Abstract:
:Aging is associated with a reduction in the maximum density of n-methyl-d-aspartate (NMDA)-sensitive glutamate binding sites in the hippocampus of Fischer 344 rats. This study was designed to investigate the effect of acetyl-l-carnitine (ALCAR) on NMDA receptors in the old rat (24 months) after chronic or single-dose treatments. The number of NMDA receptors was significantly decreased in the old rat hippocampus by 19.5% compared with the young rat. A six-month treatment with ALCAR in the old rat attenuated the loss of NMDA binding sites in the hippocampus. A single-dose treatment with ALCAR in the old rat increased the Bmax value by 35%, while no change was observed in the young group. We conclude that ALCAR can exert two actions: a trophic/neuro-preserving one when chronically administered during aging, and a stimulatory one when given at a single dose in the aged rat.
journal_name
Exp Gerontoljournal_title
Experimental gerontologyauthors
Castorina M,Ambrosini AM,Giuliani A,Pacifici L,Ramacci MT,Angelucci Ldoi
10.1016/0531-5565(93)90042-csubject
Has Abstractpub_date
1993-11-01 00:00:00pages
537-48issue
6eissn
0531-5565issn
1873-6815journal_volume
28pub_type
杂志文章abstract::Dietary restriction extends lifespan in a variety of organisms, but the key nutritional components driving this process and how they interact remain uncertain. In Drosophila, while a substantial body of research suggests that protein is the major dietary component affecting longevity, recent studies claim that carbohy...
journal_title:Experimental gerontology
pub_type: 杂志文章
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更新日期:2013-10-01 00:00:00
abstract::Orally-administered catechin has long been known to have several beneficial effects on the mammalian host, however, the effects of orally supplemented catechin on the host through gingival tissues have not yet been established. Here, we elucidated the effects of orally supplemented catechin in the rat heart blood mito...
journal_title:Experimental gerontology
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abstract::Ageing is highly complex, involving multiple mechanisms at different levels. Nevertheless, recent evidence suggests that several of the most important mechanisms are linked via endogenous stress-induced DNA damage caused by reactive oxygen species (ROS). Understanding how such damage contributes to age-related changes...
journal_title:Experimental gerontology
pub_type: 杂志文章,评审
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doi:10.1016/j.exger.2021.111259
更新日期:2021-01-28 00:00:00
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journal_title:Experimental gerontology
pub_type: 杂志文章
doi:10.1016/0531-5565(92)90034-w
更新日期:1992-01-01 00:00:00
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journal_title:Experimental gerontology
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journal_title:Experimental gerontology
pub_type: 杂志文章
doi:10.1016/j.exger.2016.04.022
更新日期:2016-08-01 00:00:00
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journal_title:Experimental gerontology
pub_type: 杂志文章
doi:10.1016/0531-5565(94)00053-0
更新日期:1995-03-01 00:00:00
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journal_title:Experimental gerontology
pub_type: 杂志文章
doi:10.1016/j.exger.2013.07.007
更新日期:2013-11-01 00:00:00
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journal_title:Experimental gerontology
pub_type: 杂志文章
doi:10.1016/0531-5565(87)90048-9
更新日期:1987-01-01 00:00:00
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journal_title:Experimental gerontology
pub_type: 杂志文章,评审
doi:10.1016/j.exger.2006.01.011
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journal_title:Experimental gerontology
pub_type: 杂志文章,评审
doi:10.1016/j.exger.2019.110817
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journal_title:Experimental gerontology
pub_type: 杂志文章
doi:10.1016/j.exger.2016.02.012
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journal_title:Experimental gerontology
pub_type: 杂志文章
doi:10.1016/j.exger.2019.110640
更新日期:2019-09-01 00:00:00
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journal_title:Experimental gerontology
pub_type: 杂志文章
doi:10.1016/j.exger.2014.01.022
更新日期:2014-04-01 00:00:00
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journal_title:Experimental gerontology
pub_type: 杂志文章,评审
doi:10.1016/j.exger.2014.02.011
更新日期:2014-08-01 00:00:00
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journal_title:Experimental gerontology
pub_type: 杂志文章
doi:10.1016/j.exger.2019.110663
更新日期:2019-10-01 00:00:00
abstract::Heat shock proteins (HSP's) closely interact with 20S proteasome and have been shown to maintain catalytic activity, responsible for the prevention of protein aggregation. A decrease in both proteasome activity and heat shock proteins (HSP's) has been observed with age. We investigated whether life-long calorie restri...
journal_title:Experimental gerontology
pub_type: 杂志文章
doi:10.1016/j.exger.2004.08.012
更新日期:2005-01-01 00:00:00
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journal_title:Experimental gerontology
pub_type: 杂志文章
doi:10.1016/j.exger.2015.08.011
更新日期:2015-10-01 00:00:00
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journal_title:Experimental gerontology
pub_type: 杂志文章
doi:10.1016/j.exger.2020.110840
更新日期:2020-04-01 00:00:00
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journal_title:Experimental gerontology
pub_type: 杂志文章
doi:10.1016/j.exger.2007.07.005
更新日期:2007-10-01 00:00:00
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journal_title:Experimental gerontology
pub_type: 杂志文章
doi:10.1016/j.exger.2010.09.012
更新日期:2010-12-01 00:00:00
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journal_title:Experimental gerontology
pub_type: 杂志文章
doi:10.1016/j.exger.2017.05.015
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abstract::Aging is associated with impaired mitochondrial function, whereas exercise training enhances mitochondrial content and function in part through activation of PGC-1α. Mitochondria form dynamic networks regulated by fission and fusion with profound effects on mitochondrial functions, yet the effects of aging and exercis...
journal_title:Experimental gerontology
pub_type: 杂志文章
doi:10.1016/j.exger.2017.05.020
更新日期:2017-10-01 00:00:00
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journal_title:Experimental gerontology
pub_type: 杂志文章
doi:10.1016/j.exger.2013.02.001
更新日期:2013-04-01 00:00:00
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journal_title:Experimental gerontology
pub_type: 杂志文章
doi:10.1016/s0531-5565(00)00101-7
更新日期:2000-08-01 00:00:00
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journal_title:Experimental gerontology
pub_type: 杂志文章,评审
doi:10.1016/s0531-5565(01)00133-4
更新日期:2001-09-01 00:00:00
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journal_title:Experimental gerontology
pub_type: 杂志文章
doi:10.1016/0531-5565(87)90045-3
更新日期:1987-01-01 00:00:00
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journal_title:Experimental gerontology
pub_type: 杂志文章,评审
doi:10.1016/j.exger.2006.11.015
更新日期:2007-05-01 00:00:00
abstract::As recently reported, it is possible to detect and quantify the amount of the deleted human mitochondrial DNA (mtDNA) in whole blood, platelets and peripheral blood mononuclear cells using real-time PCR. The aim of this study was to identify the cell types in human blood carrying the 4977 bp deleted mtDNA and their ac...
journal_title:Experimental gerontology
pub_type: 杂志文章
doi:10.1016/j.exger.2003.10.011
更新日期:2004-02-01 00:00:00