| Carboxyfullerene SOD mimetic treatment | Administration of a small-molecule synthetic enzyme superoxide dismutase mimetic to wild-type (i.e. non-transgenicm non-senescence accelerated) mice starting at middle age significantly extends lifespan and reduces age-associated oxidative stress and mitochondrial radical production. Treatment also improves performance on Morris water maze learning and memory task and therefore rescues age-related cognitive impairment [17079053]. | — | — | — | — |
| NAM treatment | Treatment with NAM reduces mean and maximum replicative lifespan by 28 and 37%. NAM treatment blocks the lifespan extending effect of rapamycn [20947565]. | Yeast | -28 | — | -37 |
| Ascrobate treatment | Hypersensitivity to oxygene and significantly decreased replicative lifespan of SOD1 deletion can be ameliorated by exogenous ascorbate. If acorbate's negative effects of auto-oxidation are prevented by exchange of medium, ascorbate prolongs mean and maximum replicative lifespan in the atmosphere of air and pure oxygene [15621721].
| Yeast | — | — | — |
| D-glucosamine treatment | Addition of 0.5 mg/ml D-glucosamine to the growth media suppresses the short replicative lifespan and temperature sensitive growth of mpt5 mutant, but fails to extend the lifespan of wild-type cells [11805047]. | Yeast | — | — | — |
| Hesperidin treatment | Hesperidin derived from the Citrus genus extends replicative lifespan at doses of 5 and 10 microMolar. Hesperdin inihibts ROS and UTH1 gene expression, but increases Sir2 and SOD gene expression. UTH1 and SKN7 are involved in lifespan extension mediated by hesperidin [22484922]. | Yeast | — | — | — |
| Gonadermasides D treatment | Application of gonadermasides D significantly increases the replicative lifespan in the K6001 strain by regulating UTH1 [21512225]. | Yeast | — | — | — |
| Ganodermasides C treatment | Application of gonadermasides C significantly increases the replicative lifespan in the K6001 strain by regulating UTH1 [21512225]. | Yeast | — | — | — |
| Ganodermasides A treatment | Application of Ganodermasides A extends the replicative lifespan in K6001 strain by regulating UTH1 expression [20093034]. | Yeast | — | — | — |
| Ganodermasides B treatment | Application of Ganodermasides B extends the replicative lifespan in K6001 strain by regulating UTH1 expression [20093034]. | Yeast | — | — | — |
| Beauveriolide I treatment | Treatment with beauveriolide I (20 microgram/mL) extends chronological lifespan in BY4741 by around 50% [22790951]. | Yeast | +50 | — | — |
| Methionine restriction | Restriction of the methionine content in the culture extends mean and maximum lifespan by up to 29 and 16% (1/10 methionine content) [15141092]. | Yeast | +29 | — | +16 |
| Resveratrol supplementation | Resveratrol significantly extends the lifespan [12939617]. | Yeast | — | — | — |
| Rapamycin treatment | Treatment with rapamcyin increases mean and maximum replicative lifespan by 19 and 16% Rapamycin fails to extend the lifespan of sir2 mutants or NAM treated wild-type cells [20947565]. Rapamcyin treatment increases mean chronological lifespan by by approximately by 80% in BY4742 [22790951].
Rapamycin extends chronological lifespan proportional with increasing concentrations from 100 pg/mL to 1 ng/mL [16418483] | Yeast | +19 to +50 | — | +16 |
| concA treatment | The specific V-ATPase inhibitor concanatmycin A (concA) blocks VMA1 or VPH2 overexpression mutations ability to produce normal, tubular mitochondria. Treatment of young cells causes vacuolar acidity and loss of mitochondrial depolarization. Loss of ΔΨ is followed by mitochondrial fragmentation and aggregation that resembles mitochondrial phenotypes present in aged cells [23172144]. | Yeast | — | — | — |
| Moderate DR | Moderate DR is the restriction of glucose concentration from 2% (*ad libitum*) to 0.5%, which extends the mean, median and maximum replicative lifespan by 45 - 52%, 43 - 50% and 50 - 52%, respectively [23172144]
Moderate DR increases vacuolar acidity in young cells and prevents the decline of vacuolar acidity in aging cells. DR also suppresses mitochondrial dysfunciton of aged cells (21 divisions) in a V-ATPase-dependent manner [23172144].
Constitutively activating PKA signaling by deleting the Ras GTPase-activating protein IRA2 reduces vacuolar acidity and accelerates the development of mitochondrial dysfunction in aging cells and prevents DR-mediated enhancement of vacuolar acidity and suppression of mitochondrial dysfunction [23172144].
Lifespan extension by DR is prevented in a strain lacking V-ATPase activity [23172144]. | Yeast | +45.2 to +51.7 | +42.9 to +50.0 | +50.0 to +52.0 |
| Rapamycin treatment | Treatment with rapamcyin increases mean, median, 75th %ile and maximum lifespan by 19-29, 17-29, 24-32 an 19%, respectively on OP50. On HT115 rapamycyin extends mean, median and 75th %ile of lifespan by 8-36, 4-46 and 12-44%, respectively. Rapamycin robustly increases lifespan in two daf-16 mutants (mgDf47 and mu86) with or without FUdR and with growth on either the standard strain OP50 or the feeding RNAi strain HT115 [22560223]. | Worm | +8 to +29 | +4 to +46 | +19 |
| Icariin treatment | Icariin and its derivate icariside II extend lifespan. Animals treated with icariin have high levels of icariside II [22216122]. | Worm | — | — | — |
| Icariside II treatment | Icariside II and its derivate icarrin extend lifespan. Animals treated with icariin have high levels of icariside II. Icariside II also increases thermo and oxidative stress tolerance, slow locomotion decline in late adulthood and delay the onset of paralysis mediated by polyQ and ABeta(1-42) proteotoxicity. Lifespan extension by Icariside II is dependent on IIS, since daf-16(mu86) and daf-2(e1370) fails to sho exhibit lifespan extension upon icariside treatment. Incariside II treatment upregulates expression of DAF-16 targets in wild-type. HSF-1 has also a role in icariside II-dependent lifespan extension [22216122]. | Worm | — | — | — |
| Quercetin treatment | Quercitin significantly extends the lifespan. Lifespan extension by quercitin has no effect on reproduction and body length. Quercitin induced lifespan extenison was neither dependent on a dietary restriction mimetic nor on sir-2.1 [19043800]. | Worm | — | — | — |
| NAD supplementation | Supplementation with NAD extended lifespan and this extension was dependent on sir-2.1 and daf-16 and associated with upregulation of sod-3 [19370397]. | Worm | — | — | — |
| Apply polyphenol treatment | Treatment with 100 microgram/mL apple polyphenol increases mean lifespan of wild-type N2 and FEM-1 by 12.0 and 5.3%, respectively [20717869]. | Worm | +5.3 to 12.0 | — | — |
| (-)-epicatechin treatment | Treatment with (-)-epidcatechin do no extend lifespan [20717869]. | Worm | — | — | — |
| Procyanidin treatment | Treatment with 65 microgram/mL Procyanidins from apple extends the lifespan of N2 and FEM-1 by 12.1 to 8.4%, respectively and does not modify grwoth, food intake of fecundity. Procyanidin treatment has no effect on mev-1 or sir-2.1 mutants [20717869]. | Worm | +8.4 to +12.1 | — | — |
| Eleutherococcus senticosus treatment | Plant adaptogen Eleutherococcus senticosus (SHE-3; alias Acantopanax senticosus) increase stress resistance and mean lifespan in a dose-dependent manner. 250 microgram/ml SHE-3 signinifanclty increases lifespan between 10 and 20% 9 (P < 0.001), increase maximum lifepsan with 2-3 days and pospones the moment when the first individuals die. With higher concentrations, the effect is weakerm wheras at the highest concentrations (2500 microgram/mL) a lifespan shortenening effect of 15-25% (P < 0.001) occurs. Treatment with SHE-3 induces translocation of DAF-16 and activation of HSP-16 [18536978]. | Worm | +10 to +20 | — | — |
| Rhodiola rosea treatment | Plant adaptogen Rhodiola rosea (SHE-5) increase stress resistance and mean lifespan in a dose-dependent manner. 10-25 microgram/ml SHE-5 signinifanclty increases lifespan between 10 and 20% 9 (P < 0.001), increase maximum lifepsan with 2-3 days and pospones the moment when the first individuals die. With higher concentrations, the effect is weaker whereas at the highest concentrations (250 microgram/mL) a lifespan shortenening effect of 15-25% (P < 0.001) occurs. Treatment with SHE-5 induces translocation of DAF-16 and activation of HSP-16 [18536978]. | Worm | +10 to +20 | — | — |
GenAge
GenDR
