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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Bibliographic Details
Published inRejuvenation research Vol. 15; no. 1; p. 98
Main Authors Mendelsohn, Andrew R, Larrick, James W
Format Journal Article
LanguageEnglish
Published United States 01.02.2012
Subjects
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
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Summary: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.
ISSN:1557-8577
DOI:10.1089/rej.2012.1312