PUBLICATION

Long-term Acetylcholinesterase Depletion Alters the Levels of Key Synaptic Proteins while Maintaining Neuronal Markers in the Aging Zebrafish (Danio rerio) Brain

Authors
Karoglu-Eravsar, E.T., Tuz-Sasik, M.U., Karaduman, A., Keskus, A.G., Arslan-Ergul, A., Konu, O., Kafaligonul, H., Adams, M.M.
ID
ZDB-PUB-231005-63
Date
2023
Source
Gerontology   69(12): 1424-1436 (Journal)
Registered Authors
Keywords
none
MeSH Terms
  • Acetylcholinesterase*/metabolism
  • Aging
  • Animals
  • Brain/metabolism
  • Cholinergic Agents/metabolism
  • Humans
  • Neurodegenerative Diseases*
  • Zebrafish/metabolism
PubMed
37793352 Full text @ Gerontology
Abstract
Interventions targeting cholinergic neurotransmission like acetylcholinesterase (AChE) inhibition distinguish potential mechanisms to delay age-related impairments and attenuate deficits related to neurodegenerative diseases. However, the chronic effects of these interventions are not well-described.
In the current study, global levels of cholinergic, cellular, synaptic, and inflammation-mediating proteins were assessed within the context of aging and chronic reduction of AChE activity. Long-term depletion of AChE activity was induced by using a mutant zebrafish line and they were compared with the wildtype group at young and old ages.
Results demonstrated that AChE activity was lower in both young and old mutants and this decrease coincided with a reduction in ACh content. Additionally, an overall age-related reduction in AChE activity and the AChE/ACh ratio was observed, this decline was more prominent in wildtype groups. The levels of an immature neuronal marker were upregulated in mutants, while a glial marker showed an overall reduction. Mutants had preserved levels of inhibitory and presynaptic elements with aging, whereas glutamate receptor subunit levels declined.
Long-term AChE activity depletion induces synaptic and cellular alterations. These data provide further insights into molecular targets and adaptive responses following the long-term reduction of AChE activity that was also targeted pharmacologically to treat neurodegenerative diseases in human subjects.
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Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
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Mapping