ArticleAging cell2017
Anti-aging drugs reduce hypothalamic inflammation in a sex-specific manner.
Article in Aging cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
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Who cites it
54 citing papers in PubMed, 81 citations in OpenAlex.
- Redefining the timeline: a three-phase framework of hypothalamic microinflammation in metabolic disease.Reviews in endocrine & metabolic disorders · 2026Review
- Acarbose modulates microglial Pkm2 acetylation to reshape immunometabolism and preserve retinal neurons after ischemia-reperfusion.Journal of neuroinflammation · 2026Article
- Acarbose improves cognitive function in a mouse model of normal aging but not Alzheimer's disease.bioRxiv : the preprint server for biology · 2026Article
- Ginsenoside Rb1 Ameliorates Age-Related Cognitive Impairment Potentially by Modulating the NF-κB Signaling Pathway.Brain and behavior · 2026Article
- The geroprotectors trametinib and rapamycin combine additively to extend mouse healthspan and lifespan.Nature aging · 2025Article
- Protection against APOE4-associated phenotypes with the longevity-promoting intervention 17α-estradiol in middle-aged male mice.Communications medicine · 2025Article
- Microglial ER stress response via IRE1α regulates diet-induced metabolic imbalance and obesity in mice.Molecular metabolism · 2025Article
- Acarbose ameliorates Western diet-induced metabolic and cognitive impairments in the 3xTg mouse model of Alzheimer's disease.GeroScience · 2025Article
- Characterization of craniofacial tissue aging in genetically diverse HET3 male mice with longevity treatment of 17-alpha estradiol.Archives of oral biology · 2025Article
- Update on Hypothalamic Inflammation and Gliosis: Expanding Evidence of Relevance Beyond Obesity.Current obesity reports · 2025Review
- A cocktail of rapamycin, acarbose, and phenylbutyrate prevents age-related cognitive decline in mice by targeting multiple aging pathways.GeroScience · 2024Article
- Hypothalamic MRI-derived microstructure is associated with neurocognitive aging in humans.Neurobiology of aging · 2024Article
- Proteomic changes induced by longevity-promoting interventions in mice.GeroScience · 2024Article
- AAV-BDNF gene therapy ameliorates a hypothalamic neuroinflammatory signature in theMolecular therapy. Methods & clinical development · 2023Article
- Four anti-aging drugs and calorie-restricted diet produce parallel effects in fat, brain, muscle, macrophages, and plasma of young mice.GeroScience · 2023Article
- Growth hormone receptor (GHR) in AgRP neurons regulates thermogenesis in a sex-specific manner.GeroScience · 2023Article
- Glioprotective effects of resveratrol in hypothalamic astrocyte cultures obtained from interferon receptor knockout (IFNα/βRIn vitro cellular & developmental biology. Animal · 2023Article
- Repurposing Canagliflozin to target brain aging.Aging · 2023Article
- Canagliflozin retards age-related lesions in heart, kidney, liver, and adrenal gland in genetically heterogenous male mice.GeroScience · 2023Article
- Trends in Gliosis in Obesity, and the Role of Antioxidants as a Therapeutic Alternative.Antioxidants (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Aging leads to hypothalamic inflammation, but does so more slowly in mice whose lifespan has been extended by mutations that affect GH/IGF-1 signals. Early-life exposure to GH by injection, or to nutrient restriction in the first 3 weeks of life, also modulate both lifespan and the pace of hypothalamic inflammation. Three drugs extend lifespan of UM-HET3 mice in a sex-specific way: acarbose (ACA), 17-α-estradiol (17αE2), and nordihydroguaiaretic acid (NDGA), with more dramatic longevity increases in males in each case. In this study, we examined the effect of these anti-aging drugs on neuro-inflammation in hypothalamus and hippocampus. We found that age-associated hypothalamic inflammation is reduced in males but not in females at 12 months of age by ACA and 17αE2 and at 22 months of age in NDGA-treated mice. The three drugs blocked indices of hypothalamic reactive gliosis associated with aging, such as Iba-1-positive microglia and GFAP-positive astrocytes, as well as age-associated overproduction of TNF-α. This effect was not observed in drug-treated female mice or in the hippocampus of the drug-treated animals. On the other hand, caloric restriction (CR; an intervention that extends the lifespan in both sexes) significantly reduced hypothalamic microglia and TNF-α in both sexes at 12 months of age. Together, these results suggest that the extent of drug-induced changes in hypothalamic inflammatory processes is sexually dimorphic in a pattern that parallels the effects of these agents on mouse longevity and that mimics the changes seen, in both sexes, of long-lived nutrient restricted or mutant mice.
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