IKKβ Alleviates Neuron Injury in Alzheimer’s Disease via Regulating Autophagy and RIPK1-Mediated Necroptosis
Alzheimer’s disease (AD), featured with memory loss and multiple cognitive impairments, is a devastating neurodegenerative disease that affects millions of people in the world, especially the elder people. IKKβ plays important role in the development of neurodegenerative diseases. However, the molec...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Wang, Wei [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2022 |
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| Schlagwörter: |
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| Anmerkung: |
© The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021 |
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| Übergeordnetes Werk: |
Enthalten in: Molecular neurobiology - Totowa, NJ : Humana Press, 1987, 59(2022), 4 vom: 27. Jan., Seite 2407-2423 |
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| Übergeordnetes Werk: |
volume:59 ; year:2022 ; number:4 ; day:27 ; month:01 ; pages:2407-2423 |
| Links: |
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| DOI / URN: |
10.1007/s12035-021-02652-y |
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| Katalog-ID: |
SPR046785175 |
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| 520 | |a Alzheimer’s disease (AD), featured with memory loss and multiple cognitive impairments, is a devastating neurodegenerative disease that affects millions of people in the world, especially the elder people. IKKβ plays important role in the development of neurodegenerative diseases. However, the molecular mechanism of IKKβ, especially related with autophagy and necroptosis, in AD, is still unclear. Here, we studied the function of IKKβ in regulating autophagy and RIPK1-induced necroptosis in SH-SY5Y cells and APP/PS1 mice. By silencing IKKβ in the SH-SY5Y cells, we found that inhibition of IKKβ could promote the RIPK1-induced necroptosis caused by Aβ accumulation as well as suppress the autophagy of SH-SY5Y cells. Furthermore, we discovered that autophagy was significantly enhanced, and RIPK1-induced necroptosis was inhibited when IKKβ was constitutively activated in SH-SY5Y cells. Then, using APP/PS1 mouse model, we demonstrated that silencing IKKβ could significantly enhance the accumulation of Aβ but have not impact on the mice behavior and cognitive ability. Even the controversial results about the role of IKKβ in AD is not fully understood, our results might provide an important potential therapeutic target for slowing AD. Graphical abstract . | ||
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10.1007/s12035-021-02652-y doi (DE-627)SPR046785175 (SPR)s12035-021-02652-y-e DE-627 ger DE-627 rakwb eng Wang, Wei verfasserin aut IKKβ Alleviates Neuron Injury in Alzheimer’s Disease via Regulating Autophagy and RIPK1-Mediated Necroptosis 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021 Alzheimer’s disease (AD), featured with memory loss and multiple cognitive impairments, is a devastating neurodegenerative disease that affects millions of people in the world, especially the elder people. IKKβ plays important role in the development of neurodegenerative diseases. However, the molecular mechanism of IKKβ, especially related with autophagy and necroptosis, in AD, is still unclear. Here, we studied the function of IKKβ in regulating autophagy and RIPK1-induced necroptosis in SH-SY5Y cells and APP/PS1 mice. By silencing IKKβ in the SH-SY5Y cells, we found that inhibition of IKKβ could promote the RIPK1-induced necroptosis caused by Aβ accumulation as well as suppress the autophagy of SH-SY5Y cells. Furthermore, we discovered that autophagy was significantly enhanced, and RIPK1-induced necroptosis was inhibited when IKKβ was constitutively activated in SH-SY5Y cells. Then, using APP/PS1 mouse model, we demonstrated that silencing IKKβ could significantly enhance the accumulation of Aβ but have not impact on the mice behavior and cognitive ability. Even the controversial results about the role of IKKβ in AD is not fully understood, our results might provide an important potential therapeutic target for slowing AD. Graphical abstract . Alzheimer’s disease (dpeaa)DE-He213 IKKβ (dpeaa)DE-He213 RIPK1 (dpeaa)DE-He213 Necroptosis (dpeaa)DE-He213 Autophagy (dpeaa)DE-He213 Gu, Xunhu aut Cheng, Zhijuan aut Lu, Xiaoqing aut Xie, Shuhua aut Liu, Xu (orcid)0000-0002-3913-7720 aut Enthalten in Molecular neurobiology Totowa, NJ : Humana Press, 1987 59(2022), 4 vom: 27. Jan., Seite 2407-2423 (DE-627)34858444X (DE-600)2079384-4 1559-1182 nnns volume:59 year:2022 number:4 day:27 month:01 pages:2407-2423 https://dx.doi.org/10.1007/s12035-021-02652-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 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_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 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_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 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_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 59 2022 4 27 01 2407-2423 |
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10.1007/s12035-021-02652-y doi (DE-627)SPR046785175 (SPR)s12035-021-02652-y-e DE-627 ger DE-627 rakwb eng Wang, Wei verfasserin aut IKKβ Alleviates Neuron Injury in Alzheimer’s Disease via Regulating Autophagy and RIPK1-Mediated Necroptosis 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021 Alzheimer’s disease (AD), featured with memory loss and multiple cognitive impairments, is a devastating neurodegenerative disease that affects millions of people in the world, especially the elder people. IKKβ plays important role in the development of neurodegenerative diseases. However, the molecular mechanism of IKKβ, especially related with autophagy and necroptosis, in AD, is still unclear. Here, we studied the function of IKKβ in regulating autophagy and RIPK1-induced necroptosis in SH-SY5Y cells and APP/PS1 mice. By silencing IKKβ in the SH-SY5Y cells, we found that inhibition of IKKβ could promote the RIPK1-induced necroptosis caused by Aβ accumulation as well as suppress the autophagy of SH-SY5Y cells. Furthermore, we discovered that autophagy was significantly enhanced, and RIPK1-induced necroptosis was inhibited when IKKβ was constitutively activated in SH-SY5Y cells. Then, using APP/PS1 mouse model, we demonstrated that silencing IKKβ could significantly enhance the accumulation of Aβ but have not impact on the mice behavior and cognitive ability. Even the controversial results about the role of IKKβ in AD is not fully understood, our results might provide an important potential therapeutic target for slowing AD. Graphical abstract . Alzheimer’s disease (dpeaa)DE-He213 IKKβ (dpeaa)DE-He213 RIPK1 (dpeaa)DE-He213 Necroptosis (dpeaa)DE-He213 Autophagy (dpeaa)DE-He213 Gu, Xunhu aut Cheng, Zhijuan aut Lu, Xiaoqing aut Xie, Shuhua aut Liu, Xu (orcid)0000-0002-3913-7720 aut Enthalten in Molecular neurobiology Totowa, NJ : Humana Press, 1987 59(2022), 4 vom: 27. Jan., Seite 2407-2423 (DE-627)34858444X (DE-600)2079384-4 1559-1182 nnns volume:59 year:2022 number:4 day:27 month:01 pages:2407-2423 https://dx.doi.org/10.1007/s12035-021-02652-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 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_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 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_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 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_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 59 2022 4 27 01 2407-2423 |
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10.1007/s12035-021-02652-y doi (DE-627)SPR046785175 (SPR)s12035-021-02652-y-e DE-627 ger DE-627 rakwb eng Wang, Wei verfasserin aut IKKβ Alleviates Neuron Injury in Alzheimer’s Disease via Regulating Autophagy and RIPK1-Mediated Necroptosis 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021 Alzheimer’s disease (AD), featured with memory loss and multiple cognitive impairments, is a devastating neurodegenerative disease that affects millions of people in the world, especially the elder people. IKKβ plays important role in the development of neurodegenerative diseases. However, the molecular mechanism of IKKβ, especially related with autophagy and necroptosis, in AD, is still unclear. Here, we studied the function of IKKβ in regulating autophagy and RIPK1-induced necroptosis in SH-SY5Y cells and APP/PS1 mice. By silencing IKKβ in the SH-SY5Y cells, we found that inhibition of IKKβ could promote the RIPK1-induced necroptosis caused by Aβ accumulation as well as suppress the autophagy of SH-SY5Y cells. Furthermore, we discovered that autophagy was significantly enhanced, and RIPK1-induced necroptosis was inhibited when IKKβ was constitutively activated in SH-SY5Y cells. Then, using APP/PS1 mouse model, we demonstrated that silencing IKKβ could significantly enhance the accumulation of Aβ but have not impact on the mice behavior and cognitive ability. Even the controversial results about the role of IKKβ in AD is not fully understood, our results might provide an important potential therapeutic target for slowing AD. Graphical abstract . Alzheimer’s disease (dpeaa)DE-He213 IKKβ (dpeaa)DE-He213 RIPK1 (dpeaa)DE-He213 Necroptosis (dpeaa)DE-He213 Autophagy (dpeaa)DE-He213 Gu, Xunhu aut Cheng, Zhijuan aut Lu, Xiaoqing aut Xie, Shuhua aut Liu, Xu (orcid)0000-0002-3913-7720 aut Enthalten in Molecular neurobiology Totowa, NJ : Humana Press, 1987 59(2022), 4 vom: 27. Jan., Seite 2407-2423 (DE-627)34858444X (DE-600)2079384-4 1559-1182 nnns volume:59 year:2022 number:4 day:27 month:01 pages:2407-2423 https://dx.doi.org/10.1007/s12035-021-02652-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 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_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 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_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 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_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 59 2022 4 27 01 2407-2423 |
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10.1007/s12035-021-02652-y doi (DE-627)SPR046785175 (SPR)s12035-021-02652-y-e DE-627 ger DE-627 rakwb eng Wang, Wei verfasserin aut IKKβ Alleviates Neuron Injury in Alzheimer’s Disease via Regulating Autophagy and RIPK1-Mediated Necroptosis 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021 Alzheimer’s disease (AD), featured with memory loss and multiple cognitive impairments, is a devastating neurodegenerative disease that affects millions of people in the world, especially the elder people. IKKβ plays important role in the development of neurodegenerative diseases. However, the molecular mechanism of IKKβ, especially related with autophagy and necroptosis, in AD, is still unclear. Here, we studied the function of IKKβ in regulating autophagy and RIPK1-induced necroptosis in SH-SY5Y cells and APP/PS1 mice. By silencing IKKβ in the SH-SY5Y cells, we found that inhibition of IKKβ could promote the RIPK1-induced necroptosis caused by Aβ accumulation as well as suppress the autophagy of SH-SY5Y cells. Furthermore, we discovered that autophagy was significantly enhanced, and RIPK1-induced necroptosis was inhibited when IKKβ was constitutively activated in SH-SY5Y cells. Then, using APP/PS1 mouse model, we demonstrated that silencing IKKβ could significantly enhance the accumulation of Aβ but have not impact on the mice behavior and cognitive ability. Even the controversial results about the role of IKKβ in AD is not fully understood, our results might provide an important potential therapeutic target for slowing AD. Graphical abstract . Alzheimer’s disease (dpeaa)DE-He213 IKKβ (dpeaa)DE-He213 RIPK1 (dpeaa)DE-He213 Necroptosis (dpeaa)DE-He213 Autophagy (dpeaa)DE-He213 Gu, Xunhu aut Cheng, Zhijuan aut Lu, Xiaoqing aut Xie, Shuhua aut Liu, Xu (orcid)0000-0002-3913-7720 aut Enthalten in Molecular neurobiology Totowa, NJ : Humana Press, 1987 59(2022), 4 vom: 27. Jan., Seite 2407-2423 (DE-627)34858444X (DE-600)2079384-4 1559-1182 nnns volume:59 year:2022 number:4 day:27 month:01 pages:2407-2423 https://dx.doi.org/10.1007/s12035-021-02652-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 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_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 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_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 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_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 59 2022 4 27 01 2407-2423 |
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10.1007/s12035-021-02652-y doi (DE-627)SPR046785175 (SPR)s12035-021-02652-y-e DE-627 ger DE-627 rakwb eng Wang, Wei verfasserin aut IKKβ Alleviates Neuron Injury in Alzheimer’s Disease via Regulating Autophagy and RIPK1-Mediated Necroptosis 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021 Alzheimer’s disease (AD), featured with memory loss and multiple cognitive impairments, is a devastating neurodegenerative disease that affects millions of people in the world, especially the elder people. IKKβ plays important role in the development of neurodegenerative diseases. However, the molecular mechanism of IKKβ, especially related with autophagy and necroptosis, in AD, is still unclear. Here, we studied the function of IKKβ in regulating autophagy and RIPK1-induced necroptosis in SH-SY5Y cells and APP/PS1 mice. By silencing IKKβ in the SH-SY5Y cells, we found that inhibition of IKKβ could promote the RIPK1-induced necroptosis caused by Aβ accumulation as well as suppress the autophagy of SH-SY5Y cells. Furthermore, we discovered that autophagy was significantly enhanced, and RIPK1-induced necroptosis was inhibited when IKKβ was constitutively activated in SH-SY5Y cells. Then, using APP/PS1 mouse model, we demonstrated that silencing IKKβ could significantly enhance the accumulation of Aβ but have not impact on the mice behavior and cognitive ability. Even the controversial results about the role of IKKβ in AD is not fully understood, our results might provide an important potential therapeutic target for slowing AD. Graphical abstract . Alzheimer’s disease (dpeaa)DE-He213 IKKβ (dpeaa)DE-He213 RIPK1 (dpeaa)DE-He213 Necroptosis (dpeaa)DE-He213 Autophagy (dpeaa)DE-He213 Gu, Xunhu aut Cheng, Zhijuan aut Lu, Xiaoqing aut Xie, Shuhua aut Liu, Xu (orcid)0000-0002-3913-7720 aut Enthalten in Molecular neurobiology Totowa, NJ : Humana Press, 1987 59(2022), 4 vom: 27. Jan., Seite 2407-2423 (DE-627)34858444X (DE-600)2079384-4 1559-1182 nnns volume:59 year:2022 number:4 day:27 month:01 pages:2407-2423 https://dx.doi.org/10.1007/s12035-021-02652-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 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_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 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_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 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_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 59 2022 4 27 01 2407-2423 |
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Enthalten in Molecular neurobiology 59(2022), 4 vom: 27. Jan., Seite 2407-2423 volume:59 year:2022 number:4 day:27 month:01 pages:2407-2423 |
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Wang, Wei @@aut@@ Gu, Xunhu @@aut@@ Cheng, Zhijuan @@aut@@ Lu, Xiaoqing @@aut@@ Xie, Shuhua @@aut@@ Liu, Xu @@aut@@ |
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IKKβ plays important role in the development of neurodegenerative diseases. However, the molecular mechanism of IKKβ, especially related with autophagy and necroptosis, in AD, is still unclear. Here, we studied the function of IKKβ in regulating autophagy and RIPK1-induced necroptosis in SH-SY5Y cells and APP/PS1 mice. By silencing IKKβ in the SH-SY5Y cells, we found that inhibition of IKKβ could promote the RIPK1-induced necroptosis caused by Aβ accumulation as well as suppress the autophagy of SH-SY5Y cells. Furthermore, we discovered that autophagy was significantly enhanced, and RIPK1-induced necroptosis was inhibited when IKKβ was constitutively activated in SH-SY5Y cells. Then, using APP/PS1 mouse model, we demonstrated that silencing IKKβ could significantly enhance the accumulation of Aβ but have not impact on the mice behavior and cognitive ability. Even the controversial results about the role of IKKβ in AD is not fully understood, our results might provide an important potential therapeutic target for slowing AD. 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Wang, Wei |
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Wang, Wei misc Alzheimer’s disease misc IKKβ misc RIPK1 misc Necroptosis misc Autophagy IKKβ Alleviates Neuron Injury in Alzheimer’s Disease via Regulating Autophagy and RIPK1-Mediated Necroptosis |
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IKKβ Alleviates Neuron Injury in Alzheimer’s Disease via Regulating Autophagy and RIPK1-Mediated Necroptosis Alzheimer’s disease (dpeaa)DE-He213 IKKβ (dpeaa)DE-He213 RIPK1 (dpeaa)DE-He213 Necroptosis (dpeaa)DE-He213 Autophagy (dpeaa)DE-He213 |
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misc Alzheimer’s disease misc IKKβ misc RIPK1 misc Necroptosis misc Autophagy |
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IKKβ Alleviates Neuron Injury in Alzheimer’s Disease via Regulating Autophagy and RIPK1-Mediated Necroptosis |
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ikkβ alleviates neuron injury in alzheimer’s disease via regulating autophagy and ripk1-mediated necroptosis |
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IKKβ Alleviates Neuron Injury in Alzheimer’s Disease via Regulating Autophagy and RIPK1-Mediated Necroptosis |
| abstract |
Alzheimer’s disease (AD), featured with memory loss and multiple cognitive impairments, is a devastating neurodegenerative disease that affects millions of people in the world, especially the elder people. IKKβ plays important role in the development of neurodegenerative diseases. However, the molecular mechanism of IKKβ, especially related with autophagy and necroptosis, in AD, is still unclear. Here, we studied the function of IKKβ in regulating autophagy and RIPK1-induced necroptosis in SH-SY5Y cells and APP/PS1 mice. By silencing IKKβ in the SH-SY5Y cells, we found that inhibition of IKKβ could promote the RIPK1-induced necroptosis caused by Aβ accumulation as well as suppress the autophagy of SH-SY5Y cells. Furthermore, we discovered that autophagy was significantly enhanced, and RIPK1-induced necroptosis was inhibited when IKKβ was constitutively activated in SH-SY5Y cells. Then, using APP/PS1 mouse model, we demonstrated that silencing IKKβ could significantly enhance the accumulation of Aβ but have not impact on the mice behavior and cognitive ability. Even the controversial results about the role of IKKβ in AD is not fully understood, our results might provide an important potential therapeutic target for slowing AD. Graphical abstract . © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021 |
| abstractGer |
Alzheimer’s disease (AD), featured with memory loss and multiple cognitive impairments, is a devastating neurodegenerative disease that affects millions of people in the world, especially the elder people. IKKβ plays important role in the development of neurodegenerative diseases. However, the molecular mechanism of IKKβ, especially related with autophagy and necroptosis, in AD, is still unclear. Here, we studied the function of IKKβ in regulating autophagy and RIPK1-induced necroptosis in SH-SY5Y cells and APP/PS1 mice. By silencing IKKβ in the SH-SY5Y cells, we found that inhibition of IKKβ could promote the RIPK1-induced necroptosis caused by Aβ accumulation as well as suppress the autophagy of SH-SY5Y cells. Furthermore, we discovered that autophagy was significantly enhanced, and RIPK1-induced necroptosis was inhibited when IKKβ was constitutively activated in SH-SY5Y cells. Then, using APP/PS1 mouse model, we demonstrated that silencing IKKβ could significantly enhance the accumulation of Aβ but have not impact on the mice behavior and cognitive ability. Even the controversial results about the role of IKKβ in AD is not fully understood, our results might provide an important potential therapeutic target for slowing AD. Graphical abstract . © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021 |
| abstract_unstemmed |
Alzheimer’s disease (AD), featured with memory loss and multiple cognitive impairments, is a devastating neurodegenerative disease that affects millions of people in the world, especially the elder people. IKKβ plays important role in the development of neurodegenerative diseases. However, the molecular mechanism of IKKβ, especially related with autophagy and necroptosis, in AD, is still unclear. Here, we studied the function of IKKβ in regulating autophagy and RIPK1-induced necroptosis in SH-SY5Y cells and APP/PS1 mice. By silencing IKKβ in the SH-SY5Y cells, we found that inhibition of IKKβ could promote the RIPK1-induced necroptosis caused by Aβ accumulation as well as suppress the autophagy of SH-SY5Y cells. Furthermore, we discovered that autophagy was significantly enhanced, and RIPK1-induced necroptosis was inhibited when IKKβ was constitutively activated in SH-SY5Y cells. Then, using APP/PS1 mouse model, we demonstrated that silencing IKKβ could significantly enhance the accumulation of Aβ but have not impact on the mice behavior and cognitive ability. Even the controversial results about the role of IKKβ in AD is not fully understood, our results might provide an important potential therapeutic target for slowing AD. Graphical abstract . © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021 |
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IKKβ Alleviates Neuron Injury in Alzheimer’s Disease via Regulating Autophagy and RIPK1-Mediated Necroptosis |
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https://dx.doi.org/10.1007/s12035-021-02652-y |
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Gu, Xunhu Cheng, Zhijuan Lu, Xiaoqing Xie, Shuhua Liu, Xu |
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2024-07-04T00:23:21.242Z |
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| score |
7.3985615 |