攝入富含多胺的食物能夠延緩果蠅因年齡引起的記憶力下降,,10月《自然—神經(jīng)科學(xué)》上的一項研究得出該結(jié)論。很多食物都含有多胺,,研究證明,,多胺會隨著人年齡增大而自然減少,此外,,其對其他模式生物的壽命也有促進作用,。此項最新研究則進一步證明增加飲食中的多胺能夠幫助延緩與年齡相關(guān)的記憶力減退。
大多數(shù)器官利用多胺調(diào)節(jié)細胞的生理過程比如細胞存活和細胞繁殖,。哺乳動物細胞自身能夠合成多胺——雖然目前相關(guān)的原始分子機制幾乎仍是未知,。另外,人們已經(jīng)知道大腦中的多胺水平會隨著年齡增大而降低,。
由于多胺能夠延長無脊椎模式生物的壽命,,Stephan Sigrist, Frank Madeo等人便研究果蠅的這種記憶力減退能否通過攝入多胺發(fā)生逆轉(zhuǎn)。他們發(fā)現(xiàn),當(dāng)較老果蠅難以記住預(yù)示著輕微電擊的特定線索時,,那些經(jīng)過高含量多胺喂養(yǎng)的較老果蠅則沒有發(fā)生這種問題,,它們在這項任務(wù)中的表現(xiàn)同那些較年輕的果蠅一樣。研究人員還注意到,,多胺會通過促進細胞自噬作用(一種細胞的自我吞噬過程,,會清理掉有缺陷的細胞器)的方式調(diào)節(jié)平衡這種有益影響(生物谷Bioon.com)。
生物谷推薦的英文摘要
Nature Neuroscience DOI:10.1038/nn.3512
Restoring polyamines protects from age-induced memory impairment in an autophagy-dependent manner
Varun K Gupta,,Lisa Scheunemann,,Tobias Eisenberg,Sara Mertel,,Anuradha Bhukel,,Tom S Koemans,Jamie M Kramer,,Karen S Y Liu,,Sabrina Schroeder,Hendrik G Stunnenberg,,F(xiàn)rank Sinner,,Christoph Magnes,Thomas R Pieber,,Shubham Dipt,,André Fiala,Annette Schenck,,Martin Schwaerzel,,F(xiàn)rank Madeo & Stephan J Sigrist
Age-dependent memory impairment is known to occur in several organisms, including Drosophila,, mouse and human. However,, the fundamental cellular mechanisms that underlie these impairments are still poorly understood, effectively hampering the development of pharmacological strategies to treat the condition. Polyamines are among the substances found to decrease with age in the human brain. We found that levels of polyamines (spermidine,, putrescine) decreased in aging fruit flies,, concomitant with declining memory abilities. Simple spermidine feeding not only restored juvenile polyamine levels, but also suppressed age-induced memory impairment. Ornithine decarboxylase-1,, the rate-limiting enzyme for de novo polyamine synthesis,, also protected olfactory memories in aged flies when expressed specifically in Kenyon cells, which are crucial for olfactory memory formation. Spermidine-fed flies showed enhanced autophagy (a form of cellular self-digestion),, and genetic deficits in the autophagic machinery prevented spermidine-mediated rescue of memory impairments. Our findings indicate that autophagy is critical for suppression of memory impairments by spermidine and that polyamines,, which are endogenously present, are candidates for pharmacological intervention.