1 Ocak 2023 Dergi makalesi Açık Erişim

Karoglu-Eravsar, Elif Tugce; Tuz-Sasik, Melek Umay; Karaduman, Aysenur; Keskus, Ayse Gokce; Arslan-Ergul, Ayca; Konu, Ozlen; Kafaligonul, Hulusi; Adams, Michelle M.

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  <identifier identifierType="URL">https://aperta.ulakbim.gov.tr/record/270528</identifier>
  <creators>
    <creator>
      <creatorName>Karoglu-Eravsar, Elif Tugce</creatorName>
      <givenName>Elif Tugce</givenName>
      <familyName>Karoglu-Eravsar</familyName>
    </creator>
    <creator>
      <creatorName>Tuz-Sasik, Melek Umay</creatorName>
      <givenName>Melek Umay</givenName>
      <familyName>Tuz-Sasik</familyName>
    </creator>
    <creator>
      <creatorName>Karaduman, Aysenur</creatorName>
      <givenName>Aysenur</givenName>
      <familyName>Karaduman</familyName>
    </creator>
    <creator>
      <creatorName>Keskus, Ayse Gokce</creatorName>
      <givenName>Ayse Gokce</givenName>
      <familyName>Keskus</familyName>
    </creator>
    <creator>
      <creatorName>Arslan-Ergul, Ayca</creatorName>
      <givenName>Ayca</givenName>
      <familyName>Arslan-Ergul</familyName>
    </creator>
    <creator>
      <creatorName>Konu, Ozlen</creatorName>
      <givenName>Ozlen</givenName>
      <familyName>Konu</familyName>
    </creator>
    <creator>
      <creatorName>Kafaligonul, Hulusi</creatorName>
      <givenName>Hulusi</givenName>
      <familyName>Kafaligonul</familyName>
    </creator>
    <creator>
      <creatorName>Adams, Michelle M.</creatorName>
      <givenName>Michelle M.</givenName>
      <familyName>Adams</familyName>
    </creator>
  </creators>
  <titles>
    <title>Long-Term Acetylcholinesterase Depletion Alters The Levels Of Key Synaptic Proteins While Maintaining Neuronal Markers In The Aging Zebrafish (Danio Rerio) Brain</title>
  </titles>
  <publisher>Aperta</publisher>
  <publicationYear>2023</publicationYear>
  <dates>
    <date dateType="Issued">2023-01-01</date>
  </dates>
  <resourceType resourceTypeGeneral="Text">Journal article</resourceType>
  <alternateIdentifiers>
    <alternateIdentifier alternateIdentifierType="url">https://aperta.ulakbim.gov.tr/record/270528</alternateIdentifier>
  </alternateIdentifiers>
  <relatedIdentifiers>
    <relatedIdentifier relatedIdentifierType="DOI" relationType="IsIdenticalTo">10.1159/000534343</relatedIdentifier>
  </relatedIdentifiers>
  <rightsList>
    <rights rightsURI="http://www.opendefinition.org/licenses/cc-by">Creative Commons Attribution</rights>
    <rights rightsURI="info:eu-repo/semantics/openAccess">Open Access</rights>
  </rightsList>
  <descriptions>
    <description descriptionType="Abstract">&lt;p&gt;Introduction: 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. Methods: 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: 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. Discussion/Conclusion: 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.&lt;/p&gt;</description>
  </descriptions>
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