期刊
NEUROBIOLOGY OF AGING
卷 26, 期 1, 页码 69-76出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2004.02.013
关键词
advanced glycosylation end product; anti-ageing; antioxidant; blood transport; caloric restriction; carbonyl; CNS biopsy; degradability; deleteriousness; exocytosis; free radical; glial uptake; hormesis; insulin receptor gene; in vivo; late-life mortality decline; longitudinal sampling
The prospect of removing cellular deposits of lipofuscin is of considerable interest because they may contribute to age related functional decline and disease. Here, we use a decapod crustacean model to circumvent a number of problems inherent in previous studies on lipofuscin loss. We employ (a) validated lipofuscin quantification methods, (b) an in vivo context, (c) essentially natural environmental conditions and (d) a situation without accelerated production of residual material or (e) application of pharmacological compounds. We use a novel CNS biopsy technique that produces both an anti-ageing effect and also permits longitudinal sampling of individuals, thus (f) avoiding conventional purely cross-sectional population data that may suffer from selective mortality biases. We quantitatively demonstrate that lipofuscin, accrued through normal ageing, can be lost from neural tissue. The mechanism of loss probably involves exocytosis and possibly blood transport. If non-disruptive ways to accelerate lipofuscin removal can be found, our results suggest that therapeutic reversal of this most universal manifestation of cellular ageing may be possible. (C) 2004 Elsevier Inc. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据