Effect of methylglyoxal on Parkinson’s disease pathophysiology in the rotenone model
Objective: Type 2 diabetes mellitus patients have been reported to have a higher incidence of Parkinson’s disease. This study aimed to explore the effect of advanced glycation end products precursor methylglyoxal (MGO) on the pathophysiology of Parkinson’s disease in a rotenone model. Materials and...
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| Veröffentlicht in: | Marmara Medical Journal 2024-01, Vol.37 (2), p.166-177 |
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| container_title | Marmara Medical Journal |
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| creator | Çulpan, Yekta Ozden, Lara Gozderesi, Yakup Kocak, Beril Baltaci, Zeynep Hazal Denizli, Ayberk Yılmaz, Betul Gülhan, Rezzan |
| description | Objective: Type 2 diabetes mellitus patients have been reported to have a higher incidence of Parkinson’s disease. This study aimed to
explore the effect of advanced glycation end products precursor methylglyoxal (MGO) on the pathophysiology of Parkinson’s disease
in a rotenone model.
Materials and Methods: Adult female Wistar rats (n=42) were divided into four groups. Rotenone toxicity was assessed by daily weight
measurements and mortality rates. Effect of MGO on blood glucose was evaluated. Locomotor activity, rearing, and rotarod tests
were performed to evaluate motor functions, and for neurodegeneration, tyrosine hydroxylase immunoreactivity in the striatum and
substantia nigra regions was assessed.
Results: The mortality rate was 9% in the rotenone-applied rats. The mean weight, locomotor activity, rearing activity, and longest time
spent on a rotarod were lower in the MGO+Rotenone group than in the Control group. Tyrosine hydroxylase immunoreactivity in the
striatum rostral to the anterior commissure in the MGO+Rotenone group was lower than that in the Control and MGO groups. The
number of tyrosine hydroxylase positive cells in the substantia nigra pars compacta was comparable among the groups.
Conclusion: When nigrostriatal degeneration was triggered, MGO was found to worsen motor dysfunction and increase damage to
dopaminergic neuron projections. |
| doi_str_mv | 10.5472/marumj.1480086 |
| format | Article |
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explore the effect of advanced glycation end products precursor methylglyoxal (MGO) on the pathophysiology of Parkinson’s disease
in a rotenone model.
Materials and Methods: Adult female Wistar rats (n=42) were divided into four groups. Rotenone toxicity was assessed by daily weight
measurements and mortality rates. Effect of MGO on blood glucose was evaluated. Locomotor activity, rearing, and rotarod tests
were performed to evaluate motor functions, and for neurodegeneration, tyrosine hydroxylase immunoreactivity in the striatum and
substantia nigra regions was assessed.
Results: The mortality rate was 9% in the rotenone-applied rats. The mean weight, locomotor activity, rearing activity, and longest time
spent on a rotarod were lower in the MGO+Rotenone group than in the Control group. Tyrosine hydroxylase immunoreactivity in the
striatum rostral to the anterior commissure in the MGO+Rotenone group was lower than that in the Control and MGO groups. The
number of tyrosine hydroxylase positive cells in the substantia nigra pars compacta was comparable among the groups.
Conclusion: When nigrostriatal degeneration was triggered, MGO was found to worsen motor dysfunction and increase damage to
dopaminergic neuron projections.</description><identifier>ISSN: 1019-1941</identifier><identifier>EISSN: 1309-9469</identifier><identifier>DOI: 10.5472/marumj.1480086</identifier><language>eng</language><publisher>Istanbul: Marmara University</publisher><subject>Mortality ; Pathophysiology</subject><ispartof>Marmara Medical Journal, 2024-01, Vol.37 (2), p.166-177</ispartof><rights>2024. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the associated terms available at https://dergipark.org.tr/en/pub/marumj/about-journal</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c192t-f818b8aa8b7a161d9c15fb6d8f52bfb428b6532cc13fb0cdebd3c1ef4c9170c3</cites><orcidid>0000-0003-4229-6391 ; 0000-0003-1762-0284 ; 0000-0001-8110-7691 ; 0000-0002-6213-7286 ; 0009-0004-3696-3412 ; 0009-0005-2046-865X ; 0000-0002-1519-3170 ; 0000-0001-7548-4095</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids></links><search><creatorcontrib>Çulpan, Yekta</creatorcontrib><creatorcontrib>Ozden, Lara</creatorcontrib><creatorcontrib>Gozderesi, Yakup</creatorcontrib><creatorcontrib>Kocak, Beril</creatorcontrib><creatorcontrib>Baltaci, Zeynep Hazal</creatorcontrib><creatorcontrib>Denizli, Ayberk</creatorcontrib><creatorcontrib>Yılmaz, Betul</creatorcontrib><creatorcontrib>Gülhan, Rezzan</creatorcontrib><title>Effect of methylglyoxal on Parkinson’s disease pathophysiology in the rotenone model</title><title>Marmara Medical Journal</title><description>Objective: Type 2 diabetes mellitus patients have been reported to have a higher incidence of Parkinson’s disease. This study aimed to
explore the effect of advanced glycation end products precursor methylglyoxal (MGO) on the pathophysiology of Parkinson’s disease
in a rotenone model.
Materials and Methods: Adult female Wistar rats (n=42) were divided into four groups. Rotenone toxicity was assessed by daily weight
measurements and mortality rates. Effect of MGO on blood glucose was evaluated. Locomotor activity, rearing, and rotarod tests
were performed to evaluate motor functions, and for neurodegeneration, tyrosine hydroxylase immunoreactivity in the striatum and
substantia nigra regions was assessed.
Results: The mortality rate was 9% in the rotenone-applied rats. The mean weight, locomotor activity, rearing activity, and longest time
spent on a rotarod were lower in the MGO+Rotenone group than in the Control group. Tyrosine hydroxylase immunoreactivity in the
striatum rostral to the anterior commissure in the MGO+Rotenone group was lower than that in the Control and MGO groups. The
number of tyrosine hydroxylase positive cells in the substantia nigra pars compacta was comparable among the groups.
Conclusion: When nigrostriatal degeneration was triggered, MGO was found to worsen motor dysfunction and increase damage to
dopaminergic neuron projections.</description><subject>Mortality</subject><subject>Pathophysiology</subject><issn>1019-1941</issn><issn>1309-9469</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNotkL1OwzAYRS0EEqWwMltiTvFnJ6k9oqr8SJVgqFgt27GblCQOtiuRjdfg9XgSgtrp3uHoXukgdAtkUeRLet-pcOj2C8g5Ibw8QzNgRGQiL8X51AmIDEQOl-gqxj0hBSeinKH3tXPWJOwd7myqx3bXjv5Ltdj3-E2Fj6aPvv_9_om4aqJV0eJBpdoP9Rgb3_rdiJsep9ri4JPtfW9x5yvbXqMLp9pob045R9vH9Xb1nG1en15WD5vMgKApcxy45kpxvVRQQiUMFE6XFXcF1U7nlOuyYNQYYE4TU1ldMQPW5UbAkhg2R3fH2SH4z4ONSe79IfTTo2RAOaUsJ2SiFkfKBB9jsE4OoZlsjRKI_Fcnj-rkSR37AyhsZik</recordid><startdate>20240101</startdate><enddate>20240101</enddate><creator>Çulpan, Yekta</creator><creator>Ozden, Lara</creator><creator>Gozderesi, Yakup</creator><creator>Kocak, Beril</creator><creator>Baltaci, Zeynep Hazal</creator><creator>Denizli, Ayberk</creator><creator>Yılmaz, Betul</creator><creator>Gülhan, Rezzan</creator><general>Marmara University</general><scope>AAYXX</scope><scope>CITATION</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>COVID</scope><scope>DWQXO</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><orcidid>https://orcid.org/0000-0003-4229-6391</orcidid><orcidid>https://orcid.org/0000-0003-1762-0284</orcidid><orcidid>https://orcid.org/0000-0001-8110-7691</orcidid><orcidid>https://orcid.org/0000-0002-6213-7286</orcidid><orcidid>https://orcid.org/0009-0004-3696-3412</orcidid><orcidid>https://orcid.org/0009-0005-2046-865X</orcidid><orcidid>https://orcid.org/0000-0002-1519-3170</orcidid><orcidid>https://orcid.org/0000-0001-7548-4095</orcidid></search><sort><creationdate>20240101</creationdate><title>Effect of methylglyoxal on Parkinson’s disease pathophysiology in the rotenone model</title><author>Çulpan, Yekta ; Ozden, Lara ; Gozderesi, Yakup ; Kocak, Beril ; Baltaci, Zeynep Hazal ; Denizli, Ayberk ; Yılmaz, Betul ; Gülhan, Rezzan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c192t-f818b8aa8b7a161d9c15fb6d8f52bfb428b6532cc13fb0cdebd3c1ef4c9170c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Mortality</topic><topic>Pathophysiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Çulpan, Yekta</creatorcontrib><creatorcontrib>Ozden, Lara</creatorcontrib><creatorcontrib>Gozderesi, Yakup</creatorcontrib><creatorcontrib>Kocak, Beril</creatorcontrib><creatorcontrib>Baltaci, Zeynep Hazal</creatorcontrib><creatorcontrib>Denizli, Ayberk</creatorcontrib><creatorcontrib>Yılmaz, Betul</creatorcontrib><creatorcontrib>Gülhan, Rezzan</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Coronavirus Research Database</collection><collection>ProQuest Central Korea</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>Marmara Medical Journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Çulpan, Yekta</au><au>Ozden, Lara</au><au>Gozderesi, Yakup</au><au>Kocak, Beril</au><au>Baltaci, Zeynep Hazal</au><au>Denizli, Ayberk</au><au>Yılmaz, Betul</au><au>Gülhan, Rezzan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of methylglyoxal on Parkinson’s disease pathophysiology in the rotenone model</atitle><jtitle>Marmara Medical Journal</jtitle><date>2024-01-01</date><risdate>2024</risdate><volume>37</volume><issue>2</issue><spage>166</spage><epage>177</epage><pages>166-177</pages><issn>1019-1941</issn><eissn>1309-9469</eissn><abstract>Objective: Type 2 diabetes mellitus patients have been reported to have a higher incidence of Parkinson’s disease. This study aimed to
explore the effect of advanced glycation end products precursor methylglyoxal (MGO) on the pathophysiology of Parkinson’s disease
in a rotenone model.
Materials and Methods: Adult female Wistar rats (n=42) were divided into four groups. Rotenone toxicity was assessed by daily weight
measurements and mortality rates. Effect of MGO on blood glucose was evaluated. Locomotor activity, rearing, and rotarod tests
were performed to evaluate motor functions, and for neurodegeneration, tyrosine hydroxylase immunoreactivity in the striatum and
substantia nigra regions was assessed.
Results: The mortality rate was 9% in the rotenone-applied rats. The mean weight, locomotor activity, rearing activity, and longest time
spent on a rotarod were lower in the MGO+Rotenone group than in the Control group. Tyrosine hydroxylase immunoreactivity in the
striatum rostral to the anterior commissure in the MGO+Rotenone group was lower than that in the Control and MGO groups. The
number of tyrosine hydroxylase positive cells in the substantia nigra pars compacta was comparable among the groups.
Conclusion: When nigrostriatal degeneration was triggered, MGO was found to worsen motor dysfunction and increase damage to
dopaminergic neuron projections.</abstract><cop>Istanbul</cop><pub>Marmara University</pub><doi>10.5472/marumj.1480086</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0003-4229-6391</orcidid><orcidid>https://orcid.org/0000-0003-1762-0284</orcidid><orcidid>https://orcid.org/0000-0001-8110-7691</orcidid><orcidid>https://orcid.org/0000-0002-6213-7286</orcidid><orcidid>https://orcid.org/0009-0004-3696-3412</orcidid><orcidid>https://orcid.org/0009-0005-2046-865X</orcidid><orcidid>https://orcid.org/0000-0002-1519-3170</orcidid><orcidid>https://orcid.org/0000-0001-7548-4095</orcidid><oa>free_for_read</oa></addata></record> |
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| title | Effect of methylglyoxal on Parkinson’s disease pathophysiology in the rotenone model |
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