Effects of intrahippocampal CT105, a carboxyl terminal fragment of β-amyloid precursor protein, alone/with inflammatory cytokines on working memory in rats
In this study, we examined the effects of a 105 amino acid carboxyl terminal fragment of β-amyloid precursor protein (CT105) and inflammatory cytokines on working memory in rats, by using a three-panel runway set-up. CT105 at 10 nmol/side significantly impaired working memory when it was administere...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Matsumoto, Yuji [verfasserIn] Watanabe, Shigenori [verfasserIn] Suh, Yoo-Hun [verfasserIn] |
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| Format: |
E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Science Ltd ; 2002 |
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| Schlagwörter: |
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| Umfang: |
Online-Ressource |
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| Reproduktion: |
2002 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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| Übergeordnetes Werk: |
In: Journal of neurochemistry - Oxford : Wiley-Blackwell, 1956, 82(2002), 2, Seite 0 |
| Übergeordnetes Werk: |
volume:82 ; year:2002 ; number:2 ; pages:0 |
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| DOI / URN: |
10.1046/j.1471-4159.2002.00944.x |
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| 520 | |a In this study, we examined the effects of a 105 amino acid carboxyl terminal fragment of β-amyloid precursor protein (CT105) and inflammatory cytokines on working memory in rats, by using a three-panel runway set-up. CT105 at 10 nmol/side significantly impaired working memory when it was administered bilaterally into the hippocampus. Furthermore, to elucidate the interaction of CT105 with inflammatory cytokines, we co-administered tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) in combination with CT105. Concurrent injections of CT105 (1.0 nmol/side) and TNF-α (100 ng/side) produced a synergistic deficit of working memory, whereas IL-1β (100 ng/side) combined with CT105 (1.0 nmol/side) did not affect the working memory performance. These results indicate that the CT105-induced impairment of working memory is strongly aggravated by an increase in the level of the inflammatory cytokine TNF-α, which may occur in the brains of patients with Alzheimer's disease. | ||
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10.1046/j.1471-4159.2002.00944.x doi (DE-627)NLEJ24313679X DE-627 ger DE-627 rakwb Matsumoto, Yuji verfasserin aut Effects of intrahippocampal CT105, a carboxyl terminal fragment of β-amyloid precursor protein, alone/with inflammatory cytokines on working memory in rats Oxford, UK Blackwell Science Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier In this study, we examined the effects of a 105 amino acid carboxyl terminal fragment of β-amyloid precursor protein (CT105) and inflammatory cytokines on working memory in rats, by using a three-panel runway set-up. CT105 at 10 nmol/side significantly impaired working memory when it was administered bilaterally into the hippocampus. Furthermore, to elucidate the interaction of CT105 with inflammatory cytokines, we co-administered tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) in combination with CT105. Concurrent injections of CT105 (1.0 nmol/side) and TNF-α (100 ng/side) produced a synergistic deficit of working memory, whereas IL-1β (100 ng/side) combined with CT105 (1.0 nmol/side) did not affect the working memory performance. These results indicate that the CT105-induced impairment of working memory is strongly aggravated by an increase in the level of the inflammatory cytokine TNF-α, which may occur in the brains of patients with Alzheimer's disease. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| carboxyl terminal fragment of β-amyloid precursor protein Watanabe, Shigenori verfasserin aut Suh, Yoo-Hun verfasserin aut Yamamoto, Tsuneyuki oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 82(2002), 2, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:82 year:2002 number:2 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2002.00944.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 82 2002 2 0 |
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10.1046/j.1471-4159.2002.00944.x doi (DE-627)NLEJ24313679X DE-627 ger DE-627 rakwb Matsumoto, Yuji verfasserin aut Effects of intrahippocampal CT105, a carboxyl terminal fragment of β-amyloid precursor protein, alone/with inflammatory cytokines on working memory in rats Oxford, UK Blackwell Science Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier In this study, we examined the effects of a 105 amino acid carboxyl terminal fragment of β-amyloid precursor protein (CT105) and inflammatory cytokines on working memory in rats, by using a three-panel runway set-up. CT105 at 10 nmol/side significantly impaired working memory when it was administered bilaterally into the hippocampus. Furthermore, to elucidate the interaction of CT105 with inflammatory cytokines, we co-administered tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) in combination with CT105. Concurrent injections of CT105 (1.0 nmol/side) and TNF-α (100 ng/side) produced a synergistic deficit of working memory, whereas IL-1β (100 ng/side) combined with CT105 (1.0 nmol/side) did not affect the working memory performance. These results indicate that the CT105-induced impairment of working memory is strongly aggravated by an increase in the level of the inflammatory cytokine TNF-α, which may occur in the brains of patients with Alzheimer's disease. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| carboxyl terminal fragment of β-amyloid precursor protein Watanabe, Shigenori verfasserin aut Suh, Yoo-Hun verfasserin aut Yamamoto, Tsuneyuki oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 82(2002), 2, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:82 year:2002 number:2 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2002.00944.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 82 2002 2 0 |
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10.1046/j.1471-4159.2002.00944.x doi (DE-627)NLEJ24313679X DE-627 ger DE-627 rakwb Matsumoto, Yuji verfasserin aut Effects of intrahippocampal CT105, a carboxyl terminal fragment of β-amyloid precursor protein, alone/with inflammatory cytokines on working memory in rats Oxford, UK Blackwell Science Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier In this study, we examined the effects of a 105 amino acid carboxyl terminal fragment of β-amyloid precursor protein (CT105) and inflammatory cytokines on working memory in rats, by using a three-panel runway set-up. CT105 at 10 nmol/side significantly impaired working memory when it was administered bilaterally into the hippocampus. Furthermore, to elucidate the interaction of CT105 with inflammatory cytokines, we co-administered tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) in combination with CT105. Concurrent injections of CT105 (1.0 nmol/side) and TNF-α (100 ng/side) produced a synergistic deficit of working memory, whereas IL-1β (100 ng/side) combined with CT105 (1.0 nmol/side) did not affect the working memory performance. These results indicate that the CT105-induced impairment of working memory is strongly aggravated by an increase in the level of the inflammatory cytokine TNF-α, which may occur in the brains of patients with Alzheimer's disease. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| carboxyl terminal fragment of β-amyloid precursor protein Watanabe, Shigenori verfasserin aut Suh, Yoo-Hun verfasserin aut Yamamoto, Tsuneyuki oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 82(2002), 2, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:82 year:2002 number:2 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2002.00944.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 82 2002 2 0 |
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10.1046/j.1471-4159.2002.00944.x doi (DE-627)NLEJ24313679X DE-627 ger DE-627 rakwb Matsumoto, Yuji verfasserin aut Effects of intrahippocampal CT105, a carboxyl terminal fragment of β-amyloid precursor protein, alone/with inflammatory cytokines on working memory in rats Oxford, UK Blackwell Science Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier In this study, we examined the effects of a 105 amino acid carboxyl terminal fragment of β-amyloid precursor protein (CT105) and inflammatory cytokines on working memory in rats, by using a three-panel runway set-up. CT105 at 10 nmol/side significantly impaired working memory when it was administered bilaterally into the hippocampus. Furthermore, to elucidate the interaction of CT105 with inflammatory cytokines, we co-administered tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) in combination with CT105. Concurrent injections of CT105 (1.0 nmol/side) and TNF-α (100 ng/side) produced a synergistic deficit of working memory, whereas IL-1β (100 ng/side) combined with CT105 (1.0 nmol/side) did not affect the working memory performance. These results indicate that the CT105-induced impairment of working memory is strongly aggravated by an increase in the level of the inflammatory cytokine TNF-α, which may occur in the brains of patients with Alzheimer's disease. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| carboxyl terminal fragment of β-amyloid precursor protein Watanabe, Shigenori verfasserin aut Suh, Yoo-Hun verfasserin aut Yamamoto, Tsuneyuki oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 82(2002), 2, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:82 year:2002 number:2 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2002.00944.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 82 2002 2 0 |
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10.1046/j.1471-4159.2002.00944.x doi (DE-627)NLEJ24313679X DE-627 ger DE-627 rakwb Matsumoto, Yuji verfasserin aut Effects of intrahippocampal CT105, a carboxyl terminal fragment of β-amyloid precursor protein, alone/with inflammatory cytokines on working memory in rats Oxford, UK Blackwell Science Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier In this study, we examined the effects of a 105 amino acid carboxyl terminal fragment of β-amyloid precursor protein (CT105) and inflammatory cytokines on working memory in rats, by using a three-panel runway set-up. CT105 at 10 nmol/side significantly impaired working memory when it was administered bilaterally into the hippocampus. Furthermore, to elucidate the interaction of CT105 with inflammatory cytokines, we co-administered tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) in combination with CT105. Concurrent injections of CT105 (1.0 nmol/side) and TNF-α (100 ng/side) produced a synergistic deficit of working memory, whereas IL-1β (100 ng/side) combined with CT105 (1.0 nmol/side) did not affect the working memory performance. These results indicate that the CT105-induced impairment of working memory is strongly aggravated by an increase in the level of the inflammatory cytokine TNF-α, which may occur in the brains of patients with Alzheimer's disease. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| carboxyl terminal fragment of β-amyloid precursor protein Watanabe, Shigenori verfasserin aut Suh, Yoo-Hun verfasserin aut Yamamoto, Tsuneyuki oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 82(2002), 2, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:82 year:2002 number:2 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2002.00944.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 82 2002 2 0 |
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Effects of intrahippocampal CT105, a carboxyl terminal fragment of β-amyloid precursor protein, alone/with inflammatory cytokines on working memory in rats |
| abstract |
In this study, we examined the effects of a 105 amino acid carboxyl terminal fragment of β-amyloid precursor protein (CT105) and inflammatory cytokines on working memory in rats, by using a three-panel runway set-up. CT105 at 10 nmol/side significantly impaired working memory when it was administered bilaterally into the hippocampus. Furthermore, to elucidate the interaction of CT105 with inflammatory cytokines, we co-administered tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) in combination with CT105. Concurrent injections of CT105 (1.0 nmol/side) and TNF-α (100 ng/side) produced a synergistic deficit of working memory, whereas IL-1β (100 ng/side) combined with CT105 (1.0 nmol/side) did not affect the working memory performance. These results indicate that the CT105-induced impairment of working memory is strongly aggravated by an increase in the level of the inflammatory cytokine TNF-α, which may occur in the brains of patients with Alzheimer's disease. |
| abstractGer |
In this study, we examined the effects of a 105 amino acid carboxyl terminal fragment of β-amyloid precursor protein (CT105) and inflammatory cytokines on working memory in rats, by using a three-panel runway set-up. CT105 at 10 nmol/side significantly impaired working memory when it was administered bilaterally into the hippocampus. Furthermore, to elucidate the interaction of CT105 with inflammatory cytokines, we co-administered tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) in combination with CT105. Concurrent injections of CT105 (1.0 nmol/side) and TNF-α (100 ng/side) produced a synergistic deficit of working memory, whereas IL-1β (100 ng/side) combined with CT105 (1.0 nmol/side) did not affect the working memory performance. These results indicate that the CT105-induced impairment of working memory is strongly aggravated by an increase in the level of the inflammatory cytokine TNF-α, which may occur in the brains of patients with Alzheimer's disease. |
| abstract_unstemmed |
In this study, we examined the effects of a 105 amino acid carboxyl terminal fragment of β-amyloid precursor protein (CT105) and inflammatory cytokines on working memory in rats, by using a three-panel runway set-up. CT105 at 10 nmol/side significantly impaired working memory when it was administered bilaterally into the hippocampus. Furthermore, to elucidate the interaction of CT105 with inflammatory cytokines, we co-administered tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) in combination with CT105. Concurrent injections of CT105 (1.0 nmol/side) and TNF-α (100 ng/side) produced a synergistic deficit of working memory, whereas IL-1β (100 ng/side) combined with CT105 (1.0 nmol/side) did not affect the working memory performance. These results indicate that the CT105-induced impairment of working memory is strongly aggravated by an increase in the level of the inflammatory cytokine TNF-α, which may occur in the brains of patients with Alzheimer's disease. |
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Watanabe, Shigenori Suh, Yoo-Hun Yamamoto, Tsuneyuki |
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Watanabe, Shigenori Suh, Yoo-Hun Yamamoto, Tsuneyuki |
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10.1046/j.1471-4159.2002.00944.x |
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