Oxidation and Cognitive Impairment in the Aging Zebrafish
Background: The zebrafish has become an established model organism in aging research giving insight into general aging processes in vertebrates. Oxidative stress in aging may damage proteins and lipids in brain cells. Enhanced levels of oxidized macromolecules exert neurotoxic effects that could lea...
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| Veröffentlicht in: | Gerontology (Basel) 2015-12, Vol.62 (1), p.47-57 |
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| creator | Ruhl, Tim Jonas, Annika Seidel, Nathan Ian Prinz, Nicole Albayram, Onder Bilkei-Gorzo, Andras von der Emde, Gerhard |
| description | Background: The zebrafish has become an established model organism in aging research giving insight into general aging processes in vertebrates. Oxidative stress in aging may damage proteins and lipids in brain cells. Enhanced levels of oxidized macromolecules exert neurotoxic effects that could lead to disturbances in neuronal functioning and cognitive skills. Objective: This study aims to investigate a possible relation between oxidative stress and learning deficits during aging in zebrafish. Methods: We tested zebrafish of different ages in a color discrimination paradigm for associative learning and in a hole board task for spatial learning abilities. Afterwards, we determined the levels of oxidized lipids and proteins as well as the amount of lipofuscin in the learning-relevant brain regions of animals of the same age. Results: While young zebrafish at the age of 1 year successfully completed both learning tasks, cognitive abilities were significantly impaired in older animals. Learning deficits occurred at the age of 2 years, where we also detected significantly increased levels of lipofuscin and oxidized proteins in the zebrafish medial and lateral pallial areas of the dorsal telencephalon. Conclusion: These data suggest that enhanced oxidative stress may contribute to behavioral and cognitive impairments in the aging zebrafish. |
| doi_str_mv | 10.1159/000433534 |
| format | Article |
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Oxidative stress in aging may damage proteins and lipids in brain cells. Enhanced levels of oxidized macromolecules exert neurotoxic effects that could lead to disturbances in neuronal functioning and cognitive skills. Objective: This study aims to investigate a possible relation between oxidative stress and learning deficits during aging in zebrafish. Methods: We tested zebrafish of different ages in a color discrimination paradigm for associative learning and in a hole board task for spatial learning abilities. Afterwards, we determined the levels of oxidized lipids and proteins as well as the amount of lipofuscin in the learning-relevant brain regions of animals of the same age. Results: While young zebrafish at the age of 1 year successfully completed both learning tasks, cognitive abilities were significantly impaired in older animals. Learning deficits occurred at the age of 2 years, where we also detected significantly increased levels of lipofuscin and oxidized proteins in the zebrafish medial and lateral pallial areas of the dorsal telencephalon. Conclusion: These data suggest that enhanced oxidative stress may contribute to behavioral and cognitive impairments in the aging zebrafish.</description><identifier>ISSN: 0304-324X</identifier><identifier>EISSN: 1423-0003</identifier><identifier>DOI: 10.1159/000433534</identifier><identifier>PMID: 26183067</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Aging ; Aging - physiology ; Analysis ; Animals ; Association Learning - physiology ; Associative learning ; Cognition & reasoning ; Cognition Disorders - physiopathology ; Danio rerio ; Discrimination Learning - physiology ; Experimental Section / Original Paper ; Geriatric cognitive disorders ; Gerontology ; Learning - physiology ; Lipid Peroxidation ; Lipofuscin - metabolism ; Oxidation-reduction reactions ; Oxidative stress ; Oxidative Stress - physiology ; Physiological aspects ; Protein Carbonylation ; Risk factors ; Spatial Learning - physiology ; Telencephalon - metabolism ; Thiobarbituric Acid Reactive Substances - metabolism ; Zebrafish</subject><ispartof>Gerontology (Basel), 2015-12, Vol.62 (1), p.47-57</ispartof><rights>2015 S. Karger AG, Basel</rights><rights>2015 S. Karger AG, Basel.</rights><rights>COPYRIGHT 2015 S. Karger AG</rights><rights>Copyright S. Karger AG Dec 2015</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c492t-9d56212c14f4a209884999f6cfc423dae1e25c7570dbca30ffe08a33cb9455e43</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,2429,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26183067$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ruhl, Tim</creatorcontrib><creatorcontrib>Jonas, Annika</creatorcontrib><creatorcontrib>Seidel, Nathan Ian</creatorcontrib><creatorcontrib>Prinz, Nicole</creatorcontrib><creatorcontrib>Albayram, Onder</creatorcontrib><creatorcontrib>Bilkei-Gorzo, Andras</creatorcontrib><creatorcontrib>von der Emde, Gerhard</creatorcontrib><title>Oxidation and Cognitive Impairment in the Aging Zebrafish</title><title>Gerontology (Basel)</title><addtitle>Gerontology</addtitle><description>Background: The zebrafish has become an established model organism in aging research giving insight into general aging processes in vertebrates. Oxidative stress in aging may damage proteins and lipids in brain cells. Enhanced levels of oxidized macromolecules exert neurotoxic effects that could lead to disturbances in neuronal functioning and cognitive skills. Objective: This study aims to investigate a possible relation between oxidative stress and learning deficits during aging in zebrafish. Methods: We tested zebrafish of different ages in a color discrimination paradigm for associative learning and in a hole board task for spatial learning abilities. Afterwards, we determined the levels of oxidized lipids and proteins as well as the amount of lipofuscin in the learning-relevant brain regions of animals of the same age. Results: While young zebrafish at the age of 1 year successfully completed both learning tasks, cognitive abilities were significantly impaired in older animals. Learning deficits occurred at the age of 2 years, where we also detected significantly increased levels of lipofuscin and oxidized proteins in the zebrafish medial and lateral pallial areas of the dorsal telencephalon. Conclusion: These data suggest that enhanced oxidative stress may contribute to behavioral and cognitive impairments in the aging zebrafish.</description><subject>Aging</subject><subject>Aging - physiology</subject><subject>Analysis</subject><subject>Animals</subject><subject>Association Learning - physiology</subject><subject>Associative learning</subject><subject>Cognition & reasoning</subject><subject>Cognition Disorders - physiopathology</subject><subject>Danio rerio</subject><subject>Discrimination Learning - physiology</subject><subject>Experimental Section / Original Paper</subject><subject>Geriatric cognitive disorders</subject><subject>Gerontology</subject><subject>Learning - physiology</subject><subject>Lipid Peroxidation</subject><subject>Lipofuscin - metabolism</subject><subject>Oxidation-reduction reactions</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - physiology</subject><subject>Physiological aspects</subject><subject>Protein Carbonylation</subject><subject>Risk factors</subject><subject>Spatial Learning - physiology</subject><subject>Telencephalon - metabolism</subject><subject>Thiobarbituric Acid Reactive Substances - metabolism</subject><subject>Zebrafish</subject><issn>0304-324X</issn><issn>1423-0003</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqN0c9rFDEUB_Agil2rB-8iAwXRw2iSl0wmx2WptVAoFAXxErKZl9nU-bEmM6L_fbNM3YP00FPg5ZOXvHwJec3oR8ak_kQpFQASxBOyYoJDmQvwlKwoUFECF99PyIuUbnORckafkxNesRpopVZEX_8JjZ3COBR2aIrN2A5hCr-xuOz3NsQeh6kIQzHtsFi3YWiLH7iN1oe0e0meedslfHW_npJvn8-_br6UV9cXl5v1VemE5lOpG1lxxh0TXlhOdV0LrbWvnHf5pY1Fhlw6JRVtts4C9R5pbQHcVgspUcApeb_03cfx14xpMn1IDrvODjjOyTBV00NLqB5BhT5MzmimZ__R23GOQx4kKymVUsBUVu8W1doOzQ5tN-3S2M2H_0pmXYHiVDJgGX5YoItjShG92cfQ2_jXMGoOGZljRtm-vb963vbYHOW_UDJ4s4CfNrYYj-B4_uzB7Yvzm0WYfePhDkuSnJQ</recordid><startdate>20151201</startdate><enddate>20151201</enddate><creator>Ruhl, Tim</creator><creator>Jonas, Annika</creator><creator>Seidel, Nathan Ian</creator><creator>Prinz, Nicole</creator><creator>Albayram, Onder</creator><creator>Bilkei-Gorzo, Andras</creator><creator>von der Emde, Gerhard</creator><general>S. Karger AG</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>0-V</scope><scope>3V.</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>88I</scope><scope>88J</scope><scope>8AF</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ALSLI</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M2P</scope><scope>M2R</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>S0X</scope><scope>7X8</scope></search><sort><creationdate>20151201</creationdate><title>Oxidation and Cognitive Impairment in the Aging Zebrafish</title><author>Ruhl, Tim ; Jonas, Annika ; Seidel, Nathan Ian ; Prinz, Nicole ; Albayram, Onder ; Bilkei-Gorzo, Andras ; von der Emde, Gerhard</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c492t-9d56212c14f4a209884999f6cfc423dae1e25c7570dbca30ffe08a33cb9455e43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Aging</topic><topic>Aging - physiology</topic><topic>Analysis</topic><topic>Animals</topic><topic>Association Learning - physiology</topic><topic>Associative learning</topic><topic>Cognition & reasoning</topic><topic>Cognition Disorders - physiopathology</topic><topic>Danio rerio</topic><topic>Discrimination Learning - physiology</topic><topic>Experimental Section / Original Paper</topic><topic>Geriatric cognitive disorders</topic><topic>Gerontology</topic><topic>Learning - physiology</topic><topic>Lipid Peroxidation</topic><topic>Lipofuscin - metabolism</topic><topic>Oxidation-reduction reactions</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - physiology</topic><topic>Physiological aspects</topic><topic>Protein Carbonylation</topic><topic>Risk factors</topic><topic>Spatial Learning - physiology</topic><topic>Telencephalon - metabolism</topic><topic>Thiobarbituric Acid Reactive Substances - metabolism</topic><topic>Zebrafish</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ruhl, Tim</creatorcontrib><creatorcontrib>Jonas, Annika</creatorcontrib><creatorcontrib>Seidel, Nathan Ian</creatorcontrib><creatorcontrib>Prinz, Nicole</creatorcontrib><creatorcontrib>Albayram, Onder</creatorcontrib><creatorcontrib>Bilkei-Gorzo, Andras</creatorcontrib><creatorcontrib>von der Emde, Gerhard</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Social Sciences Premium Collection</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>Science Database (Alumni Edition)</collection><collection>Social Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Social Science Premium Collection</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>Science Database</collection><collection>Social Science Database</collection><collection>Nursing & Allied Health Premium</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><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>SIRS Editorial</collection><collection>MEDLINE - Academic</collection><jtitle>Gerontology (Basel)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ruhl, Tim</au><au>Jonas, Annika</au><au>Seidel, Nathan Ian</au><au>Prinz, Nicole</au><au>Albayram, Onder</au><au>Bilkei-Gorzo, Andras</au><au>von der Emde, Gerhard</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oxidation and Cognitive Impairment in the Aging Zebrafish</atitle><jtitle>Gerontology (Basel)</jtitle><addtitle>Gerontology</addtitle><date>2015-12-01</date><risdate>2015</risdate><volume>62</volume><issue>1</issue><spage>47</spage><epage>57</epage><pages>47-57</pages><issn>0304-324X</issn><eissn>1423-0003</eissn><abstract>Background: The zebrafish has become an established model organism in aging research giving insight into general aging processes in vertebrates. Oxidative stress in aging may damage proteins and lipids in brain cells. Enhanced levels of oxidized macromolecules exert neurotoxic effects that could lead to disturbances in neuronal functioning and cognitive skills. Objective: This study aims to investigate a possible relation between oxidative stress and learning deficits during aging in zebrafish. Methods: We tested zebrafish of different ages in a color discrimination paradigm for associative learning and in a hole board task for spatial learning abilities. Afterwards, we determined the levels of oxidized lipids and proteins as well as the amount of lipofuscin in the learning-relevant brain regions of animals of the same age. Results: While young zebrafish at the age of 1 year successfully completed both learning tasks, cognitive abilities were significantly impaired in older animals. Learning deficits occurred at the age of 2 years, where we also detected significantly increased levels of lipofuscin and oxidized proteins in the zebrafish medial and lateral pallial areas of the dorsal telencephalon. Conclusion: These data suggest that enhanced oxidative stress may contribute to behavioral and cognitive impairments in the aging zebrafish.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>26183067</pmid><doi>10.1159/000433534</doi><tpages>11</tpages></addata></record> |
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| subjects | Aging Aging - physiology Analysis Animals Association Learning - physiology Associative learning Cognition & reasoning Cognition Disorders - physiopathology Danio rerio Discrimination Learning - physiology Experimental Section / Original Paper Geriatric cognitive disorders Gerontology Learning - physiology Lipid Peroxidation Lipofuscin - metabolism Oxidation-reduction reactions Oxidative stress Oxidative Stress - physiology Physiological aspects Protein Carbonylation Risk factors Spatial Learning - physiology Telencephalon - metabolism Thiobarbituric Acid Reactive Substances - metabolism Zebrafish |
| title | Oxidation and Cognitive Impairment in the Aging Zebrafish |
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