Spermidine-triggered autophagy ameliorates memory during aging

Sigrist, Stephan J.; Carmona-Gutiérrez, Didac; Gupta, Varun; Bhukel, Anuradha; Mertel, Sara; Eisenberg, Tobias; Madeo, Frank

doi:10.4161/auto.26918

Cited by 63 publications

(47 citation statements)

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“…It has been confirmed that Spd inhibits cell senescence induced by neuroinflammation and oxidative stress in striatum 36 and protects against aging-induced synaptic senescence. 15,37,38 These previous findings offered a reasonable explanation for the results obtained in the present study. Furthermore, the present work demonstrated that Spd also overcame HG-induced neurotoxicity in HT-22 cells.…”

Section: Discussionsupporting

confidence: 91%

“…These results indicated that Spd is able to suppress HG‐induced senescence in HT‐22 cells. It has been confirmed that Spd inhibits cell senescence induced by neuroinflammation and oxidative stress in striatum and protects against aging‐induced synaptic senescence . These previous findings offered a reasonable explanation for the results obtained in the present study.…”

Section: Discussionsupporting

confidence: 91%

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Spermidine prevents high glucose‐induced senescence in HT‐22 cells by upregulation of CB1 receptor

Zhu

Fan

Tang

et al. 2018

Clin Exp Pharma Physio

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Hyperglycaemia-induced neurotoxicity involved in the pathogenesis of diabetic encephalopathy and neuronal senescence is one of the worst effects of hyperglyceamic neurotoxicity. Cannabinoid receptor type 1 (CB1) has neuroprotective function in a series of neuropathy. Spermidine (Spd) has anti-aging function in many tissues. However, the role of Spd in hyperglyceamia-induced neuronal senescence remains unexplored. Therefore, we used high glucose (HG)-treated HT-22 cell as vitro model to investigate whether Spd protects neurons against hyperglyceamia-induced senescence and the mediatory role of CB1 receptor. The HT-22 cells were cultured in HG condition in the presence of different dose of Spd. Then, the viability of cells was measured by Cell Counting Kit-8 (CCK-8) assay. The senescence of cells was detected by Senescence-associated β-galactosidase (SA-β-Gal) staining. The expressions of p16 , p21 and CB1 receptor were measured by western blot. We found that Spd inhibited HG-induced neurotoxicity (the loss of cell viability) and senescence (the increase of SA-β-Gal positive cells, the upregulation of p16 and p21 ) in HT-22 cells. Also, Spd prevented HG-induced downregulation of CB1 receptor in HT-22 cells. Furthermore, we demonstrated that AM251 (a specific inhibitor of the CB1 receptor) reversed the protective effects of Spd on HG-induced neurotoxicity and senescence. These results indicated that Spd prevents HG-induced neurotoxicity and senescence via the upregulation of CB1 receptor. Our findings provide a promising future of Spd-based preventions and therapies for diabetic encephalopathy.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 91%

Spermidine prevents high glucose‐induced senescence in HT‐22 cells by upregulation of CB1 receptor

Zhu

Fan

Tang

et al. 2018

Clin Exp Pharma Physio

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“…285 Treatments with SPD, agmatine, and by genetic modulation that increase endogenous PA levels resulted in not only an increase in life span 97 , but also in memory restoration. 97, 101, 199 PA-rich nutrition increased the life span of aging mice 98, 99, 100, 286 while some amines and PAs (such as agmatine, arginine, putrescine, spermidine, spermine) are lost during aging and in the diseased CNS. 97, 102, 157, 179–182, 286 Also, PAs inhibit age-associated changes in global DNA methylation as well as dimethylhydrazine-induced tumor genesis.…”

Section: Polyamines: Role In the Cns Disordersmentioning

confidence: 99%

The Role of Glia in Stress

Skatchkov

Woodbury-Fariña

Eaton

2014

Psychiatric Clinics of North America

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Synopsis This review focuses on the roles of glia and polyamines (PAs) in brain function and dysfunction, highlighting how PAs are one of the principal differences between glia and neurons as they are surprisingly stored, but not synthesized, almost exclusively in glial cells from which they can be released to regulate neuronal synaptic activity. The review includes the novel role of PAs, such as putrescine (PUT), spermidine (SPD) and spermine (SPM) and their precursors and derivatives. However: (i) PAs have not yet been a focus of much glial research; (ii) PAs affect many neuronal and glial receptors, channels and transporters; (iii) PAs are therefore key elements in the development of many diseases and syndromes (iv) thus forming the rationale for PA and glia focused therapy for these conditions.

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“…There has been increased # p values after log transformation. (37)(38)(39)(40). In fact, polyamine levels have been shown to decline with age in many organisms (41).…”

Section: Amino Acids and Biogenic Aminesmentioning

confidence: 99%

Plasma Biomarkers of Poor Muscle Quality in Older Men and Women from the Baltimore Longitudinal Study of Aging

Moaddel

Fabbri

Khadeer

et al. 2016

GERONA

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Aging is characterized by progressive decline in muscle mass, strength, and quality all of which contribute to functional impairment, falls, mobility disability, and frailty. Circulating factors may provide clues on the mechanisms for decline in muscle quality with aging. Characterizing the metabolic profile associated with reduced muscle quality in older persons could have important translational implications for the early identification of subjects at high risk of developing sarcopenia and the identification of targets for new preventive strategies and treatments. In a pilot cross-sectional, case-control study nested in the Baltimore Longitudinal Study on Aging, we compared circulating metabolites between 79 participants with low muscle quality ratio and 79 controls with high muscle quality, matched by age, sex, and height. The concentrations of 180 metabolites were determined by LC MS/MS, using the Biocrates p180 system, a targeted metabolomics approach. Participants with low muscle quality had significantly higher levels of leucine, isoleucine, tryptophan, serotonin, and methionine, while those with high muscle quality had significantly lower levels of putrescine and the selected phophatidylcholine (PCs) and lysoPCs. The results of this study open a new road for future investigations aimed at identifying new metabolic pathways involved in the decline of muscle quality with aging.

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Spermidine-triggered autophagy ameliorates memory during aging

Cited by 63 publications

References 0 publications

Spermidine prevents high glucose‐induced senescence in HT‐22 cells by upregulation of CB1 receptor

Spermidine prevents high glucose‐induced senescence in HT‐22 cells by upregulation of CB1 receptor

The Role of Glia in Stress

Plasma Biomarkers of Poor Muscle Quality in Older Men and Women from the Baltimore Longitudinal Study of Aging

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