Effects of Huperzin-A on the Beta-amyloid accumulation in the brain and skeletal muscle cells of a rat model for Alzheimer's disease
Aims: Alzheimer's Disease (AD) is characterized by a loss of cognitive function and also the accumulation of β-amyloid peptide (βAP) in the brain parenchyma, which plays an important role in this disease. However, it is often also associated with the non-cognitive symptoms such as loss of muscl...
Ausführliche Beschreibung
Autor*in: |
Turkseven, Cagatay Han [verfasserIn] Buyukakilli, Belgin [verfasserIn] Balli, Ebru [verfasserIn] Yetkin, Derya [verfasserIn] Erdal, Mehmet Emin [verfasserIn] Yilmaz, Senay Gorucu [verfasserIn] Sahin, Leyla [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2017 |
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Schlagwörter: |
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Übergeordnetes Werk: |
Enthalten in: Life sciences - New York, NY [u.a.] : Elsevier Science, 1963, 184, Seite 47-57 |
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Übergeordnetes Werk: |
volume:184 ; pages:47-57 |
DOI / URN: |
10.1016/j.lfs.2017.07.012 |
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Katalog-ID: |
ELV008780293 |
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245 | 1 | 0 | |a Effects of Huperzin-A on the Beta-amyloid accumulation in the brain and skeletal muscle cells of a rat model for Alzheimer's disease |
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520 | |a Aims: Alzheimer's Disease (AD) is characterized by a loss of cognitive function and also the accumulation of β-amyloid peptide (βAP) in the brain parenchyma, which plays an important role in this disease. However, it is often also associated with the non-cognitive symptoms such as loss of muscle function (Inclusion-Body Myositis-IBM).Main methods: Sprague-Dawley rats (13 weeks-n=68) were randomly assigned into five groups: Group C: Control; Group D: d-galactose; Group O+D: Bilateral oophorectomy+ d-galactose; Group O: Bilateral oophorectomy; Group O+D+H: Bilateral oophorectomy+ d-galactose+Hup-A. Tissue fixation was performed with the perfusion method. The Compound Muscle Action Potential (CMAP) and mechanical muscle activity were recorded using the standard electro-biophysical techniques. Immune staining was performed with specific antibodies, and the pathological changes were examined. RNA was obtained from brain tissue samples with the Trizol Method. Then, the expression data of mature-miRNAs (rno-miR-9-5p, rno-miR-29a-3p, rno-miR-106a-5p, rno-miR-107 and rno-miR-125a-3p), which may be effective in AD, were taken with Real-Time PCR.Key findings: Impairments occurred in behavioral tests of the rats in the O+D group. βAP accumulation and AChE activity increased significantly in the forebrain in the O+D group compared to the C group. It was seen that Huperzine-A (Hup-A) reduced AChE activity and destructed βAP accumulation. There was a significant decrease in the maximum contractile force at different frequencies in the O+D group and in the O group compared to the C group.Significance: It was found that Hup-A contributed to the healing process in rats for damage occurring both in the brain and in the neuro-muscular system. | ||
650 | 4 | |a Alzheimer's disease | |
650 | 4 | |a β-amyloid peptide | |
650 | 4 | |a Motor dysfunction | |
650 | 4 | |a Electromyography | |
650 | 4 | |a Huperzine-a | |
650 | 4 | |a Inclusion body myositis | |
700 | 1 | |a Buyukakilli, Belgin |e verfasserin |0 (orcid)0000-0003-1153-2558 |4 aut | |
700 | 1 | |a Balli, Ebru |e verfasserin |4 aut | |
700 | 1 | |a Yetkin, Derya |e verfasserin |4 aut | |
700 | 1 | |a Erdal, Mehmet Emin |e verfasserin |4 aut | |
700 | 1 | |a Yilmaz, Senay Gorucu |e verfasserin |4 aut | |
700 | 1 | |a Sahin, Leyla |e verfasserin |4 aut | |
773 | 0 | 8 | |i Enthalten in |t Life sciences |d New York, NY [u.a.] : Elsevier Science, 1963 |g 184, Seite 47-57 |h Online-Ressource |w (DE-627)320515605 |w (DE-600)2013911-1 |w (DE-576)09095503X |x 1879-0631 |7 nnns |
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10.1016/j.lfs.2017.07.012 doi (DE-627)ELV008780293 (ELSEVIER)S0024-3205(17)30332-6 DE-627 ger DE-627 rda eng 570 DE-600 BIODIV DE-30 fid 42.00 bkl 44.40 bkl Turkseven, Cagatay Han verfasserin aut Effects of Huperzin-A on the Beta-amyloid accumulation in the brain and skeletal muscle cells of a rat model for Alzheimer's disease 2017 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Aims: Alzheimer's Disease (AD) is characterized by a loss of cognitive function and also the accumulation of β-amyloid peptide (βAP) in the brain parenchyma, which plays an important role in this disease. However, it is often also associated with the non-cognitive symptoms such as loss of muscle function (Inclusion-Body Myositis-IBM).Main methods: Sprague-Dawley rats (13 weeks-n=68) were randomly assigned into five groups: Group C: Control; Group D: d-galactose; Group O+D: Bilateral oophorectomy+ d-galactose; Group O: Bilateral oophorectomy; Group O+D+H: Bilateral oophorectomy+ d-galactose+Hup-A. Tissue fixation was performed with the perfusion method. The Compound Muscle Action Potential (CMAP) and mechanical muscle activity were recorded using the standard electro-biophysical techniques. Immune staining was performed with specific antibodies, and the pathological changes were examined. RNA was obtained from brain tissue samples with the Trizol Method. Then, the expression data of mature-miRNAs (rno-miR-9-5p, rno-miR-29a-3p, rno-miR-106a-5p, rno-miR-107 and rno-miR-125a-3p), which may be effective in AD, were taken with Real-Time PCR.Key findings: Impairments occurred in behavioral tests of the rats in the O+D group. βAP accumulation and AChE activity increased significantly in the forebrain in the O+D group compared to the C group. It was seen that Huperzine-A (Hup-A) reduced AChE activity and destructed βAP accumulation. There was a significant decrease in the maximum contractile force at different frequencies in the O+D group and in the O group compared to the C group.Significance: It was found that Hup-A contributed to the healing process in rats for damage occurring both in the brain and in the neuro-muscular system. Alzheimer's disease β-amyloid peptide Motor dysfunction Electromyography Huperzine-a Inclusion body myositis Buyukakilli, Belgin verfasserin (orcid)0000-0003-1153-2558 aut Balli, Ebru verfasserin aut Yetkin, Derya verfasserin aut Erdal, Mehmet Emin verfasserin aut Yilmaz, Senay Gorucu verfasserin aut Sahin, Leyla verfasserin aut Enthalten in Life sciences New York, NY [u.a.] : Elsevier Science, 1963 184, Seite 47-57 Online-Ressource (DE-627)320515605 (DE-600)2013911-1 (DE-576)09095503X 1879-0631 nnns volume:184 pages:47-57 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-BIODIV SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2098 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4313 GBV_ILN_4326 GBV_ILN_4334 GBV_ILN_4338 42.00 Biologie: Allgemeines 44.40 Pharmazie Pharmazeutika AR 184 47-57 |
spelling |
10.1016/j.lfs.2017.07.012 doi (DE-627)ELV008780293 (ELSEVIER)S0024-3205(17)30332-6 DE-627 ger DE-627 rda eng 570 DE-600 BIODIV DE-30 fid 42.00 bkl 44.40 bkl Turkseven, Cagatay Han verfasserin aut Effects of Huperzin-A on the Beta-amyloid accumulation in the brain and skeletal muscle cells of a rat model for Alzheimer's disease 2017 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Aims: Alzheimer's Disease (AD) is characterized by a loss of cognitive function and also the accumulation of β-amyloid peptide (βAP) in the brain parenchyma, which plays an important role in this disease. However, it is often also associated with the non-cognitive symptoms such as loss of muscle function (Inclusion-Body Myositis-IBM).Main methods: Sprague-Dawley rats (13 weeks-n=68) were randomly assigned into five groups: Group C: Control; Group D: d-galactose; Group O+D: Bilateral oophorectomy+ d-galactose; Group O: Bilateral oophorectomy; Group O+D+H: Bilateral oophorectomy+ d-galactose+Hup-A. Tissue fixation was performed with the perfusion method. The Compound Muscle Action Potential (CMAP) and mechanical muscle activity were recorded using the standard electro-biophysical techniques. Immune staining was performed with specific antibodies, and the pathological changes were examined. RNA was obtained from brain tissue samples with the Trizol Method. Then, the expression data of mature-miRNAs (rno-miR-9-5p, rno-miR-29a-3p, rno-miR-106a-5p, rno-miR-107 and rno-miR-125a-3p), which may be effective in AD, were taken with Real-Time PCR.Key findings: Impairments occurred in behavioral tests of the rats in the O+D group. βAP accumulation and AChE activity increased significantly in the forebrain in the O+D group compared to the C group. It was seen that Huperzine-A (Hup-A) reduced AChE activity and destructed βAP accumulation. There was a significant decrease in the maximum contractile force at different frequencies in the O+D group and in the O group compared to the C group.Significance: It was found that Hup-A contributed to the healing process in rats for damage occurring both in the brain and in the neuro-muscular system. Alzheimer's disease β-amyloid peptide Motor dysfunction Electromyography Huperzine-a Inclusion body myositis Buyukakilli, Belgin verfasserin (orcid)0000-0003-1153-2558 aut Balli, Ebru verfasserin aut Yetkin, Derya verfasserin aut Erdal, Mehmet Emin verfasserin aut Yilmaz, Senay Gorucu verfasserin aut Sahin, Leyla verfasserin aut Enthalten in Life sciences New York, NY [u.a.] : Elsevier Science, 1963 184, Seite 47-57 Online-Ressource (DE-627)320515605 (DE-600)2013911-1 (DE-576)09095503X 1879-0631 nnns volume:184 pages:47-57 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-BIODIV SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2098 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4313 GBV_ILN_4326 GBV_ILN_4334 GBV_ILN_4338 42.00 Biologie: Allgemeines 44.40 Pharmazie Pharmazeutika AR 184 47-57 |
allfields_unstemmed |
10.1016/j.lfs.2017.07.012 doi (DE-627)ELV008780293 (ELSEVIER)S0024-3205(17)30332-6 DE-627 ger DE-627 rda eng 570 DE-600 BIODIV DE-30 fid 42.00 bkl 44.40 bkl Turkseven, Cagatay Han verfasserin aut Effects of Huperzin-A on the Beta-amyloid accumulation in the brain and skeletal muscle cells of a rat model for Alzheimer's disease 2017 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Aims: Alzheimer's Disease (AD) is characterized by a loss of cognitive function and also the accumulation of β-amyloid peptide (βAP) in the brain parenchyma, which plays an important role in this disease. However, it is often also associated with the non-cognitive symptoms such as loss of muscle function (Inclusion-Body Myositis-IBM).Main methods: Sprague-Dawley rats (13 weeks-n=68) were randomly assigned into five groups: Group C: Control; Group D: d-galactose; Group O+D: Bilateral oophorectomy+ d-galactose; Group O: Bilateral oophorectomy; Group O+D+H: Bilateral oophorectomy+ d-galactose+Hup-A. Tissue fixation was performed with the perfusion method. The Compound Muscle Action Potential (CMAP) and mechanical muscle activity were recorded using the standard electro-biophysical techniques. Immune staining was performed with specific antibodies, and the pathological changes were examined. RNA was obtained from brain tissue samples with the Trizol Method. Then, the expression data of mature-miRNAs (rno-miR-9-5p, rno-miR-29a-3p, rno-miR-106a-5p, rno-miR-107 and rno-miR-125a-3p), which may be effective in AD, were taken with Real-Time PCR.Key findings: Impairments occurred in behavioral tests of the rats in the O+D group. βAP accumulation and AChE activity increased significantly in the forebrain in the O+D group compared to the C group. It was seen that Huperzine-A (Hup-A) reduced AChE activity and destructed βAP accumulation. There was a significant decrease in the maximum contractile force at different frequencies in the O+D group and in the O group compared to the C group.Significance: It was found that Hup-A contributed to the healing process in rats for damage occurring both in the brain and in the neuro-muscular system. Alzheimer's disease β-amyloid peptide Motor dysfunction Electromyography Huperzine-a Inclusion body myositis Buyukakilli, Belgin verfasserin (orcid)0000-0003-1153-2558 aut Balli, Ebru verfasserin aut Yetkin, Derya verfasserin aut Erdal, Mehmet Emin verfasserin aut Yilmaz, Senay Gorucu verfasserin aut Sahin, Leyla verfasserin aut Enthalten in Life sciences New York, NY [u.a.] : Elsevier Science, 1963 184, Seite 47-57 Online-Ressource (DE-627)320515605 (DE-600)2013911-1 (DE-576)09095503X 1879-0631 nnns volume:184 pages:47-57 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-BIODIV SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2098 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4313 GBV_ILN_4326 GBV_ILN_4334 GBV_ILN_4338 42.00 Biologie: Allgemeines 44.40 Pharmazie Pharmazeutika AR 184 47-57 |
allfieldsGer |
10.1016/j.lfs.2017.07.012 doi (DE-627)ELV008780293 (ELSEVIER)S0024-3205(17)30332-6 DE-627 ger DE-627 rda eng 570 DE-600 BIODIV DE-30 fid 42.00 bkl 44.40 bkl Turkseven, Cagatay Han verfasserin aut Effects of Huperzin-A on the Beta-amyloid accumulation in the brain and skeletal muscle cells of a rat model for Alzheimer's disease 2017 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Aims: Alzheimer's Disease (AD) is characterized by a loss of cognitive function and also the accumulation of β-amyloid peptide (βAP) in the brain parenchyma, which plays an important role in this disease. However, it is often also associated with the non-cognitive symptoms such as loss of muscle function (Inclusion-Body Myositis-IBM).Main methods: Sprague-Dawley rats (13 weeks-n=68) were randomly assigned into five groups: Group C: Control; Group D: d-galactose; Group O+D: Bilateral oophorectomy+ d-galactose; Group O: Bilateral oophorectomy; Group O+D+H: Bilateral oophorectomy+ d-galactose+Hup-A. Tissue fixation was performed with the perfusion method. The Compound Muscle Action Potential (CMAP) and mechanical muscle activity were recorded using the standard electro-biophysical techniques. Immune staining was performed with specific antibodies, and the pathological changes were examined. RNA was obtained from brain tissue samples with the Trizol Method. Then, the expression data of mature-miRNAs (rno-miR-9-5p, rno-miR-29a-3p, rno-miR-106a-5p, rno-miR-107 and rno-miR-125a-3p), which may be effective in AD, were taken with Real-Time PCR.Key findings: Impairments occurred in behavioral tests of the rats in the O+D group. βAP accumulation and AChE activity increased significantly in the forebrain in the O+D group compared to the C group. It was seen that Huperzine-A (Hup-A) reduced AChE activity and destructed βAP accumulation. There was a significant decrease in the maximum contractile force at different frequencies in the O+D group and in the O group compared to the C group.Significance: It was found that Hup-A contributed to the healing process in rats for damage occurring both in the brain and in the neuro-muscular system. Alzheimer's disease β-amyloid peptide Motor dysfunction Electromyography Huperzine-a Inclusion body myositis Buyukakilli, Belgin verfasserin (orcid)0000-0003-1153-2558 aut Balli, Ebru verfasserin aut Yetkin, Derya verfasserin aut Erdal, Mehmet Emin verfasserin aut Yilmaz, Senay Gorucu verfasserin aut Sahin, Leyla verfasserin aut Enthalten in Life sciences New York, NY [u.a.] : Elsevier Science, 1963 184, Seite 47-57 Online-Ressource (DE-627)320515605 (DE-600)2013911-1 (DE-576)09095503X 1879-0631 nnns volume:184 pages:47-57 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-BIODIV SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2098 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4313 GBV_ILN_4326 GBV_ILN_4334 GBV_ILN_4338 42.00 Biologie: Allgemeines 44.40 Pharmazie Pharmazeutika AR 184 47-57 |
allfieldsSound |
10.1016/j.lfs.2017.07.012 doi (DE-627)ELV008780293 (ELSEVIER)S0024-3205(17)30332-6 DE-627 ger DE-627 rda eng 570 DE-600 BIODIV DE-30 fid 42.00 bkl 44.40 bkl Turkseven, Cagatay Han verfasserin aut Effects of Huperzin-A on the Beta-amyloid accumulation in the brain and skeletal muscle cells of a rat model for Alzheimer's disease 2017 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Aims: Alzheimer's Disease (AD) is characterized by a loss of cognitive function and also the accumulation of β-amyloid peptide (βAP) in the brain parenchyma, which plays an important role in this disease. However, it is often also associated with the non-cognitive symptoms such as loss of muscle function (Inclusion-Body Myositis-IBM).Main methods: Sprague-Dawley rats (13 weeks-n=68) were randomly assigned into five groups: Group C: Control; Group D: d-galactose; Group O+D: Bilateral oophorectomy+ d-galactose; Group O: Bilateral oophorectomy; Group O+D+H: Bilateral oophorectomy+ d-galactose+Hup-A. Tissue fixation was performed with the perfusion method. The Compound Muscle Action Potential (CMAP) and mechanical muscle activity were recorded using the standard electro-biophysical techniques. Immune staining was performed with specific antibodies, and the pathological changes were examined. RNA was obtained from brain tissue samples with the Trizol Method. Then, the expression data of mature-miRNAs (rno-miR-9-5p, rno-miR-29a-3p, rno-miR-106a-5p, rno-miR-107 and rno-miR-125a-3p), which may be effective in AD, were taken with Real-Time PCR.Key findings: Impairments occurred in behavioral tests of the rats in the O+D group. βAP accumulation and AChE activity increased significantly in the forebrain in the O+D group compared to the C group. It was seen that Huperzine-A (Hup-A) reduced AChE activity and destructed βAP accumulation. There was a significant decrease in the maximum contractile force at different frequencies in the O+D group and in the O group compared to the C group.Significance: It was found that Hup-A contributed to the healing process in rats for damage occurring both in the brain and in the neuro-muscular system. Alzheimer's disease β-amyloid peptide Motor dysfunction Electromyography Huperzine-a Inclusion body myositis Buyukakilli, Belgin verfasserin (orcid)0000-0003-1153-2558 aut Balli, Ebru verfasserin aut Yetkin, Derya verfasserin aut Erdal, Mehmet Emin verfasserin aut Yilmaz, Senay Gorucu verfasserin aut Sahin, Leyla verfasserin aut Enthalten in Life sciences New York, NY [u.a.] : Elsevier Science, 1963 184, Seite 47-57 Online-Ressource (DE-627)320515605 (DE-600)2013911-1 (DE-576)09095503X 1879-0631 nnns volume:184 pages:47-57 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-BIODIV SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2098 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4313 GBV_ILN_4326 GBV_ILN_4334 GBV_ILN_4338 42.00 Biologie: Allgemeines 44.40 Pharmazie Pharmazeutika AR 184 47-57 |
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Alzheimer's disease β-amyloid peptide Motor dysfunction Electromyography Huperzine-a Inclusion body myositis |
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Turkseven, Cagatay Han @@aut@@ Buyukakilli, Belgin @@aut@@ Balli, Ebru @@aut@@ Yetkin, Derya @@aut@@ Erdal, Mehmet Emin @@aut@@ Yilmaz, Senay Gorucu @@aut@@ Sahin, Leyla @@aut@@ |
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Turkseven, Cagatay Han |
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Turkseven, Cagatay Han ddc 570 fid BIODIV bkl 42.00 bkl 44.40 misc Alzheimer's disease misc β-amyloid peptide misc Motor dysfunction misc Electromyography misc Huperzine-a misc Inclusion body myositis Effects of Huperzin-A on the Beta-amyloid accumulation in the brain and skeletal muscle cells of a rat model for Alzheimer's disease |
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570 DE-600 BIODIV DE-30 fid 42.00 bkl 44.40 bkl Effects of Huperzin-A on the Beta-amyloid accumulation in the brain and skeletal muscle cells of a rat model for Alzheimer's disease Alzheimer's disease β-amyloid peptide Motor dysfunction Electromyography Huperzine-a Inclusion body myositis |
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Effects of Huperzin-A on the Beta-amyloid accumulation in the brain and skeletal muscle cells of a rat model for Alzheimer's disease |
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Effects of Huperzin-A on the Beta-amyloid accumulation in the brain and skeletal muscle cells of a rat model for Alzheimer's disease |
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Turkseven, Cagatay Han Buyukakilli, Belgin Balli, Ebru Yetkin, Derya Erdal, Mehmet Emin Yilmaz, Senay Gorucu Sahin, Leyla |
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effects of huperzin-a on the beta-amyloid accumulation in the brain and skeletal muscle cells of a rat model for alzheimer's disease |
title_auth |
Effects of Huperzin-A on the Beta-amyloid accumulation in the brain and skeletal muscle cells of a rat model for Alzheimer's disease |
abstract |
Aims: Alzheimer's Disease (AD) is characterized by a loss of cognitive function and also the accumulation of β-amyloid peptide (βAP) in the brain parenchyma, which plays an important role in this disease. However, it is often also associated with the non-cognitive symptoms such as loss of muscle function (Inclusion-Body Myositis-IBM).Main methods: Sprague-Dawley rats (13 weeks-n=68) were randomly assigned into five groups: Group C: Control; Group D: d-galactose; Group O+D: Bilateral oophorectomy+ d-galactose; Group O: Bilateral oophorectomy; Group O+D+H: Bilateral oophorectomy+ d-galactose+Hup-A. Tissue fixation was performed with the perfusion method. The Compound Muscle Action Potential (CMAP) and mechanical muscle activity were recorded using the standard electro-biophysical techniques. Immune staining was performed with specific antibodies, and the pathological changes were examined. RNA was obtained from brain tissue samples with the Trizol Method. Then, the expression data of mature-miRNAs (rno-miR-9-5p, rno-miR-29a-3p, rno-miR-106a-5p, rno-miR-107 and rno-miR-125a-3p), which may be effective in AD, were taken with Real-Time PCR.Key findings: Impairments occurred in behavioral tests of the rats in the O+D group. βAP accumulation and AChE activity increased significantly in the forebrain in the O+D group compared to the C group. It was seen that Huperzine-A (Hup-A) reduced AChE activity and destructed βAP accumulation. There was a significant decrease in the maximum contractile force at different frequencies in the O+D group and in the O group compared to the C group.Significance: It was found that Hup-A contributed to the healing process in rats for damage occurring both in the brain and in the neuro-muscular system. |
abstractGer |
Aims: Alzheimer's Disease (AD) is characterized by a loss of cognitive function and also the accumulation of β-amyloid peptide (βAP) in the brain parenchyma, which plays an important role in this disease. However, it is often also associated with the non-cognitive symptoms such as loss of muscle function (Inclusion-Body Myositis-IBM).Main methods: Sprague-Dawley rats (13 weeks-n=68) were randomly assigned into five groups: Group C: Control; Group D: d-galactose; Group O+D: Bilateral oophorectomy+ d-galactose; Group O: Bilateral oophorectomy; Group O+D+H: Bilateral oophorectomy+ d-galactose+Hup-A. Tissue fixation was performed with the perfusion method. The Compound Muscle Action Potential (CMAP) and mechanical muscle activity were recorded using the standard electro-biophysical techniques. Immune staining was performed with specific antibodies, and the pathological changes were examined. RNA was obtained from brain tissue samples with the Trizol Method. Then, the expression data of mature-miRNAs (rno-miR-9-5p, rno-miR-29a-3p, rno-miR-106a-5p, rno-miR-107 and rno-miR-125a-3p), which may be effective in AD, were taken with Real-Time PCR.Key findings: Impairments occurred in behavioral tests of the rats in the O+D group. βAP accumulation and AChE activity increased significantly in the forebrain in the O+D group compared to the C group. It was seen that Huperzine-A (Hup-A) reduced AChE activity and destructed βAP accumulation. There was a significant decrease in the maximum contractile force at different frequencies in the O+D group and in the O group compared to the C group.Significance: It was found that Hup-A contributed to the healing process in rats for damage occurring both in the brain and in the neuro-muscular system. |
abstract_unstemmed |
Aims: Alzheimer's Disease (AD) is characterized by a loss of cognitive function and also the accumulation of β-amyloid peptide (βAP) in the brain parenchyma, which plays an important role in this disease. However, it is often also associated with the non-cognitive symptoms such as loss of muscle function (Inclusion-Body Myositis-IBM).Main methods: Sprague-Dawley rats (13 weeks-n=68) were randomly assigned into five groups: Group C: Control; Group D: d-galactose; Group O+D: Bilateral oophorectomy+ d-galactose; Group O: Bilateral oophorectomy; Group O+D+H: Bilateral oophorectomy+ d-galactose+Hup-A. Tissue fixation was performed with the perfusion method. The Compound Muscle Action Potential (CMAP) and mechanical muscle activity were recorded using the standard electro-biophysical techniques. Immune staining was performed with specific antibodies, and the pathological changes were examined. RNA was obtained from brain tissue samples with the Trizol Method. Then, the expression data of mature-miRNAs (rno-miR-9-5p, rno-miR-29a-3p, rno-miR-106a-5p, rno-miR-107 and rno-miR-125a-3p), which may be effective in AD, were taken with Real-Time PCR.Key findings: Impairments occurred in behavioral tests of the rats in the O+D group. βAP accumulation and AChE activity increased significantly in the forebrain in the O+D group compared to the C group. It was seen that Huperzine-A (Hup-A) reduced AChE activity and destructed βAP accumulation. There was a significant decrease in the maximum contractile force at different frequencies in the O+D group and in the O group compared to the C group.Significance: It was found that Hup-A contributed to the healing process in rats for damage occurring both in the brain and in the neuro-muscular system. |
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Effects of Huperzin-A on the Beta-amyloid accumulation in the brain and skeletal muscle cells of a rat model for Alzheimer's disease |
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However, it is often also associated with the non-cognitive symptoms such as loss of muscle function (Inclusion-Body Myositis-IBM).Main methods: Sprague-Dawley rats (13 weeks-n=68) were randomly assigned into five groups: Group C: Control; Group D: d-galactose; Group O+D: Bilateral oophorectomy+ d-galactose; Group O: Bilateral oophorectomy; Group O+D+H: Bilateral oophorectomy+ d-galactose+Hup-A. Tissue fixation was performed with the perfusion method. The Compound Muscle Action Potential (CMAP) and mechanical muscle activity were recorded using the standard electro-biophysical techniques. Immune staining was performed with specific antibodies, and the pathological changes were examined. RNA was obtained from brain tissue samples with the Trizol Method. Then, the expression data of mature-miRNAs (rno-miR-9-5p, rno-miR-29a-3p, rno-miR-106a-5p, rno-miR-107 and rno-miR-125a-3p), which may be effective in AD, were taken with Real-Time PCR.Key findings: Impairments occurred in behavioral tests of the rats in the O+D group. βAP accumulation and AChE activity increased significantly in the forebrain in the O+D group compared to the C group. It was seen that Huperzine-A (Hup-A) reduced AChE activity and destructed βAP accumulation. There was a significant decrease in the maximum contractile force at different frequencies in the O+D group and in the O group compared to the C group.Significance: It was found that Hup-A contributed to the healing process in rats for damage occurring both in the brain and in the neuro-muscular system.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Alzheimer's disease</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">β-amyloid peptide</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Motor dysfunction</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Electromyography</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Huperzine-a</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Inclusion body myositis</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Buyukakilli, 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