Apomorphine treatment in Alzheimer mice promoting amyloid-β degradation
Objective: Intracellular amyloid β‐protein (Aβ) contributes to neurodegeneration in Alzheimer disease (AD). Apomorphine (APO) is a dopamine receptor agonist for Parkinson disease and also protects against oxidative stress. Efficacy of APO for an AD mouse model and effects of APO on cell cultures are...
Gespeichert in:
| Veröffentlicht in: | Annals of neurology 2011-02, Vol.69 (2), p.248-256 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 256 |
|---|---|
| container_issue | 2 |
| container_start_page | 248 |
| container_title | Annals of neurology |
| container_volume | 69 |
| creator | Himeno, Eri Ohyagi, Yasumasa Ma, Linqing Nakamura, Norimichi Miyoshi, Katsue Sakae, Nobutaka Motomura, Kyoko Soejima, Naoko Yamasaki, Ryo Hashimoto, Tetsuya Tabira, Takeshi M. LaFerla, Frank Kira, Jun-ichi |
| description | Objective:
Intracellular amyloid β‐protein (Aβ) contributes to neurodegeneration in Alzheimer disease (AD). Apomorphine (APO) is a dopamine receptor agonist for Parkinson disease and also protects against oxidative stress. Efficacy of APO for an AD mouse model and effects of APO on cell cultures are studied.
Methods:
The triple transgenic AD mouse model (3xTg‐AD) has 2 familial AD‐related gene mutations (APPKM670/671NL/PS1M146V) and a tau gene mutation (TauP301L). Six‐month‐old 3xTg‐AD mice were treated with subcutaneous injections of APO once a week for 1 month. Memory function was evaluated by Morris water maze before and after the treatment. Brain tissues were examined by immunohistochemical staining and Western blotting. Effects of APO on intracellular Aβ degradation, activity of Aβ‐degrading enzymes, and protection against oxidative stress were studied in cultured SH‐SY5Y cells.
Results:
After APO treatment, short‐term memory function was dramatically improved. Significant decreases in the levels of intraneuronal Aβ, hyper‐phosphorylated tau (p‐tau), p53, and heme oxygenase‐1 proteins were observed. Moreover, APO promoted degradation of intracellular Aβ, increased activity of proteasome and insulin‐degrading enzyme, protected against H2O2 toxicity, and decreased p53 protein levels in the cultured cells.
Interpretation:
3xTg‐AD mice show intraneuronal Aβ accumulation and memory disturbances before extracellular Aβ deposition. Our data demonstrating improvement of memory function of 3xTg‐AD mice with decreases in intraneuronal Aβ and p‐tau levels by APO treatment strongly suggest that intraneuronal Aβ is an important therapeutic target and APO will be a novel drug for AD. Ann Neurol 2011 |
| doi_str_mv | 10.1002/ana.22319 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_856404389</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>856404389</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3929-488faebaf0170b902275e904897773d1f1c2373e99fade4cdadcb8a109c997df3</originalsourceid><addsrcrecordid>eNp1kMtOwzAQRS0EgvJY8AMoG4RYBPxI4ngZIaBI5SEEYmlN7QkY8ih2KiifxYfwTQRaYMVqNmfunTmEbDN6wCjlh9DAAeeCqSUyYKlgcc4TtUwGVGRJnDKRrJH1EB4ppSpjdJWscSZyKSQdkGExaevWTx5cg1HnEboamy5yTVRUbw_oavRR7QxGE99znWvuI6hnVets_PEeWbz3YKFzbbNJVkqoAm4t5ga5PTm-ORrGo8vTs6NiFBuhuIqTPC8Bx1BSJulYUc5lioomuZJSCstKZriQApUqwWJiLFgzzoFRZZSSthQbZG-e2x_0PMXQ6doFg1UFDbbToPM0S2gictWT-3PS-DYEj6WeeFeDn2lG9Zc33XvT3956dmeROh3XaH_JH1E9sLsAIBioSg-NceGP658TLPsKOpxzL67C2f-Nurgofqrj-YYLHb7-boB_0llfneq7i1M9VNcZP78a6SvxCWrIk_E</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>856404389</pqid></control><display><type>article</type><title>Apomorphine treatment in Alzheimer mice promoting amyloid-β degradation</title><source>MEDLINE</source><source>Wiley Online Library All Journals</source><creator>Himeno, Eri ; Ohyagi, Yasumasa ; Ma, Linqing ; Nakamura, Norimichi ; Miyoshi, Katsue ; Sakae, Nobutaka ; Motomura, Kyoko ; Soejima, Naoko ; Yamasaki, Ryo ; Hashimoto, Tetsuya ; Tabira, Takeshi ; M. LaFerla, Frank ; Kira, Jun-ichi</creator><creatorcontrib>Himeno, Eri ; Ohyagi, Yasumasa ; Ma, Linqing ; Nakamura, Norimichi ; Miyoshi, Katsue ; Sakae, Nobutaka ; Motomura, Kyoko ; Soejima, Naoko ; Yamasaki, Ryo ; Hashimoto, Tetsuya ; Tabira, Takeshi ; M. LaFerla, Frank ; Kira, Jun-ichi</creatorcontrib><description>Objective:
Intracellular amyloid β‐protein (Aβ) contributes to neurodegeneration in Alzheimer disease (AD). Apomorphine (APO) is a dopamine receptor agonist for Parkinson disease and also protects against oxidative stress. Efficacy of APO for an AD mouse model and effects of APO on cell cultures are studied.
Methods:
The triple transgenic AD mouse model (3xTg‐AD) has 2 familial AD‐related gene mutations (APPKM670/671NL/PS1M146V) and a tau gene mutation (TauP301L). Six‐month‐old 3xTg‐AD mice were treated with subcutaneous injections of APO once a week for 1 month. Memory function was evaluated by Morris water maze before and after the treatment. Brain tissues were examined by immunohistochemical staining and Western blotting. Effects of APO on intracellular Aβ degradation, activity of Aβ‐degrading enzymes, and protection against oxidative stress were studied in cultured SH‐SY5Y cells.
Results:
After APO treatment, short‐term memory function was dramatically improved. Significant decreases in the levels of intraneuronal Aβ, hyper‐phosphorylated tau (p‐tau), p53, and heme oxygenase‐1 proteins were observed. Moreover, APO promoted degradation of intracellular Aβ, increased activity of proteasome and insulin‐degrading enzyme, protected against H2O2 toxicity, and decreased p53 protein levels in the cultured cells.
Interpretation:
3xTg‐AD mice show intraneuronal Aβ accumulation and memory disturbances before extracellular Aβ deposition. Our data demonstrating improvement of memory function of 3xTg‐AD mice with decreases in intraneuronal Aβ and p‐tau levels by APO treatment strongly suggest that intraneuronal Aβ is an important therapeutic target and APO will be a novel drug for AD. Ann Neurol 2011</description><identifier>ISSN: 0364-5134</identifier><identifier>EISSN: 1531-8249</identifier><identifier>DOI: 10.1002/ana.22319</identifier><identifier>PMID: 21387370</identifier><identifier>CODEN: ANNED3</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Alzheimer Disease - drug therapy ; Alzheimer Disease - metabolism ; Amyloid beta-Peptides - metabolism ; Animals ; Apomorphine - pharmacology ; Apomorphine - therapeutic use ; Biological and medical sciences ; Blotting, Western ; Brain - drug effects ; Brain - metabolism ; Cells, Cultured ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Disease Models, Animal ; Dopamine Agonists - pharmacology ; Dopamine Agonists - therapeutic use ; Immunohistochemistry ; Insulysin - metabolism ; Maze Learning - drug effects ; Medical sciences ; Memory, Short-Term - drug effects ; Mice ; Mice, Transgenic ; Neprilysin - metabolism ; Neurology ; Neurons - drug effects ; Neurons - metabolism ; Oxidative Stress - drug effects ; Oxidative Stress - physiology ; Phosphorylation - drug effects ; Proteasome Endopeptidase Complex - metabolism ; Statistics, Nonparametric ; tau Proteins - metabolism</subject><ispartof>Annals of neurology, 2011-02, Vol.69 (2), p.248-256</ispartof><rights>Copyright © 2011 American Neurological Association</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2011 American Neurological Association.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3929-488faebaf0170b902275e904897773d1f1c2373e99fade4cdadcb8a109c997df3</citedby><cites>FETCH-LOGICAL-c3929-488faebaf0170b902275e904897773d1f1c2373e99fade4cdadcb8a109c997df3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fana.22319$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fana.22319$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23923169$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21387370$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Himeno, Eri</creatorcontrib><creatorcontrib>Ohyagi, Yasumasa</creatorcontrib><creatorcontrib>Ma, Linqing</creatorcontrib><creatorcontrib>Nakamura, Norimichi</creatorcontrib><creatorcontrib>Miyoshi, Katsue</creatorcontrib><creatorcontrib>Sakae, Nobutaka</creatorcontrib><creatorcontrib>Motomura, Kyoko</creatorcontrib><creatorcontrib>Soejima, Naoko</creatorcontrib><creatorcontrib>Yamasaki, Ryo</creatorcontrib><creatorcontrib>Hashimoto, Tetsuya</creatorcontrib><creatorcontrib>Tabira, Takeshi</creatorcontrib><creatorcontrib>M. LaFerla, Frank</creatorcontrib><creatorcontrib>Kira, Jun-ichi</creatorcontrib><title>Apomorphine treatment in Alzheimer mice promoting amyloid-β degradation</title><title>Annals of neurology</title><addtitle>Ann Neurol</addtitle><description>Objective:
Intracellular amyloid β‐protein (Aβ) contributes to neurodegeneration in Alzheimer disease (AD). Apomorphine (APO) is a dopamine receptor agonist for Parkinson disease and also protects against oxidative stress. Efficacy of APO for an AD mouse model and effects of APO on cell cultures are studied.
Methods:
The triple transgenic AD mouse model (3xTg‐AD) has 2 familial AD‐related gene mutations (APPKM670/671NL/PS1M146V) and a tau gene mutation (TauP301L). Six‐month‐old 3xTg‐AD mice were treated with subcutaneous injections of APO once a week for 1 month. Memory function was evaluated by Morris water maze before and after the treatment. Brain tissues were examined by immunohistochemical staining and Western blotting. Effects of APO on intracellular Aβ degradation, activity of Aβ‐degrading enzymes, and protection against oxidative stress were studied in cultured SH‐SY5Y cells.
Results:
After APO treatment, short‐term memory function was dramatically improved. Significant decreases in the levels of intraneuronal Aβ, hyper‐phosphorylated tau (p‐tau), p53, and heme oxygenase‐1 proteins were observed. Moreover, APO promoted degradation of intracellular Aβ, increased activity of proteasome and insulin‐degrading enzyme, protected against H2O2 toxicity, and decreased p53 protein levels in the cultured cells.
Interpretation:
3xTg‐AD mice show intraneuronal Aβ accumulation and memory disturbances before extracellular Aβ deposition. Our data demonstrating improvement of memory function of 3xTg‐AD mice with decreases in intraneuronal Aβ and p‐tau levels by APO treatment strongly suggest that intraneuronal Aβ is an important therapeutic target and APO will be a novel drug for AD. Ann Neurol 2011</description><subject>Alzheimer Disease - drug therapy</subject><subject>Alzheimer Disease - metabolism</subject><subject>Amyloid beta-Peptides - metabolism</subject><subject>Animals</subject><subject>Apomorphine - pharmacology</subject><subject>Apomorphine - therapeutic use</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Brain - drug effects</subject><subject>Brain - metabolism</subject><subject>Cells, Cultured</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Disease Models, Animal</subject><subject>Dopamine Agonists - pharmacology</subject><subject>Dopamine Agonists - therapeutic use</subject><subject>Immunohistochemistry</subject><subject>Insulysin - metabolism</subject><subject>Maze Learning - drug effects</subject><subject>Medical sciences</subject><subject>Memory, Short-Term - drug effects</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Neprilysin - metabolism</subject><subject>Neurology</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Oxidative Stress - drug effects</subject><subject>Oxidative Stress - physiology</subject><subject>Phosphorylation - drug effects</subject><subject>Proteasome Endopeptidase Complex - metabolism</subject><subject>Statistics, Nonparametric</subject><subject>tau Proteins - metabolism</subject><issn>0364-5134</issn><issn>1531-8249</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kMtOwzAQRS0EgvJY8AMoG4RYBPxI4ngZIaBI5SEEYmlN7QkY8ih2KiifxYfwTQRaYMVqNmfunTmEbDN6wCjlh9DAAeeCqSUyYKlgcc4TtUwGVGRJnDKRrJH1EB4ppSpjdJWscSZyKSQdkGExaevWTx5cg1HnEboamy5yTVRUbw_oavRR7QxGE99znWvuI6hnVets_PEeWbz3YKFzbbNJVkqoAm4t5ga5PTm-ORrGo8vTs6NiFBuhuIqTPC8Bx1BSJulYUc5lioomuZJSCstKZriQApUqwWJiLFgzzoFRZZSSthQbZG-e2x_0PMXQ6doFg1UFDbbToPM0S2gictWT-3PS-DYEj6WeeFeDn2lG9Zc33XvT3956dmeROh3XaH_JH1E9sLsAIBioSg-NceGP658TLPsKOpxzL67C2f-Nurgofqrj-YYLHb7-boB_0llfneq7i1M9VNcZP78a6SvxCWrIk_E</recordid><startdate>201102</startdate><enddate>201102</enddate><creator>Himeno, Eri</creator><creator>Ohyagi, Yasumasa</creator><creator>Ma, Linqing</creator><creator>Nakamura, Norimichi</creator><creator>Miyoshi, Katsue</creator><creator>Sakae, Nobutaka</creator><creator>Motomura, Kyoko</creator><creator>Soejima, Naoko</creator><creator>Yamasaki, Ryo</creator><creator>Hashimoto, Tetsuya</creator><creator>Tabira, Takeshi</creator><creator>M. LaFerla, Frank</creator><creator>Kira, Jun-ichi</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley-Liss</general><scope>BSCLL</scope><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>7X8</scope></search><sort><creationdate>201102</creationdate><title>Apomorphine treatment in Alzheimer mice promoting amyloid-β degradation</title><author>Himeno, Eri ; Ohyagi, Yasumasa ; Ma, Linqing ; Nakamura, Norimichi ; Miyoshi, Katsue ; Sakae, Nobutaka ; Motomura, Kyoko ; Soejima, Naoko ; Yamasaki, Ryo ; Hashimoto, Tetsuya ; Tabira, Takeshi ; M. LaFerla, Frank ; Kira, Jun-ichi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3929-488faebaf0170b902275e904897773d1f1c2373e99fade4cdadcb8a109c997df3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Alzheimer Disease - drug therapy</topic><topic>Alzheimer Disease - metabolism</topic><topic>Amyloid beta-Peptides - metabolism</topic><topic>Animals</topic><topic>Apomorphine - pharmacology</topic><topic>Apomorphine - therapeutic use</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Brain - drug effects</topic><topic>Brain - metabolism</topic><topic>Cells, Cultured</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Disease Models, Animal</topic><topic>Dopamine Agonists - pharmacology</topic><topic>Dopamine Agonists - therapeutic use</topic><topic>Immunohistochemistry</topic><topic>Insulysin - metabolism</topic><topic>Maze Learning - drug effects</topic><topic>Medical sciences</topic><topic>Memory, Short-Term - drug effects</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Neprilysin - metabolism</topic><topic>Neurology</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Oxidative Stress - drug effects</topic><topic>Oxidative Stress - physiology</topic><topic>Phosphorylation - drug effects</topic><topic>Proteasome Endopeptidase Complex - metabolism</topic><topic>Statistics, Nonparametric</topic><topic>tau Proteins - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Himeno, Eri</creatorcontrib><creatorcontrib>Ohyagi, Yasumasa</creatorcontrib><creatorcontrib>Ma, Linqing</creatorcontrib><creatorcontrib>Nakamura, Norimichi</creatorcontrib><creatorcontrib>Miyoshi, Katsue</creatorcontrib><creatorcontrib>Sakae, Nobutaka</creatorcontrib><creatorcontrib>Motomura, Kyoko</creatorcontrib><creatorcontrib>Soejima, Naoko</creatorcontrib><creatorcontrib>Yamasaki, Ryo</creatorcontrib><creatorcontrib>Hashimoto, Tetsuya</creatorcontrib><creatorcontrib>Tabira, Takeshi</creatorcontrib><creatorcontrib>M. LaFerla, Frank</creatorcontrib><creatorcontrib>Kira, Jun-ichi</creatorcontrib><collection>Istex</collection><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>MEDLINE - Academic</collection><jtitle>Annals of neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Himeno, Eri</au><au>Ohyagi, Yasumasa</au><au>Ma, Linqing</au><au>Nakamura, Norimichi</au><au>Miyoshi, Katsue</au><au>Sakae, Nobutaka</au><au>Motomura, Kyoko</au><au>Soejima, Naoko</au><au>Yamasaki, Ryo</au><au>Hashimoto, Tetsuya</au><au>Tabira, Takeshi</au><au>M. LaFerla, Frank</au><au>Kira, Jun-ichi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Apomorphine treatment in Alzheimer mice promoting amyloid-β degradation</atitle><jtitle>Annals of neurology</jtitle><addtitle>Ann Neurol</addtitle><date>2011-02</date><risdate>2011</risdate><volume>69</volume><issue>2</issue><spage>248</spage><epage>256</epage><pages>248-256</pages><issn>0364-5134</issn><eissn>1531-8249</eissn><coden>ANNED3</coden><abstract>Objective:
Intracellular amyloid β‐protein (Aβ) contributes to neurodegeneration in Alzheimer disease (AD). Apomorphine (APO) is a dopamine receptor agonist for Parkinson disease and also protects against oxidative stress. Efficacy of APO for an AD mouse model and effects of APO on cell cultures are studied.
Methods:
The triple transgenic AD mouse model (3xTg‐AD) has 2 familial AD‐related gene mutations (APPKM670/671NL/PS1M146V) and a tau gene mutation (TauP301L). Six‐month‐old 3xTg‐AD mice were treated with subcutaneous injections of APO once a week for 1 month. Memory function was evaluated by Morris water maze before and after the treatment. Brain tissues were examined by immunohistochemical staining and Western blotting. Effects of APO on intracellular Aβ degradation, activity of Aβ‐degrading enzymes, and protection against oxidative stress were studied in cultured SH‐SY5Y cells.
Results:
After APO treatment, short‐term memory function was dramatically improved. Significant decreases in the levels of intraneuronal Aβ, hyper‐phosphorylated tau (p‐tau), p53, and heme oxygenase‐1 proteins were observed. Moreover, APO promoted degradation of intracellular Aβ, increased activity of proteasome and insulin‐degrading enzyme, protected against H2O2 toxicity, and decreased p53 protein levels in the cultured cells.
Interpretation:
3xTg‐AD mice show intraneuronal Aβ accumulation and memory disturbances before extracellular Aβ deposition. Our data demonstrating improvement of memory function of 3xTg‐AD mice with decreases in intraneuronal Aβ and p‐tau levels by APO treatment strongly suggest that intraneuronal Aβ is an important therapeutic target and APO will be a novel drug for AD. Ann Neurol 2011</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>21387370</pmid><doi>10.1002/ana.22319</doi><tpages>9</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0364-5134 |
| ispartof | Annals of neurology, 2011-02, Vol.69 (2), p.248-256 |
| issn | 0364-5134 1531-8249 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_856404389 |
| source | MEDLINE; Wiley Online Library All Journals |
| subjects | Alzheimer Disease - drug therapy Alzheimer Disease - metabolism Amyloid beta-Peptides - metabolism Animals Apomorphine - pharmacology Apomorphine - therapeutic use Biological and medical sciences Blotting, Western Brain - drug effects Brain - metabolism Cells, Cultured Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Disease Models, Animal Dopamine Agonists - pharmacology Dopamine Agonists - therapeutic use Immunohistochemistry Insulysin - metabolism Maze Learning - drug effects Medical sciences Memory, Short-Term - drug effects Mice Mice, Transgenic Neprilysin - metabolism Neurology Neurons - drug effects Neurons - metabolism Oxidative Stress - drug effects Oxidative Stress - physiology Phosphorylation - drug effects Proteasome Endopeptidase Complex - metabolism Statistics, Nonparametric tau Proteins - metabolism |
| title | Apomorphine treatment in Alzheimer mice promoting amyloid-β degradation |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-08T05%3A16%3A41IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Apomorphine%20treatment%20in%20Alzheimer%20mice%20promoting%20amyloid-%CE%B2%20degradation&rft.jtitle=Annals%20of%20neurology&rft.au=Himeno,%20Eri&rft.date=2011-02&rft.volume=69&rft.issue=2&rft.spage=248&rft.epage=256&rft.pages=248-256&rft.issn=0364-5134&rft.eissn=1531-8249&rft.coden=ANNED3&rft_id=info:doi/10.1002/ana.22319&rft_dat=%3Cproquest_cross%3E856404389%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=856404389&rft_id=info:pmid/21387370&rfr_iscdi=true |