Dendritic/Post-synaptic Tau and Early Pathology of Alzheimer’s Disease
Microtubule-associated protein tau forms insoluble neurofibrillary tangles (NFTs), which is one of the major histopathological hallmarks of Alzheimer’s disease (AD). Many studies have demonstrated that tau causes early functional deficits prior to the formation of neurofibrillary aggregates. The red...
Ausführliche Beschreibung
Autor*in: |
Xiaomin Yin [verfasserIn] Chenhao Zhao [verfasserIn] Yanyan Qiu [verfasserIn] Zheng Zhou [verfasserIn] Junze Bao [verfasserIn] Wei Qian [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2021 |
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Übergeordnetes Werk: |
In: Frontiers in Molecular Neuroscience - Frontiers Media S.A., 2008, 14(2021) |
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Übergeordnetes Werk: |
volume:14 ; year:2021 |
Links: |
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DOI / URN: |
10.3389/fnmol.2021.671779 |
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Katalog-ID: |
DOAJ001420380 |
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10.3389/fnmol.2021.671779 doi (DE-627)DOAJ001420380 (DE-599)DOAJf19bc41c3f604a4a8a8f5295336c4ad6 DE-627 ger DE-627 rakwb eng RC321-571 Xiaomin Yin verfasserin aut Dendritic/Post-synaptic Tau and Early Pathology of Alzheimer’s Disease 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Microtubule-associated protein tau forms insoluble neurofibrillary tangles (NFTs), which is one of the major histopathological hallmarks of Alzheimer’s disease (AD). Many studies have demonstrated that tau causes early functional deficits prior to the formation of neurofibrillary aggregates. The redistribution of tau from axons to the somatodendritic compartment of neurons and dendritic spines causes synaptic impairment, and then leads to the loss of synaptic contacts that correlates better with cognitive deficits than amyloid-β (Aβ) aggregates do in AD patients. In this review, we discuss the underlying mechanisms by which tau is mislocalized to dendritic spines and contributes to synaptic dysfunction in AD. We also discuss the synergistic effects of tau and oligomeric forms of Aβ on promoting synaptic dysfunction in AD. tau Alzheimer’s disease cognitive impairment post-synapse synaptic localization Neurosciences. Biological psychiatry. Neuropsychiatry Xiaomin Yin verfasserin aut Xiaomin Yin verfasserin aut Chenhao Zhao verfasserin aut Yanyan Qiu verfasserin aut Zheng Zhou verfasserin aut Junze Bao verfasserin aut Wei Qian verfasserin aut Wei Qian verfasserin aut Wei Qian verfasserin aut In Frontiers in Molecular Neuroscience Frontiers Media S.A., 2008 14(2021) (DE-627)579826449 (DE-600)2452967-9 16625099 nnns volume:14 year:2021 https://doi.org/10.3389/fnmol.2021.671779 kostenfrei https://doaj.org/article/f19bc41c3f604a4a8a8f5295336c4ad6 kostenfrei https://www.frontiersin.org/articles/10.3389/fnmol.2021.671779/full kostenfrei https://doaj.org/toc/1662-5099 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 2021 |
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10.3389/fnmol.2021.671779 doi (DE-627)DOAJ001420380 (DE-599)DOAJf19bc41c3f604a4a8a8f5295336c4ad6 DE-627 ger DE-627 rakwb eng RC321-571 Xiaomin Yin verfasserin aut Dendritic/Post-synaptic Tau and Early Pathology of Alzheimer’s Disease 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Microtubule-associated protein tau forms insoluble neurofibrillary tangles (NFTs), which is one of the major histopathological hallmarks of Alzheimer’s disease (AD). Many studies have demonstrated that tau causes early functional deficits prior to the formation of neurofibrillary aggregates. The redistribution of tau from axons to the somatodendritic compartment of neurons and dendritic spines causes synaptic impairment, and then leads to the loss of synaptic contacts that correlates better with cognitive deficits than amyloid-β (Aβ) aggregates do in AD patients. In this review, we discuss the underlying mechanisms by which tau is mislocalized to dendritic spines and contributes to synaptic dysfunction in AD. We also discuss the synergistic effects of tau and oligomeric forms of Aβ on promoting synaptic dysfunction in AD. tau Alzheimer’s disease cognitive impairment post-synapse synaptic localization Neurosciences. Biological psychiatry. Neuropsychiatry Xiaomin Yin verfasserin aut Xiaomin Yin verfasserin aut Chenhao Zhao verfasserin aut Yanyan Qiu verfasserin aut Zheng Zhou verfasserin aut Junze Bao verfasserin aut Wei Qian verfasserin aut Wei Qian verfasserin aut Wei Qian verfasserin aut In Frontiers in Molecular Neuroscience Frontiers Media S.A., 2008 14(2021) (DE-627)579826449 (DE-600)2452967-9 16625099 nnns volume:14 year:2021 https://doi.org/10.3389/fnmol.2021.671779 kostenfrei https://doaj.org/article/f19bc41c3f604a4a8a8f5295336c4ad6 kostenfrei https://www.frontiersin.org/articles/10.3389/fnmol.2021.671779/full kostenfrei https://doaj.org/toc/1662-5099 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 2021 |
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Dendritic/Post-synaptic Tau and Early Pathology of Alzheimer’s Disease |
abstract |
Microtubule-associated protein tau forms insoluble neurofibrillary tangles (NFTs), which is one of the major histopathological hallmarks of Alzheimer’s disease (AD). Many studies have demonstrated that tau causes early functional deficits prior to the formation of neurofibrillary aggregates. The redistribution of tau from axons to the somatodendritic compartment of neurons and dendritic spines causes synaptic impairment, and then leads to the loss of synaptic contacts that correlates better with cognitive deficits than amyloid-β (Aβ) aggregates do in AD patients. In this review, we discuss the underlying mechanisms by which tau is mislocalized to dendritic spines and contributes to synaptic dysfunction in AD. We also discuss the synergistic effects of tau and oligomeric forms of Aβ on promoting synaptic dysfunction in AD. |
abstractGer |
Microtubule-associated protein tau forms insoluble neurofibrillary tangles (NFTs), which is one of the major histopathological hallmarks of Alzheimer’s disease (AD). Many studies have demonstrated that tau causes early functional deficits prior to the formation of neurofibrillary aggregates. The redistribution of tau from axons to the somatodendritic compartment of neurons and dendritic spines causes synaptic impairment, and then leads to the loss of synaptic contacts that correlates better with cognitive deficits than amyloid-β (Aβ) aggregates do in AD patients. In this review, we discuss the underlying mechanisms by which tau is mislocalized to dendritic spines and contributes to synaptic dysfunction in AD. We also discuss the synergistic effects of tau and oligomeric forms of Aβ on promoting synaptic dysfunction in AD. |
abstract_unstemmed |
Microtubule-associated protein tau forms insoluble neurofibrillary tangles (NFTs), which is one of the major histopathological hallmarks of Alzheimer’s disease (AD). Many studies have demonstrated that tau causes early functional deficits prior to the formation of neurofibrillary aggregates. The redistribution of tau from axons to the somatodendritic compartment of neurons and dendritic spines causes synaptic impairment, and then leads to the loss of synaptic contacts that correlates better with cognitive deficits than amyloid-β (Aβ) aggregates do in AD patients. In this review, we discuss the underlying mechanisms by which tau is mislocalized to dendritic spines and contributes to synaptic dysfunction in AD. We also discuss the synergistic effects of tau and oligomeric forms of Aβ on promoting synaptic dysfunction in AD. |
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title_short |
Dendritic/Post-synaptic Tau and Early Pathology of Alzheimer’s Disease |
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