding such mutations are already active in humans, which is why we live so much longer than mice, even relative to body size. However interesting this very preliminary and unreplicated study might turn out to be, it's probably useless for human life extension.