Neural protein synthesis during aging: effects on plasticity and memory
During aging, many experience a decline in cognitive function that includes memory loss. The encoding of long-term memories depends on new protein synthesis, and this is also reduced during aging. Thus, it is possible that changes in the regulation of protein synthesis contribute to the memory impai...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2010-08-01
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| Series: | Frontiers in Aging Neuroscience |
| Subjects: | |
| Online Access: | http://journal.frontiersin.org/Journal/10.3389/fnagi.2010.00026/full |
| _version_ | 1819095915501191168 |
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| author | Lesley A Schimanski Carol A Barnes Carol A Barnes Carol A Barnes Carol A Barnes |
| author_facet | Lesley A Schimanski Carol A Barnes Carol A Barnes Carol A Barnes Carol A Barnes |
| author_sort | Lesley A Schimanski |
| collection | DOAJ |
| description | During aging, many experience a decline in cognitive function that includes memory loss. The encoding of long-term memories depends on new protein synthesis, and this is also reduced during aging. Thus, it is possible that changes in the regulation of protein synthesis contribute to the memory impairments observed in older animals. Several lines of evidence support this hypothesis. For instance, protein synthesis is required for a longer period following learning to establish long-term memory in aged rodents. Also, under some conditions, synaptic activity or pharmacological activation can induce de novo protein synthesis and lasting changes in synaptic transmission in aged, but not young, rodents; the opposite results can be observed in other conditions. These changes in plasticity likely play a role in manifesting the altered place field properties observed in awake and behaving aged rats. Thus, the collective evidence suggests a link between memory loss and the regulation of protein synthesis in senescence. In fact, pharmaceuticals that target the signaling pathways required for induction of protein synthesis have been shown to improve memory, synaptic plasticity, and place cell properties in aged animals. We suggest that a better understanding of the mechanisms that lead to different protein expression patterns in the neural circuits that change as a function of age will enable the development of more effective therapeutic treatments for memory loss. |
| first_indexed | 2024-12-21T23:50:53Z |
| format | Article |
| id | doaj.art-4da04f60081c4de3ab9a1e9692878b1a |
| institution | Directory Open Access Journal |
| issn | 1663-4365 |
| language | English |
| last_indexed | 2024-12-21T23:50:53Z |
| publishDate | 2010-08-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Aging Neuroscience |
| spelling | doaj.art-4da04f60081c4de3ab9a1e9692878b1a2022-12-21T18:45:56ZengFrontiers Media S.A.Frontiers in Aging Neuroscience1663-43652010-08-01210.3389/fnagi.2010.000261282Neural protein synthesis during aging: effects on plasticity and memoryLesley A Schimanski0Carol A Barnes1Carol A Barnes2Carol A Barnes3Carol A Barnes4University of ArizonaUniversity of ArizonaUniversity of ArizonaUniversity of ArizonaUniversity of ArizonaDuring aging, many experience a decline in cognitive function that includes memory loss. The encoding of long-term memories depends on new protein synthesis, and this is also reduced during aging. Thus, it is possible that changes in the regulation of protein synthesis contribute to the memory impairments observed in older animals. Several lines of evidence support this hypothesis. For instance, protein synthesis is required for a longer period following learning to establish long-term memory in aged rodents. Also, under some conditions, synaptic activity or pharmacological activation can induce de novo protein synthesis and lasting changes in synaptic transmission in aged, but not young, rodents; the opposite results can be observed in other conditions. These changes in plasticity likely play a role in manifesting the altered place field properties observed in awake and behaving aged rats. Thus, the collective evidence suggests a link between memory loss and the regulation of protein synthesis in senescence. In fact, pharmaceuticals that target the signaling pathways required for induction of protein synthesis have been shown to improve memory, synaptic plasticity, and place cell properties in aged animals. We suggest that a better understanding of the mechanisms that lead to different protein expression patterns in the neural circuits that change as a function of age will enable the development of more effective therapeutic treatments for memory loss.http://journal.frontiersin.org/Journal/10.3389/fnagi.2010.00026/fullAgingHippocampusMemoryplasticitytranscriptionPlace Cells |
| spellingShingle | Lesley A Schimanski Carol A Barnes Carol A Barnes Carol A Barnes Carol A Barnes Neural protein synthesis during aging: effects on plasticity and memory Frontiers in Aging Neuroscience Aging Hippocampus Memory plasticity transcription Place Cells |
| title | Neural protein synthesis during aging: effects on plasticity and memory |
| title_full | Neural protein synthesis during aging: effects on plasticity and memory |
| title_fullStr | Neural protein synthesis during aging: effects on plasticity and memory |
| title_full_unstemmed | Neural protein synthesis during aging: effects on plasticity and memory |
| title_short | Neural protein synthesis during aging: effects on plasticity and memory |
| title_sort | neural protein synthesis during aging effects on plasticity and memory |
| topic | Aging Hippocampus Memory plasticity transcription Place Cells |
| url | http://journal.frontiersin.org/Journal/10.3389/fnagi.2010.00026/full |
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