Implications of GABAergic neurotransmission in Alzheimer’s disease
Alzheimer’s disease (AD) is characterized pathologically by the deposition of -amyloid peptides (A) and the accumulation of neurofibrillary tangles (NFTs) composed of hyper-phosphorylated tau. Regardless of the pathological hallmarks, synaptic dysfunction is widely accepted as a causal event in AD...
| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2016-02-01
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| Series: | Frontiers in Aging Neuroscience |
| Subjects: | |
| Online Access: | http://journal.frontiersin.org/Journal/10.3389/fnagi.2016.00031/full |
| _version_ | 1818254215917600768 |
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| author | Yanfang eLi Hao eSun Zhicai eChen Huaxi eXu Huaxi eXu Guojun eBu Guojun eBu Hui eZheng Hui eZheng |
| author_facet | Yanfang eLi Hao eSun Zhicai eChen Huaxi eXu Huaxi eXu Guojun eBu Guojun eBu Hui eZheng Hui eZheng |
| author_sort | Yanfang eLi |
| collection | DOAJ |
| description | Alzheimer’s disease (AD) is characterized pathologically by the deposition of -amyloid peptides (A) and the accumulation of neurofibrillary tangles (NFTs) composed of hyper-phosphorylated tau. Regardless of the pathological hallmarks, synaptic dysfunction is widely accepted as a causal event in AD. Of the two major types of synapses in the CNS: glutamatergic and GABAergic, which provide excitatory and inhibitory outputs respectively, abundant data implicate an impaired glutamatergic system during disease progression. However, emerging evidence supports the notion that disrupted default neuronal network underlies impaired memory, and that alterations of GABAergic circuits, either plays a primary role or as a compensatory response to excitotoxicity, may also contribute to AD by disrupting the overall network function. The goal of this review is to provide an overview of the involvement of A, tau and apoE4, the major genetic risk factor in late-onset AD, in GABAergic neurotransmission and the potential of modulating the GABAergic function as AD therapy. |
| first_indexed | 2024-12-12T16:52:26Z |
| format | Article |
| id | doaj.art-d436799078584405ac1b8f26a30c8179 |
| institution | Directory Open Access Journal |
| issn | 1663-4365 |
| language | English |
| last_indexed | 2024-12-12T16:52:26Z |
| publishDate | 2016-02-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Aging Neuroscience |
| spelling | doaj.art-d436799078584405ac1b8f26a30c81792022-12-22T00:18:20ZengFrontiers Media S.A.Frontiers in Aging Neuroscience1663-43652016-02-01810.3389/fnagi.2016.00031180274Implications of GABAergic neurotransmission in Alzheimer’s diseaseYanfang eLi0Hao eSun1Zhicai eChen2Huaxi eXu3Huaxi eXu4Guojun eBu5Guojun eBu6Hui eZheng7Hui eZheng8Xiamen UniversityXiamen UniversityXiamen UniversityXiamen UniversitySanford-Burnham Medical Research InstituteXiamen UniversityMayo ClinicXiamen UniversityBaylor College of MedicineAlzheimer’s disease (AD) is characterized pathologically by the deposition of -amyloid peptides (A) and the accumulation of neurofibrillary tangles (NFTs) composed of hyper-phosphorylated tau. Regardless of the pathological hallmarks, synaptic dysfunction is widely accepted as a causal event in AD. Of the two major types of synapses in the CNS: glutamatergic and GABAergic, which provide excitatory and inhibitory outputs respectively, abundant data implicate an impaired glutamatergic system during disease progression. However, emerging evidence supports the notion that disrupted default neuronal network underlies impaired memory, and that alterations of GABAergic circuits, either plays a primary role or as a compensatory response to excitotoxicity, may also contribute to AD by disrupting the overall network function. The goal of this review is to provide an overview of the involvement of A, tau and apoE4, the major genetic risk factor in late-onset AD, in GABAergic neurotransmission and the potential of modulating the GABAergic function as AD therapy.http://journal.frontiersin.org/Journal/10.3389/fnagi.2016.00031/fullAmyloid beta-PeptidesApolipoproteins Etau Proteinsgabaergic neurotransmissionneuronal inhibition |
| spellingShingle | Yanfang eLi Hao eSun Zhicai eChen Huaxi eXu Huaxi eXu Guojun eBu Guojun eBu Hui eZheng Hui eZheng Implications of GABAergic neurotransmission in Alzheimer’s disease Frontiers in Aging Neuroscience Amyloid beta-Peptides Apolipoproteins E tau Proteins gabaergic neurotransmission neuronal inhibition |
| title | Implications of GABAergic neurotransmission in Alzheimer’s disease |
| title_full | Implications of GABAergic neurotransmission in Alzheimer’s disease |
| title_fullStr | Implications of GABAergic neurotransmission in Alzheimer’s disease |
| title_full_unstemmed | Implications of GABAergic neurotransmission in Alzheimer’s disease |
| title_short | Implications of GABAergic neurotransmission in Alzheimer’s disease |
| title_sort | implications of gabaergic neurotransmission in alzheimer s disease |
| topic | Amyloid beta-Peptides Apolipoproteins E tau Proteins gabaergic neurotransmission neuronal inhibition |
| url | http://journal.frontiersin.org/Journal/10.3389/fnagi.2016.00031/full |
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