Epigenetic-mediated decline in synaptic plasticity during aging
Cognitive decline observed in aging mammals is associated with decreased long-term synaptic plasticity, especially long-term potentiation (LTP). Recent work has uncovered a connection between LTP, histone acetylation, and brain-derived neurotrophic factor (BDNF)/neurotrophin receptor B (trkB) signal...
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Published in | Rejuvenation research Vol. 15; no. 1; p. 98 |
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Main Authors | , |
Format | Journal Article |
Language | English |
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United States
01.02.2012
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Abstract | Cognitive decline observed in aging mammals is associated with decreased long-term synaptic plasticity, especially long-term potentiation (LTP). Recent work has uncovered a connection between LTP, histone acetylation, and brain-derived neurotrophic factor (BDNF)/neurotrophin receptor B (trkB) signaling. LTP, histone acetylation, and BDNF/trkB signaling decrease in old animals, Because an apparent positive feedback loop links these processes, treatment with histone deacetylase inhibitors or a trkB agonist restores LTP in the hippocampus of old animals. These results coupled with exciting work on histone methylation and life span in Caneorhabditis elegans suggest that epigenetic changes may play a significant role in aging. Such dysfunctional epigenetic pathways may provide novel targets for cognitive enhancing therapeutics. |
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AbstractList | Cognitive decline observed in aging mammals is associated with decreased long-term synaptic plasticity, especially long-term potentiation (LTP). Recent work has uncovered a connection between LTP, histone acetylation, and brain-derived neurotrophic factor (BDNF)/neurotrophin receptor B (trkB) signaling. LTP, histone acetylation, and BDNF/trkB signaling decrease in old animals, Because an apparent positive feedback loop links these processes, treatment with histone deacetylase inhibitors or a trkB agonist restores LTP in the hippocampus of old animals. These results coupled with exciting work on histone methylation and life span in Caneorhabditis elegans suggest that epigenetic changes may play a significant role in aging. Such dysfunctional epigenetic pathways may provide novel targets for cognitive enhancing therapeutics. |
Author | Larrick, James W Mendelsohn, Andrew R |
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CitedBy_id | crossref_primary_10_1016_j_bbr_2015_01_052 crossref_primary_10_1016_j_molonc_2016_05_002 crossref_primary_10_1089_rej_2013_1448 crossref_primary_10_1089_rej_2013_1464 crossref_primary_10_1016_j_bbr_2013_09_029 crossref_primary_10_1002_brb3_2817 crossref_primary_10_1002_ddr_21295 crossref_primary_10_3390_ijms18020268 crossref_primary_10_1016_j_lfs_2021_119765 crossref_primary_10_3389_fnagi_2020_578719 crossref_primary_10_1016_j_neubiorev_2017_04_030 crossref_primary_10_1089_rej_2012_1375 crossref_primary_10_1007_s11357_016_9920_3 crossref_primary_10_2217_epi_12_41 |
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SubjectTerms | Acetylation Aging Animals Caenorhabditis elegans Cognition Disorders - metabolism Epigenesis, Genetic Hippocampus - metabolism Histones - metabolism Humans Long-Term Potentiation Longevity Models, Animal Neuronal Plasticity Receptor, trkB - genetics Receptor, trkB - metabolism Synapses - metabolism |
Title | Epigenetic-mediated decline in synaptic plasticity during aging |
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