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A study published in 2023 found that Menin levels declined in certain hypothalamic neurons in aging mice. Restoring Menin improved several measures, while D-serine supplementation improved learning and memory tests in older mice; neither result establishes an effective treatment for people.
A 2023 study in mice found that the age-related decline of a brain protein called Menin was associated with inflammation and changes in memory, bone mass and skin. In experiments reported by ScienceDaily, restoring Menin improved several measures in older mice, and three weeks of D-serine supplementation improved performance on learning and memory tests. The findings do not show that the amino acid prevents or treats memory loss in people.
Researchers led by Lige Leng of Xiamen University examined Menin in the hypothalamus, a brain region involved in regulating functions such as metabolism, sleep and hormone production. They found that Menin levels fell with age in certain hypothalamic neurons, while the same decline was not seen in astrocytes or microglia. Menin also helps regulate gene activity and restrain inflammation, according to the ScienceDaily account of the research.
To test whether reduced Menin could contribute to aging-related changes, the researchers used genetically modified mice with selectively reduced Menin activity. These animals developed more hypothalamic inflammation, thinner skin, lower bone mass and worse cognitive performance than controls. Their lifespans were also modestly shorter. Those results suggest that Menin loss can contribute to several changes in mice; they do not establish that it is the sole or primary driver of aging.
In a separate experiment, the team used gene delivery to increase Menin in the ventromedial hypothalamus of 20-month-old mice. After 30 days, the treated animals showed improvements in skin thickness, bone mass, learning, memory and balance, alongside reduced inflammation and changes in metabolism. The report also says treated mice lived longer in a separate survival analysis, but gives no numerical lifespan effect in the supplied material. D-serine, given in drinking water for three weeks, improved learning and memory test performance without directly restoring Menin.
A Brain Pathway With Bodywide Effects
The experiments add to research into how the brain may influence aging beyond cognitive function. The hypothalamus helps regulate systems throughout the body, so changes in its activity could be relevant to several age-related processes at once. In this study, altering Menin affected inflammation and multiple physical and cognitive measures in mice, making the protein a candidate for further investigation rather than an established treatment target.
The D-serine result offers a more specific clue about memory. The researchers linked Menin to PHGDH, an enzyme involved in the pathway that produces serine, and reported that lower Menin coincided with lower D-serine. D-serine supports signaling through NMDA receptors, which are involved in communication between nerve cells and in learning and memory. Supplementation improving mouse test scores is evidence about this experimental model, not proof that supplements improve memory in humans.
The distinction matters for readers because the study tested mice, not people, and used controlled interventions that cannot be assumed to work the same way outside a laboratory. D-serine is distinct from L-serine, the form commonly found in foods such as soybeans, eggs, fish and nuts. Eating foods containing L-serine is not equivalent to taking D-serine, and the report does not establish a safe or effective human dose.
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From Menin to D-Serine
The study builds on earlier work by Leng and colleagues identifying Menin as a protein that can help restrain inflammation in the hypothalamus. In the reported experiments, researchers first observed that Menin declined in specific neurons as mice aged, then used genetic manipulation to examine whether reducing or restoring it changed age-related measures. This sequence provides evidence of a possible role in the animals, but does not settle how much Menin contributes to normal aging or whether the same pathway has comparable effects in people.
The amino acid findings followed from the researchers’ investigation of the mechanism. They reported that Menin regulates PHGDH, which participates in the biochemical pathway that generates serine, and that restoring Menin increased D-serine in the hippocampus, a region important for memory. Giving D-serine to older mice for three weeks improved learning and memory test performance. The supplied report describes a distinct amino acid form from dietary L-serine and does not provide enough information to treat ordinary serine-rich foods as a substitute for the experimental supplement.
The original research was published in PLOS Biology in March 2023. The October 2026 ScienceDaily item revisits those results and places them alongside later research on the brain’s role in aging, but the material provided does not identify specific later studies or show that the mouse findings have been replicated in human trials.
“Some effects of aging may be influenced by biological processes in the brain that scientists could eventually learn to modify.”
— ScienceDaily report on the research
Human Benefits Remain Untested
The supplied material reports mouse experiments, not clinical trials. It does not establish whether Menin declines in the same way in humans, whether increasing it would be safe, or whether D-serine supplementation would improve memory in people. It also does not provide a human dose, long-term safety findings, or evidence that taking D-serine can prevent or reverse age-related memory problems.
Several details needed to judge the scale and reliability of the effects are not included in the report excerpt, including sample sizes and numerical results for the individual tests and survival analysis. The findings therefore support further research, but do not establish that Menin loss is the hidden driver of aging generally or that D-serine is a proven remedy. The relationship between dietary L-serine and the D-serine used in the experiments also should not be treated as interchangeable.
Replication and Human Research
The immediate research question is whether other studies can reproduce the Menin and D-serine effects and clarify how the pathway operates. Further work would need to examine which brain cells and biological mechanisms are responsible, how durable the observed changes are, and whether interventions affect different measures of aging consistently.
Before the results could support a human treatment, researchers would need to establish safety, dosing and effectiveness in appropriately designed human studies. The supplied source does not announce a clinical trial or provide a timetable for one. Until such evidence exists, the findings should be understood as an early-stage result from mice, not a basis for self-treatment with supplements.
Key Questions
What did the researchers find about Menin?
They found that Menin levels declined in certain hypothalamic neurons as mice aged. Reducing Menin activity in mice was associated with more inflammation and changes in skin, bone mass and cognitive performance.
Did restoring Menin reverse aging in the mice?
Increasing Menin in a specific hypothalamic area of 20-month-old mice improved several measured outcomes after 30 days, including skin thickness, bone mass, learning, memory and balance. The experiment does not show that aging was reversed overall or that the approach works in people.
Did D-serine improve memory in humans?
The reported experiment gave D-serine to older mice, whose performance on learning and memory tests improved after three weeks. The supplied report describes no human trial, so it does not establish a memory benefit for people.
Is D-serine the same as serine in food?
No. The report distinguishes D-serine from L-serine, the form found in foods including soybeans, eggs, fish and nuts. It says eating serine-rich foods is not equivalent to taking the form used in the experiments.
Does the study show that Menin is the cause of aging?
No. The mouse experiments suggest that changes in Menin can contribute to several aging-related measures, but they do not show that Menin is the sole cause of aging or establish how important the pathway is in humans.
Source: rss
