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Related Concept Videos

Long-term Depression01:03

Long-term Depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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Long-term Potentiation01:35

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Related Experiment Video

Updated: May 24, 2026

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology
14:57

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

Published on: March 23, 2011

Epigenetic-mediated decline in synaptic plasticity during aging.

Andrew R Mendelsohn1, James W Larrick

  • 1Panorama Research Institute and Regenerative Sciences Institute, Sunnyvale, CA 94089, USA.

Rejuvenation Research
|February 23, 2012
PubMed
Summary
This summary is machine-generated.

Aging impairs cognitive function by reducing synaptic plasticity, like long-term potentiation (LTP). Epigenetic interventions targeting histone acetylation and BDNF/trkB signaling show promise for restoring cognitive function in aging mammals.

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Last Updated: May 24, 2026

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08:58

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Area of Science:

  • Neuroscience
  • Gerontology
  • Epigenetics

Background:

  • Cognitive decline in aging mammals correlates with reduced long-term synaptic plasticity, particularly long-term potentiation (LTP).
  • A link exists between LTP, histone acetylation, and brain-derived neurotrophic factor (BDNF)/neurotrophin receptor B (trkB) signaling.
  • These key processes (LTP, histone acetylation, BDNF/trkB signaling) decline with age.

Purpose of the Study:

  • To investigate the role of epigenetic modifications in age-related cognitive decline.
  • To explore the potential of targeting epigenetic pathways for cognitive enhancement therapies.

Main Methods:

  • Utilized histone deacetylase inhibitors and a trkB agonist in aging mammal models.
  • Assessed the restoration of LTP in the hippocampus following treatments.

Main Results:

  • Treatment with histone deacetylase inhibitors or a trkB agonist successfully restored LTP in the hippocampus of aged animals.
  • This restoration suggests a functional link between epigenetic modifications and synaptic plasticity in aging.

Conclusions:

  • Epigenetic dysregulation, specifically involving histone acetylation and BDNF/trkB signaling, contributes significantly to age-related cognitive decline.
  • Targeting these dysfunctional epigenetic pathways offers a promising therapeutic strategy for developing cognitive-enhancing treatments for aging.