Learning deficits and dysfunctional synaptic plasticity induced by aggregated amyloid deposits in the dentate gyrus are rescued by chronic treatment with indomethacin
The amyloid pathology in Alzheimer's disease is accompanied by a chronic inflammatory response characterized by gliosis and activated microglial cells surrounding senile plaques. Epidemiological studies have shown nonsteroidal anti-inflammatory drug treatment reduces the risk of Alzheimer'...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Stéphan, Aline [verfasserIn] Laroche, Serge [verfasserIn] Davis, Sabrina [verfasserIn] |
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| Format: |
E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Science, Ltd ; 2003 |
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| Schlagwörter: |
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| Umfang: |
Online-Ressource |
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| Reproduktion: |
2003 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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| Übergeordnetes Werk: |
In: European journal of neuroscience - Oxford [u.a.] : Blackwell, 1989, 17(2003), 9, Seite 0 |
| Übergeordnetes Werk: |
volume:17 ; year:2003 ; number:9 ; pages:0 |
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| DOI / URN: |
10.1046/j.1460-9568.2003.02610.x |
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| 520 | |a The amyloid pathology in Alzheimer's disease is accompanied by a chronic inflammatory response characterized by gliosis and activated microglial cells surrounding senile plaques. Epidemiological studies have shown nonsteroidal anti-inflammatory drug treatment reduces the risk of Alzheimer's disease. We have previously shown that injection of a combination of Aβ40 and Aβ43 in the dentate gyrus of the rat induces aggregated amyloid deposits and inflammation associated with dysfunctional synaptic plasticity and learning deficits. Here we characterize the effectiveness of nonsteroidal anti-inflammatory treatment in this model and show that this treatment restores the working memory deficit and decremental long-term potentiation in the dentate gyrus. Importantly, we observe no qualitative difference in the presence of aggregated material but a substantial reduction in microglial-induced inflammation, suggesting that mature aggregated plaques may not be directly responsible for the deficits but may trigger an inflammatory response which has a detrimental effect on synaptic function and memory. | ||
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10.1046/j.1460-9568.2003.02610.x doi (DE-627)NLEJ242425550 DE-627 ger DE-627 rakwb Stéphan, Aline verfasserin aut Learning deficits and dysfunctional synaptic plasticity induced by aggregated amyloid deposits in the dentate gyrus are rescued by chronic treatment with indomethacin Oxford, UK Blackwell Science, Ltd 2003 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The amyloid pathology in Alzheimer's disease is accompanied by a chronic inflammatory response characterized by gliosis and activated microglial cells surrounding senile plaques. Epidemiological studies have shown nonsteroidal anti-inflammatory drug treatment reduces the risk of Alzheimer's disease. We have previously shown that injection of a combination of Aβ40 and Aβ43 in the dentate gyrus of the rat induces aggregated amyloid deposits and inflammation associated with dysfunctional synaptic plasticity and learning deficits. Here we characterize the effectiveness of nonsteroidal anti-inflammatory treatment in this model and show that this treatment restores the working memory deficit and decremental long-term potentiation in the dentate gyrus. Importantly, we observe no qualitative difference in the presence of aggregated material but a substantial reduction in microglial-induced inflammation, suggesting that mature aggregated plaques may not be directly responsible for the deficits but may trigger an inflammatory response which has a detrimental effect on synaptic function and memory. 2003 Blackwell Publishing Journal Backfiles 1879-2005 |2003|||||||||| Alzheimer's disease Laroche, Serge verfasserin aut Davis, Sabrina verfasserin aut In European journal of neuroscience Oxford [u.a.] : Blackwell, 1989 17(2003), 9, Seite 0 Online-Ressource (DE-627)NLEJ243926383 (DE-600)2005178-5 1460-9568 nnns volume:17 year:2003 number:9 pages:0 http://dx.doi.org/10.1046/j.1460-9568.2003.02610.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 17 2003 9 0 |
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10.1046/j.1460-9568.2003.02610.x doi (DE-627)NLEJ242425550 DE-627 ger DE-627 rakwb Stéphan, Aline verfasserin aut Learning deficits and dysfunctional synaptic plasticity induced by aggregated amyloid deposits in the dentate gyrus are rescued by chronic treatment with indomethacin Oxford, UK Blackwell Science, Ltd 2003 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The amyloid pathology in Alzheimer's disease is accompanied by a chronic inflammatory response characterized by gliosis and activated microglial cells surrounding senile plaques. Epidemiological studies have shown nonsteroidal anti-inflammatory drug treatment reduces the risk of Alzheimer's disease. We have previously shown that injection of a combination of Aβ40 and Aβ43 in the dentate gyrus of the rat induces aggregated amyloid deposits and inflammation associated with dysfunctional synaptic plasticity and learning deficits. Here we characterize the effectiveness of nonsteroidal anti-inflammatory treatment in this model and show that this treatment restores the working memory deficit and decremental long-term potentiation in the dentate gyrus. Importantly, we observe no qualitative difference in the presence of aggregated material but a substantial reduction in microglial-induced inflammation, suggesting that mature aggregated plaques may not be directly responsible for the deficits but may trigger an inflammatory response which has a detrimental effect on synaptic function and memory. 2003 Blackwell Publishing Journal Backfiles 1879-2005 |2003|||||||||| Alzheimer's disease Laroche, Serge verfasserin aut Davis, Sabrina verfasserin aut In European journal of neuroscience Oxford [u.a.] : Blackwell, 1989 17(2003), 9, Seite 0 Online-Ressource (DE-627)NLEJ243926383 (DE-600)2005178-5 1460-9568 nnns volume:17 year:2003 number:9 pages:0 http://dx.doi.org/10.1046/j.1460-9568.2003.02610.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 17 2003 9 0 |
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10.1046/j.1460-9568.2003.02610.x doi (DE-627)NLEJ242425550 DE-627 ger DE-627 rakwb Stéphan, Aline verfasserin aut Learning deficits and dysfunctional synaptic plasticity induced by aggregated amyloid deposits in the dentate gyrus are rescued by chronic treatment with indomethacin Oxford, UK Blackwell Science, Ltd 2003 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The amyloid pathology in Alzheimer's disease is accompanied by a chronic inflammatory response characterized by gliosis and activated microglial cells surrounding senile plaques. Epidemiological studies have shown nonsteroidal anti-inflammatory drug treatment reduces the risk of Alzheimer's disease. We have previously shown that injection of a combination of Aβ40 and Aβ43 in the dentate gyrus of the rat induces aggregated amyloid deposits and inflammation associated with dysfunctional synaptic plasticity and learning deficits. Here we characterize the effectiveness of nonsteroidal anti-inflammatory treatment in this model and show that this treatment restores the working memory deficit and decremental long-term potentiation in the dentate gyrus. Importantly, we observe no qualitative difference in the presence of aggregated material but a substantial reduction in microglial-induced inflammation, suggesting that mature aggregated plaques may not be directly responsible for the deficits but may trigger an inflammatory response which has a detrimental effect on synaptic function and memory. 2003 Blackwell Publishing Journal Backfiles 1879-2005 |2003|||||||||| Alzheimer's disease Laroche, Serge verfasserin aut Davis, Sabrina verfasserin aut In European journal of neuroscience Oxford [u.a.] : Blackwell, 1989 17(2003), 9, Seite 0 Online-Ressource (DE-627)NLEJ243926383 (DE-600)2005178-5 1460-9568 nnns volume:17 year:2003 number:9 pages:0 http://dx.doi.org/10.1046/j.1460-9568.2003.02610.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 17 2003 9 0 |
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10.1046/j.1460-9568.2003.02610.x doi (DE-627)NLEJ242425550 DE-627 ger DE-627 rakwb Stéphan, Aline verfasserin aut Learning deficits and dysfunctional synaptic plasticity induced by aggregated amyloid deposits in the dentate gyrus are rescued by chronic treatment with indomethacin Oxford, UK Blackwell Science, Ltd 2003 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The amyloid pathology in Alzheimer's disease is accompanied by a chronic inflammatory response characterized by gliosis and activated microglial cells surrounding senile plaques. Epidemiological studies have shown nonsteroidal anti-inflammatory drug treatment reduces the risk of Alzheimer's disease. We have previously shown that injection of a combination of Aβ40 and Aβ43 in the dentate gyrus of the rat induces aggregated amyloid deposits and inflammation associated with dysfunctional synaptic plasticity and learning deficits. Here we characterize the effectiveness of nonsteroidal anti-inflammatory treatment in this model and show that this treatment restores the working memory deficit and decremental long-term potentiation in the dentate gyrus. Importantly, we observe no qualitative difference in the presence of aggregated material but a substantial reduction in microglial-induced inflammation, suggesting that mature aggregated plaques may not be directly responsible for the deficits but may trigger an inflammatory response which has a detrimental effect on synaptic function and memory. 2003 Blackwell Publishing Journal Backfiles 1879-2005 |2003|||||||||| Alzheimer's disease Laroche, Serge verfasserin aut Davis, Sabrina verfasserin aut In European journal of neuroscience Oxford [u.a.] : Blackwell, 1989 17(2003), 9, Seite 0 Online-Ressource (DE-627)NLEJ243926383 (DE-600)2005178-5 1460-9568 nnns volume:17 year:2003 number:9 pages:0 http://dx.doi.org/10.1046/j.1460-9568.2003.02610.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 17 2003 9 0 |
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10.1046/j.1460-9568.2003.02610.x doi (DE-627)NLEJ242425550 DE-627 ger DE-627 rakwb Stéphan, Aline verfasserin aut Learning deficits and dysfunctional synaptic plasticity induced by aggregated amyloid deposits in the dentate gyrus are rescued by chronic treatment with indomethacin Oxford, UK Blackwell Science, Ltd 2003 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The amyloid pathology in Alzheimer's disease is accompanied by a chronic inflammatory response characterized by gliosis and activated microglial cells surrounding senile plaques. Epidemiological studies have shown nonsteroidal anti-inflammatory drug treatment reduces the risk of Alzheimer's disease. We have previously shown that injection of a combination of Aβ40 and Aβ43 in the dentate gyrus of the rat induces aggregated amyloid deposits and inflammation associated with dysfunctional synaptic plasticity and learning deficits. Here we characterize the effectiveness of nonsteroidal anti-inflammatory treatment in this model and show that this treatment restores the working memory deficit and decremental long-term potentiation in the dentate gyrus. Importantly, we observe no qualitative difference in the presence of aggregated material but a substantial reduction in microglial-induced inflammation, suggesting that mature aggregated plaques may not be directly responsible for the deficits but may trigger an inflammatory response which has a detrimental effect on synaptic function and memory. 2003 Blackwell Publishing Journal Backfiles 1879-2005 |2003|||||||||| Alzheimer's disease Laroche, Serge verfasserin aut Davis, Sabrina verfasserin aut In European journal of neuroscience Oxford [u.a.] : Blackwell, 1989 17(2003), 9, Seite 0 Online-Ressource (DE-627)NLEJ243926383 (DE-600)2005178-5 1460-9568 nnns volume:17 year:2003 number:9 pages:0 http://dx.doi.org/10.1046/j.1460-9568.2003.02610.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 17 2003 9 0 |
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The amyloid pathology in Alzheimer's disease is accompanied by a chronic inflammatory response characterized by gliosis and activated microglial cells surrounding senile plaques. Epidemiological studies have shown nonsteroidal anti-inflammatory drug treatment reduces the risk of Alzheimer's disease. We have previously shown that injection of a combination of Aβ40 and Aβ43 in the dentate gyrus of the rat induces aggregated amyloid deposits and inflammation associated with dysfunctional synaptic plasticity and learning deficits. Here we characterize the effectiveness of nonsteroidal anti-inflammatory treatment in this model and show that this treatment restores the working memory deficit and decremental long-term potentiation in the dentate gyrus. Importantly, we observe no qualitative difference in the presence of aggregated material but a substantial reduction in microglial-induced inflammation, suggesting that mature aggregated plaques may not be directly responsible for the deficits but may trigger an inflammatory response which has a detrimental effect on synaptic function and memory. |
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The amyloid pathology in Alzheimer's disease is accompanied by a chronic inflammatory response characterized by gliosis and activated microglial cells surrounding senile plaques. Epidemiological studies have shown nonsteroidal anti-inflammatory drug treatment reduces the risk of Alzheimer's disease. We have previously shown that injection of a combination of Aβ40 and Aβ43 in the dentate gyrus of the rat induces aggregated amyloid deposits and inflammation associated with dysfunctional synaptic plasticity and learning deficits. Here we characterize the effectiveness of nonsteroidal anti-inflammatory treatment in this model and show that this treatment restores the working memory deficit and decremental long-term potentiation in the dentate gyrus. Importantly, we observe no qualitative difference in the presence of aggregated material but a substantial reduction in microglial-induced inflammation, suggesting that mature aggregated plaques may not be directly responsible for the deficits but may trigger an inflammatory response which has a detrimental effect on synaptic function and memory. |
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The amyloid pathology in Alzheimer's disease is accompanied by a chronic inflammatory response characterized by gliosis and activated microglial cells surrounding senile plaques. Epidemiological studies have shown nonsteroidal anti-inflammatory drug treatment reduces the risk of Alzheimer's disease. We have previously shown that injection of a combination of Aβ40 and Aβ43 in the dentate gyrus of the rat induces aggregated amyloid deposits and inflammation associated with dysfunctional synaptic plasticity and learning deficits. Here we characterize the effectiveness of nonsteroidal anti-inflammatory treatment in this model and show that this treatment restores the working memory deficit and decremental long-term potentiation in the dentate gyrus. Importantly, we observe no qualitative difference in the presence of aggregated material but a substantial reduction in microglial-induced inflammation, suggesting that mature aggregated plaques may not be directly responsible for the deficits but may trigger an inflammatory response which has a detrimental effect on synaptic function and memory. |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ242425550</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230505204348.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">120427s2003 xx |||||o 00| ||und c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1046/j.1460-9568.2003.02610.x</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ242425550</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Stéphan, Aline</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Learning deficits and dysfunctional synaptic plasticity induced by aggregated amyloid deposits in the dentate gyrus are rescued by chronic treatment with indomethacin</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="a">Oxford, UK</subfield><subfield code="b">Blackwell Science, Ltd</subfield><subfield code="c">2003</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">The amyloid pathology in Alzheimer's disease is accompanied by a chronic inflammatory response characterized by gliosis and activated microglial cells surrounding senile plaques. Epidemiological studies have shown nonsteroidal anti-inflammatory drug treatment reduces the risk of Alzheimer's disease. We have previously shown that injection of a combination of Aβ40 and Aβ43 in the dentate gyrus of the rat induces aggregated amyloid deposits and inflammation associated with dysfunctional synaptic plasticity and learning deficits. Here we characterize the effectiveness of nonsteroidal anti-inflammatory treatment in this model and show that this treatment restores the working memory deficit and decremental long-term potentiation in the dentate gyrus. Importantly, we observe no qualitative difference in the presence of aggregated material but a substantial reduction in microglial-induced inflammation, suggesting that mature aggregated plaques may not be directly responsible for the deficits but may trigger an inflammatory response which has a detrimental effect on synaptic function and memory.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="d">2003</subfield><subfield code="f">Blackwell Publishing Journal Backfiles 1879-2005</subfield><subfield code="7">|2003||||||||||</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Alzheimer's disease</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Laroche, Serge</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Davis, Sabrina</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">European journal of neuroscience</subfield><subfield code="d">Oxford [u.a.] : Blackwell, 1989</subfield><subfield code="g">17(2003), 9, Seite 0</subfield><subfield code="h">Online-Ressource</subfield><subfield code="w">(DE-627)NLEJ243926383</subfield><subfield code="w">(DE-600)2005178-5</subfield><subfield code="x">1460-9568</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:17</subfield><subfield code="g">year:2003</subfield><subfield code="g">number:9</subfield><subfield code="g">pages:0</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1046/j.1460-9568.2003.02610.x</subfield><subfield code="q">text/html</subfield><subfield code="x">Verlag</subfield><subfield code="z">Deutschlandweit zugänglich</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-DJB</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_NL_ARTICLE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">17</subfield><subfield code="j">2003</subfield><subfield code="e">9</subfield><subfield code="h">0</subfield></datafield></record></collection>
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