期刊
SCIENTIFIC REPORTS
卷 9, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41598-019-56133-3
关键词
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资金
- Bundesministerium fur Bildung und Forschung [01GQ1420A, 01GQ1420D, 01GQ1420B, 01GQ1420C]
- Deutsche Forschungsgemeinschaft [SFB958]
- European Union
- European Social Fund [EFOP-3.6.1-16-2016-00024]
- UNKP Bolyai+ fellowship of the Hungarian Ministry of Human Capacities
- Janos Bolyai Research Fellowship of the Hungarian Academy of Sciences
- Austrian Science Fund FWF [SFB LIPOTOX F3007, F3012, W1226, P29203, P29262, P27893, P31727]
- Austrian Federal Ministry of Education, Science and Research
- University of Graz
- flysleep [BMWFW-80.109/0001-WF/V/3b/2015]
- NAWI Graz
- BioTechMed-Graz flagship project EPIAge
- Austrian Science Fund (FWF) [P29262] Funding Source: Austrian Science Fund (FWF)
Aging is associated with functional alterations of synapses thought to contribute to age-dependent memory impairment (AMI). While therapeutic avenues to protect from AMI are largely elusive, supplementation of spermidine, a polyamine normally declining with age, has been shown to restore defective proteostasis and to protect from AMI in Drosophila. Here we demonstrate that dietary spermidine protects from age-related synaptic alterations at hippocampal mossy fiber (MF)-CA3 synapses and prevents the aging-induced loss of neuronal mitochondria. Dietary spermidine rescued age-dependent decreases in synaptic vesicle density and largely restored defective presynaptic MF-CA3 long-term potentiation (LTP) at MF-CA3 synapses (MF-CA3) in aged animals. In contrast, spermidine failed to protect CA3-CA1 hippocampal synapses characterized by postsynaptic LTP from age-related changes in function and morphology. Our data demonstrate that dietary spermidine attenuates age-associated deterioration of MF-CA3 synaptic transmission and plasticity. These findings provide a physiological and molecular basis for the future therapeutic usage of spermidine.
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