Curcumin Improves Neurogenesis in Alzheimer's Disease Mice via the Upregulation of Wnt/β-Catenin and BDNF
Adult neurogenesis in the dentate gyrus (DG) is impaired during Alzheimer's disease (AD) progression. Curcumin has been reported to reduce cell apoptosis and stimulate neurogenesis. This study aimed to investigate the influence of curcumin on adult neurogenesis in AD mice and its potential mech...
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| Veröffentlicht in: | International journal of molecular sciences 2024-05, Vol.25 (10), p.5123 |
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| creator | Lou, Shengchun Gong, Danfeng Yang, Mengting Qiu, Qing Luo, Jialie Chen, Tingting |
| description | Adult neurogenesis in the dentate gyrus (DG) is impaired during Alzheimer's disease (AD) progression. Curcumin has been reported to reduce cell apoptosis and stimulate neurogenesis. This study aimed to investigate the influence of curcumin on adult neurogenesis in AD mice and its potential mechanism. Two-month-old male C57BL/6J mice were injected with soluble β-amyloid (Aβ
) using lateral ventricle stereolocalization to establish AD models. An immunofluorescence assay, including bromodeoxyuridine (BrdU), doublecortin (DCX), and neuron-specific nuclear antigen (NeuN), was used to detect hippocampal neurogenesis. Western blot and an enzyme-linked immunosorbent assay (ELISA) were used to test the expression of related proteins and the secretion of brain-derived neurotrophic factor (BDNF). A Morris water maze was used to detect the cognitive function of the mice. Our results showed that curcumin administration (100 mg/kg) rescued the impaired neurogenesis of Aβ
mice, shown as enhanced BrdU
/DCX
and BrdU
/NeuN
cells in DG. In addition, curcumin regulated the phosphatidylinositol 3 kinase (PI3K)/protein kinase B (Akt) -mediated glycogen synthase kinase-3β (GSK3β) /Wingless/Integrated (Wnt)/β-catenin pathway and cyclic adenosine monophosphate response element-binding protein (CREB)/BDNF in Aβ
mice. Inhibiting Wnt/β-catenin and depriving BDNF could reverse both the upregulated neurogenesis and cognitive function of curcumin-treated Aβ
mice. In conclusion, our study indicates that curcumin, through targeting PI3K/Akt, regulates GSK3β/Wnt/β-catenin and CREB/BDNF pathways, improving the adult neurogenesis of AD mice. |
| doi_str_mv | 10.3390/ijms25105123 |
| format | Article |
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) using lateral ventricle stereolocalization to establish AD models. An immunofluorescence assay, including bromodeoxyuridine (BrdU), doublecortin (DCX), and neuron-specific nuclear antigen (NeuN), was used to detect hippocampal neurogenesis. Western blot and an enzyme-linked immunosorbent assay (ELISA) were used to test the expression of related proteins and the secretion of brain-derived neurotrophic factor (BDNF). A Morris water maze was used to detect the cognitive function of the mice. Our results showed that curcumin administration (100 mg/kg) rescued the impaired neurogenesis of Aβ
mice, shown as enhanced BrdU
/DCX
and BrdU
/NeuN
cells in DG. In addition, curcumin regulated the phosphatidylinositol 3 kinase (PI3K)/protein kinase B (Akt) -mediated glycogen synthase kinase-3β (GSK3β) /Wingless/Integrated (Wnt)/β-catenin pathway and cyclic adenosine monophosphate response element-binding protein (CREB)/BDNF in Aβ
mice. Inhibiting Wnt/β-catenin and depriving BDNF could reverse both the upregulated neurogenesis and cognitive function of curcumin-treated Aβ
mice. In conclusion, our study indicates that curcumin, through targeting PI3K/Akt, regulates GSK3β/Wnt/β-catenin and CREB/BDNF pathways, improving the adult neurogenesis of AD mice.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms25105123</identifier><identifier>PMID: 38791161</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Advertising executives ; Alzheimer Disease - drug therapy ; Alzheimer Disease - metabolism ; Alzheimer's disease ; Amyloid beta-Peptides - metabolism ; Animals ; beta Catenin - metabolism ; Brain-derived neurotrophic factor ; Brain-Derived Neurotrophic Factor - metabolism ; Curcumin - pharmacology ; Disease ; Disease Models, Animal ; Diseases ; Doublecortin Protein - metabolism ; Ethylenediaminetetraacetic acid ; Hippocampus - drug effects ; Hippocampus - metabolism ; Kinases ; Male ; Mice ; Mice, Inbred C57BL ; Morphology ; Neurogenesis ; Neurogenesis - drug effects ; Neurons ; Phosphorylation ; Proteins ; Proto-Oncogene Proteins c-akt - metabolism ; Stem cells ; Up-Regulation - drug effects ; Wnt Signaling Pathway - drug effects</subject><ispartof>International journal of molecular sciences, 2024-05, Vol.25 (10), p.5123</ispartof><rights>COPYRIGHT 2024 MDPI AG</rights><rights>2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c381t-2441a056be4f6a4c73f7eb0de31e5da38f2fb734b03cca495cf956a7b08fe3503</cites><orcidid>0000-0001-8728-2335 ; 0009-0004-3637-1329</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38791161$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lou, Shengchun</creatorcontrib><creatorcontrib>Gong, Danfeng</creatorcontrib><creatorcontrib>Yang, Mengting</creatorcontrib><creatorcontrib>Qiu, Qing</creatorcontrib><creatorcontrib>Luo, Jialie</creatorcontrib><creatorcontrib>Chen, Tingting</creatorcontrib><title>Curcumin Improves Neurogenesis in Alzheimer's Disease Mice via the Upregulation of Wnt/β-Catenin and BDNF</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Adult neurogenesis in the dentate gyrus (DG) is impaired during Alzheimer's disease (AD) progression. Curcumin has been reported to reduce cell apoptosis and stimulate neurogenesis. This study aimed to investigate the influence of curcumin on adult neurogenesis in AD mice and its potential mechanism. Two-month-old male C57BL/6J mice were injected with soluble β-amyloid (Aβ
) using lateral ventricle stereolocalization to establish AD models. An immunofluorescence assay, including bromodeoxyuridine (BrdU), doublecortin (DCX), and neuron-specific nuclear antigen (NeuN), was used to detect hippocampal neurogenesis. Western blot and an enzyme-linked immunosorbent assay (ELISA) were used to test the expression of related proteins and the secretion of brain-derived neurotrophic factor (BDNF). A Morris water maze was used to detect the cognitive function of the mice. Our results showed that curcumin administration (100 mg/kg) rescued the impaired neurogenesis of Aβ
mice, shown as enhanced BrdU
/DCX
and BrdU
/NeuN
cells in DG. In addition, curcumin regulated the phosphatidylinositol 3 kinase (PI3K)/protein kinase B (Akt) -mediated glycogen synthase kinase-3β (GSK3β) /Wingless/Integrated (Wnt)/β-catenin pathway and cyclic adenosine monophosphate response element-binding protein (CREB)/BDNF in Aβ
mice. Inhibiting Wnt/β-catenin and depriving BDNF could reverse both the upregulated neurogenesis and cognitive function of curcumin-treated Aβ
mice. In conclusion, our study indicates that curcumin, through targeting PI3K/Akt, regulates GSK3β/Wnt/β-catenin and CREB/BDNF pathways, improving the adult neurogenesis of AD mice.</description><subject>Advertising executives</subject><subject>Alzheimer Disease - drug therapy</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer's disease</subject><subject>Amyloid beta-Peptides - metabolism</subject><subject>Animals</subject><subject>beta Catenin - metabolism</subject><subject>Brain-derived neurotrophic factor</subject><subject>Brain-Derived Neurotrophic Factor - metabolism</subject><subject>Curcumin - pharmacology</subject><subject>Disease</subject><subject>Disease Models, Animal</subject><subject>Diseases</subject><subject>Doublecortin Protein - metabolism</subject><subject>Ethylenediaminetetraacetic acid</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - metabolism</subject><subject>Kinases</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Morphology</subject><subject>Neurogenesis</subject><subject>Neurogenesis - drug effects</subject><subject>Neurons</subject><subject>Phosphorylation</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Stem cells</subject><subject>Up-Regulation - drug effects</subject><subject>Wnt Signaling Pathway - drug effects</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptkc1u1DAUhS0Eoj-wY40ssYAFaa9z43iyHKYUKpWyoWIZOc711KPEHuykEjxWH4RnwtUMqCDkha3r7xydq8PYCwEniA2cus2YSilAihIfsUNRlWUBUKvHD94H7CilDUCJpWyesgNcqEaIWhyyzWqOZh6d5xfjNoZbSvyK5hjW5Cm5xPPHcvhxQ26k-DrxM5dIJ-KfnCF-6zSfbohfbyOt50FPLngeLP_qp9Ofd8VKT-SzXvuevzu7On_Gnlg9JHq-v4_Z9fn7L6uPxeXnDxer5WVhcCGmoqwqoUHWHVW21pVRaBV10BMKkr3GhS1tp7DqAI3RVSONbWStVQcLSygBj9mbnW_e59tMaWpHlwwNg_YU5tQi1IAKFYiMvvoH3YQ5-pwuU7KpUOwM99RaD9Q6b8MUtbk3bZeqkdjUAlSmTv5D5dPT6EzwZF2e_yV4uxOYGFKKZNttdKOO31sB7X217cNqM_5yn3XuRur_wL-7xF-X9p12</recordid><startdate>20240508</startdate><enddate>20240508</enddate><creator>Lou, Shengchun</creator><creator>Gong, Danfeng</creator><creator>Yang, Mengting</creator><creator>Qiu, Qing</creator><creator>Luo, Jialie</creator><creator>Chen, Tingting</creator><general>MDPI AG</general><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-8728-2335</orcidid><orcidid>https://orcid.org/0009-0004-3637-1329</orcidid></search><sort><creationdate>20240508</creationdate><title>Curcumin Improves Neurogenesis in Alzheimer's Disease Mice via the Upregulation of Wnt/β-Catenin and BDNF</title><author>Lou, Shengchun ; 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Curcumin has been reported to reduce cell apoptosis and stimulate neurogenesis. This study aimed to investigate the influence of curcumin on adult neurogenesis in AD mice and its potential mechanism. Two-month-old male C57BL/6J mice were injected with soluble β-amyloid (Aβ
) using lateral ventricle stereolocalization to establish AD models. An immunofluorescence assay, including bromodeoxyuridine (BrdU), doublecortin (DCX), and neuron-specific nuclear antigen (NeuN), was used to detect hippocampal neurogenesis. Western blot and an enzyme-linked immunosorbent assay (ELISA) were used to test the expression of related proteins and the secretion of brain-derived neurotrophic factor (BDNF). A Morris water maze was used to detect the cognitive function of the mice. Our results showed that curcumin administration (100 mg/kg) rescued the impaired neurogenesis of Aβ
mice, shown as enhanced BrdU
/DCX
and BrdU
/NeuN
cells in DG. In addition, curcumin regulated the phosphatidylinositol 3 kinase (PI3K)/protein kinase B (Akt) -mediated glycogen synthase kinase-3β (GSK3β) /Wingless/Integrated (Wnt)/β-catenin pathway and cyclic adenosine monophosphate response element-binding protein (CREB)/BDNF in Aβ
mice. Inhibiting Wnt/β-catenin and depriving BDNF could reverse both the upregulated neurogenesis and cognitive function of curcumin-treated Aβ
mice. In conclusion, our study indicates that curcumin, through targeting PI3K/Akt, regulates GSK3β/Wnt/β-catenin and CREB/BDNF pathways, improving the adult neurogenesis of AD mice.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>38791161</pmid><doi>10.3390/ijms25105123</doi><orcidid>https://orcid.org/0000-0001-8728-2335</orcidid><orcidid>https://orcid.org/0009-0004-3637-1329</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MDPI - Multidisciplinary Digital Publishing Institute; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Advertising executives Alzheimer Disease - drug therapy Alzheimer Disease - metabolism Alzheimer's disease Amyloid beta-Peptides - metabolism Animals beta Catenin - metabolism Brain-derived neurotrophic factor Brain-Derived Neurotrophic Factor - metabolism Curcumin - pharmacology Disease Disease Models, Animal Diseases Doublecortin Protein - metabolism Ethylenediaminetetraacetic acid Hippocampus - drug effects Hippocampus - metabolism Kinases Male Mice Mice, Inbred C57BL Morphology Neurogenesis Neurogenesis - drug effects Neurons Phosphorylation Proteins Proto-Oncogene Proteins c-akt - metabolism Stem cells Up-Regulation - drug effects Wnt Signaling Pathway - drug effects |
| title | Curcumin Improves Neurogenesis in Alzheimer's Disease Mice via the Upregulation of Wnt/β-Catenin and BDNF |
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