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Karoglu-Eravsar, Elif Tugce; Tuz-Sasik, Melek Umay; Karaduman, Aysenur; Keskus, Ayse Gokce; Arslan-Ergul, Ayca; Konu, Ozlen; Kafaligonul, Hulusi; Adams, Michelle M.
<?xml version='1.0' encoding='utf-8'?> <oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"> <dc:creator>Karoglu-Eravsar, Elif Tugce</dc:creator> <dc:creator>Tuz-Sasik, Melek Umay</dc:creator> <dc:creator>Karaduman, Aysenur</dc:creator> <dc:creator>Keskus, Ayse Gokce</dc:creator> <dc:creator>Arslan-Ergul, Ayca</dc:creator> <dc:creator>Konu, Ozlen</dc:creator> <dc:creator>Kafaligonul, Hulusi</dc:creator> <dc:creator>Adams, Michelle M.</dc:creator> <dc:date>2023-01-01</dc:date> <dc:description>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.</dc:description> <dc:identifier>https://aperta.ulakbim.gov.trrecord/270528</dc:identifier> <dc:identifier>oai:aperta.ulakbim.gov.tr:270528</dc:identifier> <dc:rights>info:eu-repo/semantics/openAccess</dc:rights> <dc:rights>http://www.opendefinition.org/licenses/cc-by</dc:rights> <dc:source>GERONTOLOGY 69(12) 13</dc:source> <dc:title>Long-term Acetylcholinesterase Depletion Alters the Levels of Key Synaptic Proteins while Maintaining Neuronal Markers in the Aging Zebrafish (Danio rerio) Brain</dc:title> <dc:type>info:eu-repo/semantics/article</dc:type> <dc:type>publication-article</dc:type> </oai_dc:dc>
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