|MSRA ||methionine sulfoxide reductase A ||Animals engineered to overexpress bovine MSRA in the nervous system have an extended median lifespan by up to 70% (relative to parental control), increased resistance to oxidative stress, and delayed the onset of senescence-induced decline in activity levels and reproductive capacity . ||— |
|Pro ||L-proline ||L-proline supplementation in nematodes increases lifespan by 5.8 and 13.6% (mean and maximum lifespan) . ||— |
|Rapa ||Rapamycin ||In budding yeast 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 . Rapamcyin treatment increases mean chronological lifespan by by approximately by 80% in BY4742 . Rapamycin extends chronological lifespan proportional with increasing concentrations from 100 pg/mL to 1 ng/mL .
Treatment with rapamcyin in nemaotdes 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 .
Treatment of Drosophila imago with rapamycin induces increases of median (by 5-6%) lifespan (p < 0.01) in males and females, respectively and increase of maximum lifespan (by 33%) in females (p < 0.01) . Rapamcyin increases mouse lifespan even when administrated late in life .
Low dose of rapamycin (5 microM) slightly increase the median and maximum lifespan in fruit fly .
Rapamcyin increases mouse lifespan and healthspan even when administrated late in life (20 months) .
Rapamycin enhances learning and memory in young mice and improves these faculties in old mice thereby negating the normal decline in these functions with age. Rapamycin boost levels of neurotransmitters associated with neural plasticity. Rapamycin also lowered anxiety and depressive-like behaviour at all ages from 4, 12 and 28 months. "Happy, feel-good" neurotransmitters such as serotonin, dopamine and norepinephrine are all significantly augmented in the midbrains of rapamycin treated mice [http://denigma.de/url/37].
Treatment with rapamycin increased lifespan and suppresses spontanous tumorgenesis in inbred female mice . ||— |
|— ||Curcumin ||Curcumin increases lifespan in *C. elegans* and is associated with reduced ROS and lipofuscin during aging. Curcumin lifespan extension is attributed to its antioxidative properties. Lifespan extension had effects on body size and pharyngeal pumping rate but not on reproduction. Lifespan-extension by curcumin is abolished in osr-1, sek-1, mek-1, skn-1, unc-43, sir-2.1 and age-1 mutants, whereas curcumin treatment prolongs lifespan of mev-1 and daf-16 mutants . *C. elegans* feed low concentration of curcumin have a decreased lipofuscin levels and enhanced the resistance to heat stress and increased mean lifespan by 39% and a maximum lifespan extended by 21.4% . In fruit fly that survive an average of 64 days, an increase of mean lifespan to 80 days occurs in flies, with females of one strain and males of another strain experiencing an extension in lifespan. The lifespan response to curcimun exhibits variation in male and female, although the compound extends lifespan in both genders .
In fruit fly, 0.5 an 1.0 mg/g curcumin in the diet increases mean lifespan by 6.2 and 25% in females and by 15.5 and 12.6 in males, respectively. Lifespan extension by curcumin was associated with the increased superoxide dismutase (SOD) activity, upregulation of Ms-SOD and CuZn-SOD genes, and the downregulation of *dInR*, *ATTD*, *Def*, *CecB* and, *DptB* genes as well as reduction of lipofuscin, malondialdehyde and lipid peroxidation [22653297; 23325575]. Curcumin prolongs life and enhances activity of fruit fly Alzheimer diseased flies . ||— |
|Quercitin ||— ||Quercitin significantly extends the lifespan in C. elegans. 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 . ||— |
|NAD ||Nicotinamide Adenine Dinucleotide ||Supplementation with NAD extended lifespan of C. elegans and this extension was dependent on sir-2.1 and daf-16 and associated with upregulation of sod-3 . ||— |
|PC ||Procyanidin ||Treatment of C. elegans 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 . ||— |
|AP ||Apple polyphenol ||Apple polyphenols mainly consists of procyanidins, which are composed of (-)-epicatechins and (+)-catechins. Treatment of C. elegans with 100 microgram/mL apple polyphenol increases mean lifespan of wild-type N2 and FEM-1 by 12.0 and 5.3%, respectively .
In fruit flies, supplemention of the diet with apple polyphenol significantly extends mean lifespan by 10% and is accompanied by up-regulation of SOD1, SOD2 and CAT as well as downregulation of MTH in aged animals . ||— |
|— ||Wortmannin ||Treatment of Drosophila imago with 0.5 micromolar wortmannin increases median (by 5%) and maximum (by 39%) lifespan in males (p < 0.001), but the lifespan differences in females were statistical insignificant (p > 0.05) .
Low dose of wortmannin (5 microM) slightly increase the median and maximum lifespan . ||— |
|sod1 ||sod1 superoxide dismutase 1, soluble ||Overexpression of sod1 in C. elegans increases mean, median, and maximum lifespan by 21, 25, and 29% . ||— |
|ucp2 ||uncoupling protein 2 ||Overexpression of zebrafish's ucp2 in nematode increases mean, median, and maximum lifespan by 42, 40, and 26%, which is non-additive with sDR . ||— |
|lyz ||lysozyme ||Overexpression of lyz increases mean, median, and maximum lifespan by 26, 30 and 44% . ||— |
|SIR2RP1 ||NAD-dependent SIR2 ||Overexpression of SIR2RP1 results in a significant increase in survival of the vertebrate stage under normla axenic culture conditions, but has no effect on survival of the insect stage of the parasite. SIR2RP1 is mainly localized within the cytoplasm . ||— |
|NAM ||Nictoinamide adenine mononucleotide ||Treatment of budding yeast with NAM reduces mean and maximum replicative lifespan by 28 and 37%. NAM treatment blocks the lifespan extending effect of rapamycn .
Treatment of nematodes with NAM significantly decreases adult lifespan . ||— |
|PLD alpha ||— ||Antisense suppression of PLD alpha retards abscisic acid- and ethylene-induced senescence. Leaves detached from PLD alpha-deficient transgenic plants when inbutated in abscisic acid and ethylene exhibit a slower rate of senescence that those from wild-type and transgenic controls. PLD alpha deficient strains are associated with retardation of senescence as evidenced by delayed leaf yellowing, lower ion leakage, greater photosynthetic activity, and higher content of cholorophyl and phospholipids .
Antisense suppression of PLD alpha does not affect natural plant growth and development . ||— |
|SAG101 ||senescence-associated protein 101 ||Antisense RNA interference of SAG101 in transgenic plants delays the onset of leaf senescence for approximately 4 days, whereas chemical induced overexpression of SAG101 causes precocious senescence in both attached and detached leaves of transgenic plants . ||— |
|SAG12 ||senescence-associated protein 12 ||Expression of SAG12 is specifically activated by developmentally controlled senescence pathways but not by stress- or hormone-controlled pathways [10579486; 10579487]. ||— |
|Asc ||Ascrobate ||In budding yeast, the 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 . ||— |
|SHE-3 ||Eleutherococcus senticosus ||Treatment of nematodes with the 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 . ||— |
|SHE-5 ||Rhodiola rosea ||Treatment of nematodes with the 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 weakerm wheras at the highest concentrations (250 microgram/mL) a lifespan shortenening effect of 15-25% (P < 0.001) occurs . ||— |
|DhHP-6 ||Deterohemin-AlaHisThrValGluLys ||Deuterohemin containing peptide deterohemin-AlaHisThrValGluLys (DhHP-6) significantly increases mean lifespan (P < 0.05), but not maximum lifespan. DhHP-6 also improves survival rate in acute heat-stress (35 degree Celsius) and rescues sensitivity to paraquat in acute oxidative stress. DhHP-6 treatment up-regulates SOD-3 and also regulates stress resistance genes such as hsp-16.1, hsp16.49 and sir-2.1 daf-16 and sir-2.1 genes are essential for the beneficial effect of DhHP-6 . ||— |
|DMSO ||Dimethyl sulfoxide ||Treatment with 0.5 and 2% DMSO increases lifespan by 24.4 and 23.0%, respectively. 0.5% DMSO does not affect progeny number or lifespan under thermal stress. Treatment with 0.5% DMSO enhances the mRNA levels of hsp-16.2, hsp-70, lys-7, old-1, and sod-5 by 2.5, 2.9, 1.3, 2.3, and 4.5-fold, respectively, as well as the protein level of lys-7 by 1.5-fold. Lifespan extension confered by DMSO depends on sir-2.1 and daf-16 but not on eat-2 or hsf-1 . ||— |
|JUG ||Jugelone treatment ||High jugelone concentrations led to premature death. Low juglone concentrations are tolerated well and cause a prolongation of lifespan that is associated with increased expression of small heat-shock protein HSP-16.2, enhanced glutathione levels, and nuclear translocation of DAF-16. Silencing or deletion of daf-16 prevents jugelone-induced adaptations. RNA-interference for SIR-2.1 has the same effects as daf-16 deletion but does not affect nuclear accumulation of DAF-16. DAF-16- and SIR-2.1-dependent alterations in gene expression after challenge with reactive oxygene species lead to lifespan extension . ||— |
|WRKY6 ||WRKY transcription factor 6 ||Deletion of the WRKY6 promoter results in defects in root and leaf cell senescence .
WRKY6 is a transcription factor involved in controlling processes related to senescence and pathogen defence  and is a positive regulator of PR1 expression . WRKY6 is strongly expressed during senescence . ||— |
|— ||D-glucosamine ||In budding yeast 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 . ||— |