A progressive dopaminergic phenotype associated with neurotoxic conversion of α-synuclein in BAC-transgenic rats
Conversion of soluble α-synuclein into insoluble and fibrillar inclusions is a hallmark of Parkinson's disease and other synucleinopathies. Accumulating evidence points towards a relationship between its generation at nerve terminals and structural synaptic pathology. Little is known about the...
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| creator | NUBER, Silke HARMUTH, Florian CALAMINUS, Carsten PICHLER, Bernd J JENSEN, Poul H MÜLLER, Christian P AMATO, Davide KORNHUBER, Johannes TEISMANN, Peter YAMAKADO, Hodaka TAKAHASHI, Ryosuke WINKLER, Juergen KOHL, Zacharias MASLIAH, Eliezer RIESS, Olaf ADAME, Anthony TREJO, Margaritha SCHÖNIG, Kai ZIMMERMANN, Frank BAUER, Claudia CASADEI, Nicolas GIEL, Christiane |
| description | Conversion of soluble α-synuclein into insoluble and fibrillar inclusions is a hallmark of Parkinson's disease and other synucleinopathies. Accumulating evidence points towards a relationship between its generation at nerve terminals and structural synaptic pathology. Little is known about the pathogenic impact of α-synuclein conversion and deposition at nigrostriatal dopaminergic synapses in transgenic mice, mainly owing to expression limitations of the α-synuclein construct. Here, we explore whether both the rat as a model and expression of the bacterial artificial chromosome construct consisting of human full-length wild-type α-synuclein could exert dopaminergic neuropathological effects. We found that the human promoter induced a pan-neuronal expression, matching the rodent α-synuclein expression pattern, however, with prominent C-terminally truncated fragments. Ageing promoted conversion of both full-length and C-terminally truncated α-synuclein species into insolube and proteinase K-resistant fibres, with strongest accumulation in the striatum, resembling biochemical changes seen in human Parkinson's disease. Transgenic rats develop early changes in novelty-seeking, avoidance and smell before the progressive motor deficit. Importantly, the observed pathological changes were associated with severe loss of the dopaminergic integrity, thus resembling more closely the human pathology. |
| doi_str_mv | 10.1093/brain/aws358 |
| format | Article |
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Accumulating evidence points towards a relationship between its generation at nerve terminals and structural synaptic pathology. Little is known about the pathogenic impact of α-synuclein conversion and deposition at nigrostriatal dopaminergic synapses in transgenic mice, mainly owing to expression limitations of the α-synuclein construct. Here, we explore whether both the rat as a model and expression of the bacterial artificial chromosome construct consisting of human full-length wild-type α-synuclein could exert dopaminergic neuropathological effects. We found that the human promoter induced a pan-neuronal expression, matching the rodent α-synuclein expression pattern, however, with prominent C-terminally truncated fragments. Ageing promoted conversion of both full-length and C-terminally truncated α-synuclein species into insolube and proteinase K-resistant fibres, with strongest accumulation in the striatum, resembling biochemical changes seen in human Parkinson's disease. Transgenic rats develop early changes in novelty-seeking, avoidance and smell before the progressive motor deficit. Importantly, the observed pathological changes were associated with severe loss of the dopaminergic integrity, thus resembling more closely the human pathology.</description><identifier>ISSN: 0006-8950</identifier><identifier>EISSN: 1460-2156</identifier><identifier>DOI: 10.1093/brain/aws358</identifier><identifier>PMID: 23413261</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Aging ; alpha-Synuclein - biosynthesis ; alpha-Synuclein - genetics ; alpha-Synuclein - toxicity ; Animals ; Biological and medical sciences ; Chromosomes, Artificial, Bacterial - genetics ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Disease Models, Animal ; Disease Progression ; Dopaminergic Neurons - metabolism ; Dopaminergic Neurons - pathology ; Humans ; Medical sciences ; Neurology ; Original ; Parkinson Disease - genetics ; Parkinson Disease - metabolism ; Parkinson Disease - pathology ; Phenotype ; Rats ; Rats, Sprague-Dawley ; Rats, Transgenic</subject><ispartof>Brain (London, England : 1878), 2013-02, Vol.136 (Pt 2), p.412-432</ispartof><rights>2014 INIST-CNRS</rights><rights>The Author (2012). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oup.com 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c447t-3ed619a2202321aaa9f606ff5098b40c8b345c67137d3cff6eea7bad81b86e723</citedby><cites>FETCH-LOGICAL-c447t-3ed619a2202321aaa9f606ff5098b40c8b345c67137d3cff6eea7bad81b86e723</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=27104827$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23413261$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>NUBER, Silke</creatorcontrib><creatorcontrib>HARMUTH, Florian</creatorcontrib><creatorcontrib>CALAMINUS, Carsten</creatorcontrib><creatorcontrib>PICHLER, Bernd J</creatorcontrib><creatorcontrib>JENSEN, Poul H</creatorcontrib><creatorcontrib>MÜLLER, Christian P</creatorcontrib><creatorcontrib>AMATO, Davide</creatorcontrib><creatorcontrib>KORNHUBER, Johannes</creatorcontrib><creatorcontrib>TEISMANN, Peter</creatorcontrib><creatorcontrib>YAMAKADO, Hodaka</creatorcontrib><creatorcontrib>TAKAHASHI, Ryosuke</creatorcontrib><creatorcontrib>WINKLER, Juergen</creatorcontrib><creatorcontrib>KOHL, Zacharias</creatorcontrib><creatorcontrib>MASLIAH, Eliezer</creatorcontrib><creatorcontrib>RIESS, Olaf</creatorcontrib><creatorcontrib>ADAME, Anthony</creatorcontrib><creatorcontrib>TREJO, Margaritha</creatorcontrib><creatorcontrib>SCHÖNIG, Kai</creatorcontrib><creatorcontrib>ZIMMERMANN, Frank</creatorcontrib><creatorcontrib>BAUER, Claudia</creatorcontrib><creatorcontrib>CASADEI, Nicolas</creatorcontrib><creatorcontrib>GIEL, Christiane</creatorcontrib><title>A progressive dopaminergic phenotype associated with neurotoxic conversion of α-synuclein in BAC-transgenic rats</title><title>Brain (London, England : 1878)</title><addtitle>Brain</addtitle><description>Conversion of soluble α-synuclein into insoluble and fibrillar inclusions is a hallmark of Parkinson's disease and other synucleinopathies. Accumulating evidence points towards a relationship between its generation at nerve terminals and structural synaptic pathology. Little is known about the pathogenic impact of α-synuclein conversion and deposition at nigrostriatal dopaminergic synapses in transgenic mice, mainly owing to expression limitations of the α-synuclein construct. Here, we explore whether both the rat as a model and expression of the bacterial artificial chromosome construct consisting of human full-length wild-type α-synuclein could exert dopaminergic neuropathological effects. We found that the human promoter induced a pan-neuronal expression, matching the rodent α-synuclein expression pattern, however, with prominent C-terminally truncated fragments. Ageing promoted conversion of both full-length and C-terminally truncated α-synuclein species into insolube and proteinase K-resistant fibres, with strongest accumulation in the striatum, resembling biochemical changes seen in human Parkinson's disease. Transgenic rats develop early changes in novelty-seeking, avoidance and smell before the progressive motor deficit. Importantly, the observed pathological changes were associated with severe loss of the dopaminergic integrity, thus resembling more closely the human pathology.</description><subject>Aging</subject><subject>alpha-Synuclein - biosynthesis</subject><subject>alpha-Synuclein - genetics</subject><subject>alpha-Synuclein - toxicity</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Chromosomes, Artificial, Bacterial - genetics</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Disease Models, Animal</subject><subject>Disease Progression</subject><subject>Dopaminergic Neurons - metabolism</subject><subject>Dopaminergic Neurons - pathology</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Neurology</subject><subject>Original</subject><subject>Parkinson Disease - genetics</subject><subject>Parkinson Disease - metabolism</subject><subject>Parkinson Disease - pathology</subject><subject>Phenotype</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rats, Transgenic</subject><issn>0006-8950</issn><issn>1460-2156</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkU1r3DAQhkVpaTZpbz0XXwo9xI0-bNm-FLZLPwKBXNqzGMvjXRWv5GjsTfZn9Y_0N1XpbpMGBmZgHt55mZexN4J_ELxRF20E5y_gllRZP2MLUWieS1Hq52zBOdd53ZT8hJ0S_eRcFErql-xEqkKkSSzYzTIbY1hHJHI7zLowwtZ5jGtns3GDPkz7ETMgCtbBhF1266ZN5nGOYQp3CbLB7zCSCz4Lffb7V057P9sBnc9SfVqu8imCpzX6BEeY6BV70cNA-PrYz9iPL5-_r77lV9dfL1fLq9wWRTXlCjstGpCSSyUFADS95rrvS97UbcFt3aqitLoSquqU7XuNCFULXS3aWmMl1Rn7eNAd53aLnUWfjAxmjG4LcW8COPN0493GrMPOqLKSjdJJ4P1RIIabGWkyW0cWhwE8hpmMUOnLktf1PXp-QG0MRBH7hzOCm_uUzN-UzCGlhL_939oD_C-WBLw7AkAWhj590Dp65CrBi1pW6g92-qDp</recordid><startdate>20130201</startdate><enddate>20130201</enddate><creator>NUBER, Silke</creator><creator>HARMUTH, Florian</creator><creator>CALAMINUS, Carsten</creator><creator>PICHLER, Bernd J</creator><creator>JENSEN, Poul H</creator><creator>MÜLLER, Christian P</creator><creator>AMATO, Davide</creator><creator>KORNHUBER, Johannes</creator><creator>TEISMANN, Peter</creator><creator>YAMAKADO, Hodaka</creator><creator>TAKAHASHI, Ryosuke</creator><creator>WINKLER, Juergen</creator><creator>KOHL, Zacharias</creator><creator>MASLIAH, Eliezer</creator><creator>RIESS, Olaf</creator><creator>ADAME, Anthony</creator><creator>TREJO, Margaritha</creator><creator>SCHÖNIG, Kai</creator><creator>ZIMMERMANN, Frank</creator><creator>BAUER, Claudia</creator><creator>CASADEI, Nicolas</creator><creator>GIEL, Christiane</creator><general>Oxford University Press</general><scope>IQODW</scope><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>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>20130201</creationdate><title>A progressive dopaminergic phenotype associated with neurotoxic conversion of α-synuclein in BAC-transgenic rats</title><author>NUBER, Silke ; HARMUTH, Florian ; CALAMINUS, Carsten ; PICHLER, Bernd J ; JENSEN, Poul H ; MÜLLER, Christian P ; AMATO, Davide ; KORNHUBER, Johannes ; TEISMANN, Peter ; YAMAKADO, Hodaka ; TAKAHASHI, Ryosuke ; WINKLER, Juergen ; KOHL, Zacharias ; MASLIAH, Eliezer ; RIESS, Olaf ; ADAME, Anthony ; TREJO, Margaritha ; SCHÖNIG, Kai ; ZIMMERMANN, Frank ; BAUER, Claudia ; CASADEI, Nicolas ; GIEL, Christiane</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c447t-3ed619a2202321aaa9f606ff5098b40c8b345c67137d3cff6eea7bad81b86e723</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Aging</topic><topic>alpha-Synuclein - biosynthesis</topic><topic>alpha-Synuclein - genetics</topic><topic>alpha-Synuclein - toxicity</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Chromosomes, Artificial, Bacterial - genetics</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Disease Models, Animal</topic><topic>Disease Progression</topic><topic>Dopaminergic Neurons - metabolism</topic><topic>Dopaminergic Neurons - pathology</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Neurology</topic><topic>Original</topic><topic>Parkinson Disease - genetics</topic><topic>Parkinson Disease - metabolism</topic><topic>Parkinson Disease - pathology</topic><topic>Phenotype</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Rats, Transgenic</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>NUBER, Silke</creatorcontrib><creatorcontrib>HARMUTH, Florian</creatorcontrib><creatorcontrib>CALAMINUS, Carsten</creatorcontrib><creatorcontrib>PICHLER, Bernd J</creatorcontrib><creatorcontrib>JENSEN, Poul H</creatorcontrib><creatorcontrib>MÜLLER, Christian P</creatorcontrib><creatorcontrib>AMATO, Davide</creatorcontrib><creatorcontrib>KORNHUBER, Johannes</creatorcontrib><creatorcontrib>TEISMANN, Peter</creatorcontrib><creatorcontrib>YAMAKADO, Hodaka</creatorcontrib><creatorcontrib>TAKAHASHI, Ryosuke</creatorcontrib><creatorcontrib>WINKLER, Juergen</creatorcontrib><creatorcontrib>KOHL, Zacharias</creatorcontrib><creatorcontrib>MASLIAH, Eliezer</creatorcontrib><creatorcontrib>RIESS, Olaf</creatorcontrib><creatorcontrib>ADAME, Anthony</creatorcontrib><creatorcontrib>TREJO, Margaritha</creatorcontrib><creatorcontrib>SCHÖNIG, Kai</creatorcontrib><creatorcontrib>ZIMMERMANN, Frank</creatorcontrib><creatorcontrib>BAUER, Claudia</creatorcontrib><creatorcontrib>CASADEI, Nicolas</creatorcontrib><creatorcontrib>GIEL, Christiane</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Brain (London, England : 1878)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>NUBER, Silke</au><au>HARMUTH, Florian</au><au>CALAMINUS, Carsten</au><au>PICHLER, Bernd J</au><au>JENSEN, Poul H</au><au>MÜLLER, Christian P</au><au>AMATO, Davide</au><au>KORNHUBER, Johannes</au><au>TEISMANN, Peter</au><au>YAMAKADO, Hodaka</au><au>TAKAHASHI, Ryosuke</au><au>WINKLER, Juergen</au><au>KOHL, Zacharias</au><au>MASLIAH, Eliezer</au><au>RIESS, Olaf</au><au>ADAME, Anthony</au><au>TREJO, Margaritha</au><au>SCHÖNIG, Kai</au><au>ZIMMERMANN, Frank</au><au>BAUER, Claudia</au><au>CASADEI, Nicolas</au><au>GIEL, Christiane</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A progressive dopaminergic phenotype associated with neurotoxic conversion of α-synuclein in BAC-transgenic rats</atitle><jtitle>Brain (London, England : 1878)</jtitle><addtitle>Brain</addtitle><date>2013-02-01</date><risdate>2013</risdate><volume>136</volume><issue>Pt 2</issue><spage>412</spage><epage>432</epage><pages>412-432</pages><issn>0006-8950</issn><eissn>1460-2156</eissn><abstract>Conversion of soluble α-synuclein into insoluble and fibrillar inclusions is a hallmark of Parkinson's disease and other synucleinopathies. Accumulating evidence points towards a relationship between its generation at nerve terminals and structural synaptic pathology. Little is known about the pathogenic impact of α-synuclein conversion and deposition at nigrostriatal dopaminergic synapses in transgenic mice, mainly owing to expression limitations of the α-synuclein construct. Here, we explore whether both the rat as a model and expression of the bacterial artificial chromosome construct consisting of human full-length wild-type α-synuclein could exert dopaminergic neuropathological effects. We found that the human promoter induced a pan-neuronal expression, matching the rodent α-synuclein expression pattern, however, with prominent C-terminally truncated fragments. Ageing promoted conversion of both full-length and C-terminally truncated α-synuclein species into insolube and proteinase K-resistant fibres, with strongest accumulation in the striatum, resembling biochemical changes seen in human Parkinson's disease. Transgenic rats develop early changes in novelty-seeking, avoidance and smell before the progressive motor deficit. Importantly, the observed pathological changes were associated with severe loss of the dopaminergic integrity, thus resembling more closely the human pathology.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>23413261</pmid><doi>10.1093/brain/aws358</doi><tpages>21</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aging alpha-Synuclein - biosynthesis alpha-Synuclein - genetics alpha-Synuclein - toxicity Animals Biological and medical sciences Chromosomes, Artificial, Bacterial - genetics Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Disease Models, Animal Disease Progression Dopaminergic Neurons - metabolism Dopaminergic Neurons - pathology Humans Medical sciences Neurology Original Parkinson Disease - genetics Parkinson Disease - metabolism Parkinson Disease - pathology Phenotype Rats Rats, Sprague-Dawley Rats, Transgenic |
| title | A progressive dopaminergic phenotype associated with neurotoxic conversion of α-synuclein in BAC-transgenic rats |
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