MIT discovers common lipid aging signal in mouse lung and skin
On 21 September 2026, scientists from MIT and Massachusetts General Hospital published in Nature Aging a method called RamanOmics that combines label‑free Raman microscopy with RNA sequencing of the same tissue sections. The approach lets them study chemical signals without destroying cells.
In mouse lung and skin they found different sets of active genes with age, but a single chemical signal of aging appeared in both tissues. With age some cells enter senescence, stop dividing, linger, and affect neighbours through inflammation and tissue remodeling.
Senescent cells are usually identified by markers p21 and p16, yet neither is definitive because each appears in various cell types and stages. The authors chose p21 as the primary marker because removing p21‑positive cells prevents radiation‑induced bone loss in mice.
Earlier, the NIH suggested describing such cells by a set of coordinates that include chemical makeup; RamanOmics now provides that measurement for the first time. In 2024 MIT showed that a Raman image of a living cell can predict its transcriptional profile.
Researchers led by Jae Zhang, Salvatore Sorrentino and colleagues linked that prediction to RNA‑seq and the spatial gene‑activity map STARmap on lung and skin slices from 2‑month‑old and 26‑month‑old mice. Old mouse lungs showed inflammation and repair genes; skin showed keratinization genes — the gene sets diverged.
Yet in both tissues the same Raman peak at 1131–1135 cm⁻¹ intensified, indicating a specific lipid class that serves as the first common aging signature despite different genetic “signatures” of the organs.
From the most informative Raman peaks and genes the team built a “barcode” and trained a classifier to distinguish senescent from normal cells more accurately than any single signal. Accuracy rose from 73.7% to 77.6% in lung and from 61.8% to 65.5% in skin.
A test on a mouse skin wound excluded chance: three days after injury p21 activity increased together with the same keratinization genes and lipid peak seen during aging.
Salvatore Sorrentino said, “By combining the most important Raman features with the most important genetic signatures we created a barcode that helps find aging cells more objectively.” Jae Zhang added that one could envision an endoscope that looks inside the body and detects cellular senescence.
For now the method works only on mice; analysing about 1 mm² of tissue takes roughly 30 hours. Senescent cells are rare — fractions of a percent — so the finding is still correlative. Causality will be tested by disabling the enzymes that lengthen the lipids.
Because the aging signal is visible in scattered light, not in RNA (which requires destroying the cell), the approach can be sped up and transferred to living tissue, paving the way for non‑destructive monitoring of senescent‑cell burden and for testing whether senolytics lower that burden.
🔗 Read original →
On 21 September 2026, scientists from MIT and Massachusetts General Hospital published in Nature Aging a method called RamanOmics that combines label‑free Raman microscopy with RNA sequencing of the same tissue sections. The approach lets them study chemical signals without destroying cells.
In mouse lung and skin they found different sets of active genes with age, but a single chemical signal of aging appeared in both tissues. With age some cells enter senescence, stop dividing, linger, and affect neighbours through inflammation and tissue remodeling.
Senescent cells are usually identified by markers p21 and p16, yet neither is definitive because each appears in various cell types and stages. The authors chose p21 as the primary marker because removing p21‑positive cells prevents radiation‑induced bone loss in mice.
Earlier, the NIH suggested describing such cells by a set of coordinates that include chemical makeup; RamanOmics now provides that measurement for the first time. In 2024 MIT showed that a Raman image of a living cell can predict its transcriptional profile.
Researchers led by Jae Zhang, Salvatore Sorrentino and colleagues linked that prediction to RNA‑seq and the spatial gene‑activity map STARmap on lung and skin slices from 2‑month‑old and 26‑month‑old mice. Old mouse lungs showed inflammation and repair genes; skin showed keratinization genes — the gene sets diverged.
Yet in both tissues the same Raman peak at 1131–1135 cm⁻¹ intensified, indicating a specific lipid class that serves as the first common aging signature despite different genetic “signatures” of the organs.
From the most informative Raman peaks and genes the team built a “barcode” and trained a classifier to distinguish senescent from normal cells more accurately than any single signal. Accuracy rose from 73.7% to 77.6% in lung and from 61.8% to 65.5% in skin.
A test on a mouse skin wound excluded chance: three days after injury p21 activity increased together with the same keratinization genes and lipid peak seen during aging.
Salvatore Sorrentino said, “By combining the most important Raman features with the most important genetic signatures we created a barcode that helps find aging cells more objectively.” Jae Zhang added that one could envision an endoscope that looks inside the body and detects cellular senescence.
For now the method works only on mice; analysing about 1 mm² of tissue takes roughly 30 hours. Senescent cells are rare — fractions of a percent — so the finding is still correlative. Causality will be tested by disabling the enzymes that lengthen the lipids.
Because the aging signal is visible in scattered light, not in RNA (which requires destroying the cell), the approach can be sped up and transferred to living tissue, paving the way for non‑destructive monitoring of senescent‑cell burden and for testing whether senolytics lower that burden.
🔗 Read original →
Nature
RamanOmics decodes the spatial vibrational–molecular architecture of senescence in aging and repair
Nature Aging - Zhang, Chen, Monticolo, Sorrentino and colleagues pair label-free Raman imaging with spatial and single-cell transcriptomics to probe biochemical signatures of senescence in aging...
Menopausal Hormone Therapy Effects on Brain Depend on APOEε4 Gene and Estrogen Formulation
A large analysis of the NACC database, which includes 8741 women from over 40 U.S. dementia centers, found that the link between menopausal hormone therapy and memory or brain structure depends on both the APOEε4 gene and the estrogen formulation used.
In 2003 the Women's Health Initiative reported that women 65 years and older taking conjugated equine estrogens with medroxyprogesterone (Premarin/Prempro) had nearly double the risk of probable dementia, a risk ratio 2.05; later observational studies of estradiol suggested the opposite benefit and hinted at a role for APOEε4.
A preprint released on 20 September from Liisa Galea’s lab at CAMH in Toronto directly compared formulations within one cohort, dividing participants (average age ≈70) into five groups: no therapy, estradiol alone, estradiol + progestogen, conjugated equine estrogens (CEE) alone, and CEE + medroxyprogesterone.
After statistical adjustment for age and risk factors, estradiol showed stronger benefits for APOEε4 carriers, whereas CEE appeared more helpful for non‑carriers; CEE was linked to poorer episodic memory than estradiol or no therapy but to better verbal fluency.
The authors note that CEE mainly contains a weak estrogen with low brain‑receptor affinity, while estradiol binds strongly and has long been known to protect the hippocampus; the estradiol advantage was especially pronounced among Black participants despite their earlier, more severe menopause and lower therapy use.
In an MRI subsample of 930 women (871 untreated, 59 on estradiol), APOEε4 carriers receiving estradiol had thicker cortex in four AD‑vulnerable regions, a larger hippocampus, and fewer white‑matter lesion spots than untreated carriers; no such pattern was seen in non‑carriers.
The researchers conclude that these results reframe decades of contradictory hormone‑
🔗 Read original →
A large analysis of the NACC database, which includes 8741 women from over 40 U.S. dementia centers, found that the link between menopausal hormone therapy and memory or brain structure depends on both the APOEε4 gene and the estrogen formulation used.
In 2003 the Women's Health Initiative reported that women 65 years and older taking conjugated equine estrogens with medroxyprogesterone (Premarin/Prempro) had nearly double the risk of probable dementia, a risk ratio 2.05; later observational studies of estradiol suggested the opposite benefit and hinted at a role for APOEε4.
A preprint released on 20 September from Liisa Galea’s lab at CAMH in Toronto directly compared formulations within one cohort, dividing participants (average age ≈70) into five groups: no therapy, estradiol alone, estradiol + progestogen, conjugated equine estrogens (CEE) alone, and CEE + medroxyprogesterone.
After statistical adjustment for age and risk factors, estradiol showed stronger benefits for APOEε4 carriers, whereas CEE appeared more helpful for non‑carriers; CEE was linked to poorer episodic memory than estradiol or no therapy but to better verbal fluency.
The authors note that CEE mainly contains a weak estrogen with low brain‑receptor affinity, while estradiol binds strongly and has long been known to protect the hippocampus; the estradiol advantage was especially pronounced among Black participants despite their earlier, more severe menopause and lower therapy use.
In an MRI subsample of 930 women (871 untreated, 59 on estradiol), APOEε4 carriers receiving estradiol had thicker cortex in four AD‑vulnerable regions, a larger hippocampus, and fewer white‑matter lesion spots than untreated carriers; no such pattern was seen in non‑carriers.
The researchers conclude that these results reframe decades of contradictory hormone‑
🔗 Read original →
AI screens drug records, finds varenicline may cut dementia risk by half
Researchers at the VA Medical Center in Washington and George Washington University trained an AI model on about one million patient records without a prior hypothesis to find drugs that lower dementia risk. Varenicline, a smoking‑cessation drug approved in 2006, emerged as a strong candidate.
The team used a transformer‑type architecture to distinguish patients who later developed dementia from those who did not based on prescriptions, diagnoses, and lab results; interpretable AI then linked lower dementia risk to specific drug exposures. The findings were first reported in a preprint, 20 September.
In an independent validation cohort of 9,584 adults over 50 who were dementia‑free at baseline and started either varenicline
🔗 Read original →
Researchers at the VA Medical Center in Washington and George Washington University trained an AI model on about one million patient records without a prior hypothesis to find drugs that lower dementia risk. Varenicline, a smoking‑cessation drug approved in 2006, emerged as a strong candidate.
The team used a transformer‑type architecture to distinguish patients who later developed dementia from those who did not based on prescriptions, diagnoses, and lab results; interpretable AI then linked lower dementia risk to specific drug exposures. The findings were first reported in a preprint, 20 September.
In an independent validation cohort of 9,584 adults over 50 who were dementia‑free at baseline and started either varenicline
🔗 Read original →
medRxiv
Varenicline as a Repurposable Drug Candidate for ADRD Prevention
Objective: Effective strategies to prevent Alzheimer's disease and related dementias (ADRD) are limited. Implementing our Medication-Wide Association Study (MWAS+), we highlighted varenicline as a candidate. This study evaluated the association between varenicline…
Two Distinct Brain Pathways Protect Centenarians From Alzheimer's
Researchers at Amsterdam University Medical Center examined brain tissue from 112 centenarians who retained clear cognition into extreme age. They released their findings as a preprint, September 21.
The analysis showed that 44% of the donors had hardly accumulated amyloid‑beta, while 56% displayed amyloid levels typical of Alzheimer’s disease.
Among those with high amyloid, about 28% of the total cohort had tau spread into the presubiculum, entorhinal cortex and fusiform gyrus, mirroring the Alzheimer’s pattern and showing poorer memory. A similar proportion had comparable amyloid loads but tau barely entered those regions, and their cognition remained as sharp as in amyloid‑free individuals.
In a more detailed breakdown of 107 donors, 39% did not fit either the classic Alzheimer’s or the age‑related tau pattern, and in some high‑amyloid cases tau behaved like benign ageing. Cognition was significantly better for those with a stable, age‑like tau pattern than for those with an Alzheimer’s‑like or mixed pattern (p=0.004). The HLA‑II Hap‑B variant was linked to lower tau independent of amyloid load.
These results suggest two protective routes: preventing amyloid build‑up, or blocking its ability to trigger tau in the vulnerable medial‑temporal zones. A similar case was noted in a 115‑year‑old Dutch woman whose brain showed little amyloid or dementia‑related damage despite some tau presence.
🔗 Read original →
Researchers at Amsterdam University Medical Center examined brain tissue from 112 centenarians who retained clear cognition into extreme age. They released their findings as a preprint, September 21.
The analysis showed that 44% of the donors had hardly accumulated amyloid‑beta, while 56% displayed amyloid levels typical of Alzheimer’s disease.
Among those with high amyloid, about 28% of the total cohort had tau spread into the presubiculum, entorhinal cortex and fusiform gyrus, mirroring the Alzheimer’s pattern and showing poorer memory. A similar proportion had comparable amyloid loads but tau barely entered those regions, and their cognition remained as sharp as in amyloid‑free individuals.
In a more detailed breakdown of 107 donors, 39% did not fit either the classic Alzheimer’s or the age‑related tau pattern, and in some high‑amyloid cases tau behaved like benign ageing. Cognition was significantly better for those with a stable, age‑like tau pattern than for those with an Alzheimer’s‑like or mixed pattern (p=0.004). The HLA‑II Hap‑B variant was linked to lower tau independent of amyloid load.
These results suggest two protective routes: preventing amyloid build‑up, or blocking its ability to trigger tau in the vulnerable medial‑temporal zones. A similar case was noted in a 115‑year‑old Dutch woman whose brain showed little amyloid or dementia‑related damage despite some tau presence.
🔗 Read original →
medRxiv
Centenarians maintain cognition by resisting amyloid-β or decoupling it from tau propagation
Centenarians who maintain cognitive health provide a unique opportunity to investigate naturally occurring mechanisms that protect against Alzheimer's disease. We examined the relationship between subregional amyloid-beta and p-tau distributions in the medial…
Five longevity interventions in mice converge on a liver metabolic switch driven by glucagon
On 19 September the journal npj Aging published a study from the University of Michigan that compared five interventions known to extend mouse lifespan: the diabetes drugs acarbose and canagliflozin, a calorie‑restricted diet, and two genetic alterations—Snell dwarfism and growth‑hormone‑receptor knockout (GHRKO). All five regimens were found to remodel liver metabolism in the same way.
In each case the liver lowered the activity of enzymes that break down glucose while raising the activity of enzymes that catabolize the amino acids alanine, glutamine and asparagine. The shift was driven by the hormone glucagon, which altered the liver’s fuel preference without changing its release of glucose into the bloodstream.
Previously, the only common feature of these longevity methods was suppression of the MEK1‑ERK and mTOR growth pathways and activation of chaperone‑mediated autophagy. The downstream metabolic signal had escaped detection because broad‑omics screens filtered out a weak
🔗 Read original →
On 19 September the journal npj Aging published a study from the University of Michigan that compared five interventions known to extend mouse lifespan: the diabetes drugs acarbose and canagliflozin, a calorie‑restricted diet, and two genetic alterations—Snell dwarfism and growth‑hormone‑receptor knockout (GHRKO). All five regimens were found to remodel liver metabolism in the same way.
In each case the liver lowered the activity of enzymes that break down glucose while raising the activity of enzymes that catabolize the amino acids alanine, glutamine and asparagine. The shift was driven by the hormone glucagon, which altered the liver’s fuel preference without changing its release of glucose into the bloodstream.
Previously, the only common feature of these longevity methods was suppression of the MEK1‑ERK and mTOR growth pathways and activation of chaperone‑mediated autophagy. The downstream metabolic signal had escaped detection because broad‑omics screens filtered out a weak
🔗 Read original →
Nature
Regulation of alanine glutamine asparagine catabolism is common to mouse models that extend lifespan
npj Aging - Regulation of alanine glutamine asparagine catabolism is common to mouse models that extend lifespan
Planarian Genes Reveal How Dopamine Neurons Choose Identity and Location During Regeneration
Planarians—flatworms a few centimeters long—can regrow their entire brain after injury thanks to pluripotent stem cells. University of Georgia biologists screened 74 candidate genes active in dopamine neurons and found that loss of ten of them prevents proper numbers of new dopamine neurons from forming.
Two of the required genes, fli1-2 and irx-4/6, are needed for dopamine neurons everywhere—in brain, periphery and pharynx—controlling both their birth and survival. Four others act only in one region: lmo1/3-1 and app-L1 in the brain, soxB1-2 in the periphery, and foxA in the pharynx.
By labeling dividing stem cells, researchers showed that the cell‑type gene turns on a few hours before the location gene, but both act within the first hours after division, and disabling one set reduces activity of the other. Behavioral tests confirmed the effect: worms with these genes knocked down flipped over more slowly when placed upside down, or failed to right themselves, mirroring dopamine deficiency in other animals.
“Bad regenerative capacity is not an inherent property of the brain overall, but a specific human limitation,” says study leader Rachel Roberts‑Gelbrait of the University of Georgia in a comment to GEN. The findings were published Nature Communications, 21 September 2026.
In human Parkinson’s cell therapy, transplanted dopamine neurons mature to the correct type in fewer than 30% of cases within 6–12 weeks and often migrate to wrong locations. The first such transplants began in April 2025, with Sloan Kettering using embryonic‑derived cells and Kyoto University using patient‑reprogrammed cells; a year later the STEM‑PD trial showed grafts survived but dopamine levels did not normalize in any of the eight participants.
🔗 Read original →
Planarians—flatworms a few centimeters long—can regrow their entire brain after injury thanks to pluripotent stem cells. University of Georgia biologists screened 74 candidate genes active in dopamine neurons and found that loss of ten of them prevents proper numbers of new dopamine neurons from forming.
Two of the required genes, fli1-2 and irx-4/6, are needed for dopamine neurons everywhere—in brain, periphery and pharynx—controlling both their birth and survival. Four others act only in one region: lmo1/3-1 and app-L1 in the brain, soxB1-2 in the periphery, and foxA in the pharynx.
By labeling dividing stem cells, researchers showed that the cell‑type gene turns on a few hours before the location gene, but both act within the first hours after division, and disabling one set reduces activity of the other. Behavioral tests confirmed the effect: worms with these genes knocked down flipped over more slowly when placed upside down, or failed to right themselves, mirroring dopamine deficiency in other animals.
“Bad regenerative capacity is not an inherent property of the brain overall, but a specific human limitation,” says study leader Rachel Roberts‑Gelbrait of the University of Georgia in a comment to GEN. The findings were published Nature Communications, 21 September 2026.
In human Parkinson’s cell therapy, transplanted dopamine neurons mature to the correct type in fewer than 30% of cases within 6–12 weeks and often migrate to wrong locations. The first such transplants began in April 2025, with Sloan Kettering using embryonic‑derived cells and Kyoto University using patient‑reprogrammed cells; a year later the STEM‑PD trial showed grafts survived but dopamine levels did not normalize in any of the eight participants.
🔗 Read original →
Nature
Combinatorial mechanisms specify cellular location and neurotransmitter identity during planarian neurogenesis
Nature Communications - During regeneration, new neurons need to be made in a way that reproduces both neuronal diversity and organization. Here the authors show that a combination of factors works...
Male-only longevity drugs act via opposite IL-11 shifts in visceral fat
A study dated 16 September from Richard Miller’s lab at the University of Michigan, part of the Interventions Testing Program (ITP), examined IL-11 levels in four tissues of old mice treated with seven ITP compounds that extend lifespan only in males. Differences between the sexes appeared exclusively in visceral fat, the fat surrounding internal organs.
In visceral fat, six of the seven drugs lowered IL-11 2.5–3‑fold in males, while in females five of those six raised IL-11 1.2–2‑fold (halofuginone nearly doubled it); meclizine had no effect in either sex. Liver, muscle, and subcutaneous fat showed no sex‑specific IL-11 changes.
Two compounds from this group, mitogliatazone and astaxanthin, gave modest and non‑reproducible lifespan gains of 8% and 12% respectively; the remaining four, including canagliflozin which alone extends male lifespan by 14%, displayed a clearer IL-11 signal.
Earlier work reported in Nature, 2024 showed that IL-11 rises with age and that its deletion extends life by 24.9% (antibody treatment gave 22.5% in males and 25% in females). Testing the rapamycin + 17α‑estradiol combo, which prolongs life in both sexes by about 15% median survival, revealed IL-11 reduction in males and no significant change in females—consistent with the hypothesis that a uniform IL-11 response underlies dual‑sex benefits.
The findings reframe the ITP puzzle from “why don’t these drugs work in females?” to “what flips the sign of the IL-11 response in visceral fat by sex?”—a question now amenable to direct testing, such as blocking IL-11 specifically in visceral fat of female mice to see if male‑level lifespan extension is rescued.
🔗 Read original →
A study dated 16 September from Richard Miller’s lab at the University of Michigan, part of the Interventions Testing Program (ITP), examined IL-11 levels in four tissues of old mice treated with seven ITP compounds that extend lifespan only in males. Differences between the sexes appeared exclusively in visceral fat, the fat surrounding internal organs.
In visceral fat, six of the seven drugs lowered IL-11 2.5–3‑fold in males, while in females five of those six raised IL-11 1.2–2‑fold (halofuginone nearly doubled it); meclizine had no effect in either sex. Liver, muscle, and subcutaneous fat showed no sex‑specific IL-11 changes.
Two compounds from this group, mitogliatazone and astaxanthin, gave modest and non‑reproducible lifespan gains of 8% and 12% respectively; the remaining four, including canagliflozin which alone extends male lifespan by 14%, displayed a clearer IL-11 signal.
Earlier work reported in Nature, 2024 showed that IL-11 rises with age and that its deletion extends life by 24.9% (antibody treatment gave 22.5% in males and 25% in females). Testing the rapamycin + 17α‑estradiol combo, which prolongs life in both sexes by about 15% median survival, revealed IL-11 reduction in males and no significant change in females—consistent with the hypothesis that a uniform IL-11 response underlies dual‑sex benefits.
The findings reframe the ITP puzzle from “why don’t these drugs work in females?” to “what flips the sign of the IL-11 response in visceral fat by sex?”—a question now amenable to direct testing, such as blocking IL-11 specifically in visceral fat of female mice to see if male‑level lifespan extension is rescued.
🔗 Read original →
PubMed Central (PMC)
Canagliflozin extends life span in genetically heterogeneous male but not female mice
Canagliflozin (Cana) is an FDA-approved diabetes drug that protects against cardiovascular and kidney diseases. It also inhibits the sodium glucose transporter 2 by blocking renal reuptake and intestinal absorption of glucose. In the context of the ...
Cellular Intelligence Adds Langer, LeCun to Advisory Board, Gains Parkinson’s Therapy
On 21 September, Boston‑based Cellular Intelligence (CI) announced that its scientific advisory board now includes Moderna co‑founder Robert Langer, Turing laureate Yann LeCun, Jens Nielsen of the Novo Nordisk‑funded BioInnovation Institute, and Fabian Theis, co‑founder of the Human Cell Atlas. Langer also joined CI’s board of directors as an observer.
CI is building an AI model that predicts how a cell will respond to a signal, and it already holds the Parkinson’s therapy that Novo Nordisk abandoned when it shut down its entire cell‑therapy unit in October 2025. The company’s platform tests stem‑cell colonies with rounds of signaling molecules, using a barcode to record each colony’s treatment history. Starting from a pilot of 27 000 signal combinations in 2024, CI expanded to more than one million combinations by 2025, allowing it to distinguish skeletal‑muscle from cardiac lineages
🔗 Read original →
On 21 September, Boston‑based Cellular Intelligence (CI) announced that its scientific advisory board now includes Moderna co‑founder Robert Langer, Turing laureate Yann LeCun, Jens Nielsen of the Novo Nordisk‑funded BioInnovation Institute, and Fabian Theis, co‑founder of the Human Cell Atlas. Langer also joined CI’s board of directors as an observer.
CI is building an AI model that predicts how a cell will respond to a signal, and it already holds the Parkinson’s therapy that Novo Nordisk abandoned when it shut down its entire cell‑therapy unit in October 2025. The company’s platform tests stem‑cell colonies with rounds of signaling molecules, using a barcode to record each colony’s treatment history. Starting from a pilot of 27 000 signal combinations in 2024, CI expanded to more than one million combinations by 2025, allowing it to distinguish skeletal‑muscle from cardiac lineages
🔗 Read original →
PR Newswire
Somite Becomes Cellular Intelligence, as It Builds the First Universal Virtual Cell-Signaling Model
/PRNewswire/ -- Somite, an AI-native TechBio company building the first universal virtual cell-signaling model, today announced its new identity, Cellular...
NMN Extends Lifespan Only in Female Mice, Sinclair Lab Finds
The Sinclair laboratory tested NMN supplementation in mice from mid‑life (13 months) to death. Females showed a median lifespan increase of 8.5% and a maximum increase of 7.9%, while males derived no longevity benefit. NMN delayed frailty by 31 aging markers in both sexes.
Mice received NMN at a dose 2–3 times the clinical level — roughly ~3 g/day for a 70 kg human — throughout the treatment period. The compound equally improved markers of physical frailty regardless of sex.
NMN triggered a >10‑fold rise in the gut bacterium *Anaerotruncus colihominis*, which in vitro converted labeled NMN to NAD+ within 20 h. This microbial activity accounts for the frailty reduction and partly explains the early‑life mortality protection seen in males.
In females, hepatic and muscular genes governing mitochondrial function and DNA repair were upregulated, resembling calorie‑restriction benefits. Males exhibited suppressed mitochondrial genes and heightened inflammatory pathways driven by CD38 and PARP, which consume NAD+. The findings are detailed in the препринт лаборатории Синклера от 21 сентября, which notes Sinclair’s conflict of interest as co‑founder of MetroBiotech. Authors propose pairing NMN with CD38 or PARP blockers to extend the longevity benefit to males.
🔗 Read original →
The Sinclair laboratory tested NMN supplementation in mice from mid‑life (13 months) to death. Females showed a median lifespan increase of 8.5% and a maximum increase of 7.9%, while males derived no longevity benefit. NMN delayed frailty by 31 aging markers in both sexes.
Mice received NMN at a dose 2–3 times the clinical level — roughly ~3 g/day for a 70 kg human — throughout the treatment period. The compound equally improved markers of physical frailty regardless of sex.
NMN triggered a >10‑fold rise in the gut bacterium *Anaerotruncus colihominis*, which in vitro converted labeled NMN to NAD+ within 20 h. This microbial activity accounts for the frailty reduction and partly explains the early‑life mortality protection seen in males.
In females, hepatic and muscular genes governing mitochondrial function and DNA repair were upregulated, resembling calorie‑restriction benefits. Males exhibited suppressed mitochondrial genes and heightened inflammatory pathways driven by CD38 and PARP, which consume NAD+. The findings are detailed in the препринт лаборатории Синклера от 21 сентября, which notes Sinclair’s conflict of interest as co‑founder of MetroBiotech. Authors propose pairing NMN with CD38 or PARP blockers to extend the longevity benefit to males.
🔗 Read original →
Researchsquare
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AI progress could shift public view on aging like recent AI risk shift
On September 21, engineer and LessWrong regular Jackson Wagner posted a forecast that public attitudes toward aging could change as swiftly as views on super‑intelligent AI risk have in recent weeks. He pointed to three developments from the past week — Anthropic’s own biolab testing Claude’s autonomy, a Claude‑driven speed‑up of scientific protein‑structure models, and the launch of the Life Sciences Verification Program that gives biologists access to less‑restricted Claude versions — as signs that AI labs are laying the groundwork. Wagner’s thesis is that, by default, the energy from a future medical breakthrough will be captured by the “don’t slow the AI race” rhetoric of effective accelerationism rather than by institutional geroscience.
A viral post by Jacob Coxson on AI extinction risk recently shifted opinion: a Politico, September poll showed that about two-thirds of Americans now regard AI risk to humanity as at least moderate. Wagner argues the same preference‑cascade mechanism could work for aging, whereby people adopt the view they expect others to share, and the shift occurs abruptly once it becomes common knowledge.
While many still see combating aging as impossible, they also reject the logical conclusion that “if death is bad, we must treat aging urgently,” even though the two statements are not equivalent. Wagner puts it bluntly: “If we can cure diseases and slow or reverse aging mechanisms, we must act urgently because death is very bad.”
Anthropic’s own biolab is checking Claude’s autonomy in experiments; it recently accelerated 30 scientific models of protein structure on average 4 times; and this week it launched the Life Sciences Verification Program, which eases model restrictions for verified labs pursuing drug development. AI companies have a direct PR incentive to portray any forthcoming medical breakthrough as an argument against pausing AI, aligning with the e/acc movement that pushes technology to its limits and rejects restraints.
Wagner warns that the released longevity energy may by default flow straight into e/acc. The top comment by Mitchell_Porter predicts the opposite — a backlash resembling protests against data‑centers: “stop the rich building a sinister transhumanist world.” ACCount draws a parallel with Ozempic: acceptance of obesity collapsed not from realizing its harm but from a drug with a visible effect; a quiet 20% slowing of aging would not trigger a cascade, whereas visible rejuvenation would.
He concludes with a program for the cautious‑AI community: prepare in advance the argument that “if we die from misaligned AI while chasing immortality, we won’t gain immortality either,” and begin now investing in geroscience and drug‑regulation reform so that when the preference cascade arrives, the caution side will have the reputation of genuine anti‑aging work.
🔗 Read original →
On September 21, engineer and LessWrong regular Jackson Wagner posted a forecast that public attitudes toward aging could change as swiftly as views on super‑intelligent AI risk have in recent weeks. He pointed to three developments from the past week — Anthropic’s own biolab testing Claude’s autonomy, a Claude‑driven speed‑up of scientific protein‑structure models, and the launch of the Life Sciences Verification Program that gives biologists access to less‑restricted Claude versions — as signs that AI labs are laying the groundwork. Wagner’s thesis is that, by default, the energy from a future medical breakthrough will be captured by the “don’t slow the AI race” rhetoric of effective accelerationism rather than by institutional geroscience.
A viral post by Jacob Coxson on AI extinction risk recently shifted opinion: a Politico, September poll showed that about two-thirds of Americans now regard AI risk to humanity as at least moderate. Wagner argues the same preference‑cascade mechanism could work for aging, whereby people adopt the view they expect others to share, and the shift occurs abruptly once it becomes common knowledge.
While many still see combating aging as impossible, they also reject the logical conclusion that “if death is bad, we must treat aging urgently,” even though the two statements are not equivalent. Wagner puts it bluntly: “If we can cure diseases and slow or reverse aging mechanisms, we must act urgently because death is very bad.”
Anthropic’s own biolab is checking Claude’s autonomy in experiments; it recently accelerated 30 scientific models of protein structure on average 4 times; and this week it launched the Life Sciences Verification Program, which eases model restrictions for verified labs pursuing drug development. AI companies have a direct PR incentive to portray any forthcoming medical breakthrough as an argument against pausing AI, aligning with the e/acc movement that pushes technology to its limits and rejects restraints.
Wagner warns that the released longevity energy may by default flow straight into e/acc. The top comment by Mitchell_Porter predicts the opposite — a backlash resembling protests against data‑centers: “stop the rich building a sinister transhumanist world.” ACCount draws a parallel with Ozempic: acceptance of obesity collapsed not from realizing its harm but from a drug with a visible effect; a quiet 20% slowing of aging would not trigger a cascade, whereas visible rejuvenation would.
He concludes with a program for the cautious‑AI community: prepare in advance the argument that “if we die from misaligned AI while chasing immortality, we won’t gain immortality either,” and begin now investing in geroscience and drug‑regulation reform so that when the preference cascade arrives, the caution side will have the reputation of genuine anti‑aging work.
🔗 Read original →
Lesswrong
Jackson Wagner — LessWrong
Jackson Wagner's profile on LessWrong — A community blog devoted to refining the art of rationality
Blood protein set after menopause predicts faster brain aging and Alzheimer's risk
Researchers from the Universities of California, Toronto and Stanford determined the menopause stage in 80 women aged 43‑58 and compared their blood with that of 36 men of the same age, then validated the findings in 2,814 UK Biobank women. Among Americans over 65 with Alzheimer’s, nearly two‑thirds are women: 4.5 of 7.4 million, according to the Alzheimer’s Association. Earlier explanations pointed to female longevity or a vague “hormones” factor. The study, published Nature Medicine, September 22, 2024, identifies a blood protein signature that separates menopause from generic aging and links it to future
🔗 Read original →
Researchers from the Universities of California, Toronto and Stanford determined the menopause stage in 80 women aged 43‑58 and compared their blood with that of 36 men of the same age, then validated the findings in 2,814 UK Biobank women. Among Americans over 65 with Alzheimer’s, nearly two‑thirds are women: 4.5 of 7.4 million, according to the Alzheimer’s Association. Earlier explanations pointed to female longevity or a vague “hormones” factor. The study, published Nature Medicine, September 22, 2024, identifies a blood protein signature that separates menopause from generic aging and links it to future
🔗 Read original →
Alzheimer’s Association
Women and Alzheimer's | Alzheimer's Association
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AI model EAGLE detects esophageal cancer on routine non‑contrast CT scans
On 22 September Nature Medicine, September 2022 published an article describing the EAGLE model, which identifies esophageal cancer and precancerous lesions on standard contrast‑free CT. Validation in eight centers across three countries involved 11,466 patients and yielded 89.5% sensitivity with only a 1.5% false‑positive rate.
The system is already in use at three Chinese hospitals, where it flagged cancers missed by conventional diagnostics. Globally, esophageal cancer accounts for about 511,000 new cases and 445,000 deaths each year, with five‑year survival of 36.9 % in China and 18.5 % in the United States. No widespread screening exists because endoscopy is invasive and limited to high‑risk regions in China.
Many individuals undergo chest CT without contrast for other indications; such scans capture the entire esophagus and represent roughly 40 % of all CT examinations worldwide. Early mucosal changes are subtle, and radiologists often overlook them—most patients who later died of esophageal cancer had no suspicious findings on prior CTs, leaving the signal buried in archives.
EAGLE was constructed by Alibaba DAMO Academy and Chinese oncology centers in two stages: one neural network isolates the esophagus from the scan, a second searches that region for malignant or precancerous alterations. Training used voxel‑wise tumor outlines from contrast CT, transferred to plain images via image registration, allowing the model to discern faint early signals.
In testing, EAGLE surpassed each of 17 radiologists; with its assistance, clinicians detected cancer in 85.7 % of patients versus 71.9 % before. Sensitivity for early‑stage tumors was lower (60‑66 %) than for established lesions (89‑90 %). The model also maintains 88.4 % sensitivity on low‑dose lung‑cancer screening CTs, enabling simultaneous esophageal cancer detection without extra procedures.
Clinical deployment showed promise: an initial wave in three Chinese hospitals (21,000 patients) uncovered three cancers missed by routine work‑up, one 21 months earlier than the official diagnosis.
🔗 Read original →
On 22 September Nature Medicine, September 2022 published an article describing the EAGLE model, which identifies esophageal cancer and precancerous lesions on standard contrast‑free CT. Validation in eight centers across three countries involved 11,466 patients and yielded 89.5% sensitivity with only a 1.5% false‑positive rate.
The system is already in use at three Chinese hospitals, where it flagged cancers missed by conventional diagnostics. Globally, esophageal cancer accounts for about 511,000 new cases and 445,000 deaths each year, with five‑year survival of 36.9 % in China and 18.5 % in the United States. No widespread screening exists because endoscopy is invasive and limited to high‑risk regions in China.
Many individuals undergo chest CT without contrast for other indications; such scans capture the entire esophagus and represent roughly 40 % of all CT examinations worldwide. Early mucosal changes are subtle, and radiologists often overlook them—most patients who later died of esophageal cancer had no suspicious findings on prior CTs, leaving the signal buried in archives.
EAGLE was constructed by Alibaba DAMO Academy and Chinese oncology centers in two stages: one neural network isolates the esophagus from the scan, a second searches that region for malignant or precancerous alterations. Training used voxel‑wise tumor outlines from contrast CT, transferred to plain images via image registration, allowing the model to discern faint early signals.
In testing, EAGLE surpassed each of 17 radiologists; with its assistance, clinicians detected cancer in 85.7 % of patients versus 71.9 % before. Sensitivity for early‑stage tumors was lower (60‑66 %) than for established lesions (89‑90 %). The model also maintains 88.4 % sensitivity on low‑dose lung‑cancer screening CTs, enabling simultaneous esophageal cancer detection without extra procedures.
Clinical deployment showed promise: an initial wave in three Chinese hospitals (21,000 patients) uncovered three cancers missed by routine work‑up, one 21 months earlier than the official diagnosis.
🔗 Read original →
Nature
Large-scale esophageal cancer screening through noncontrast computed tomography and artificial intelligence
Nature Medicine - In a large-scale study, a new tool called Esophageal AI-Guided malignant Lesion Evaluation uses artificial intelligence to enhance esophageal cancer detection through noncontrast...