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Cited by 211Alzheimer's disease research and treatmentsNeuroscience and Neuropharmacology ResearchDementia and Cognitive Impairment Research

The DOI matches its Crossref record; 348 of the 353 references it cites were found in a registry or an index.

Towards a Better Understanding of GABAergic Remodeling in Alzheimer’s Disease

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Govindpani, Karan, Calvo-Flores Guzmán, Beatriz, Vinnakota, Chitra, Waldvogel, Henry, Faull, Richard, Kwakowsky, Andrea·2017·International Journal of Molecular Sciences
DOI 10.3390/ijms18081813PMC PMC5578199
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Abstract

γ-aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the vertebrate brain. In the past, there has been a major research drive focused on the dysfunction of the glutamatergic and cholinergic neurotransmitter systems in Alzheimer’s disease (AD). However, there is now growing evidence in support of a GABAergic contribution to the pathogenesis of this neurodegenerative disease. Previous studies paint a complex, convoluted and often inconsistent picture of AD-associated GABAergic remodeling. Given the importance of the GABAergic system in neuronal function and homeostasis, in the maintenance of the excitatory/inhibitory balance, and in the processes of learning and memory, such changes in GABAergic function could be an important factor in both early and later stages of AD pathogenesis. Given the limited scope of currently available therapies in modifying the course of the disease, a better understanding of GABAergic remodeling in AD could open up innovative and novel therapeutic opportunities.

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Figure 1 An overview of the γ-aminobutyric acid (GABA) signaling system. The schematic diagram represents a GABAergic synapse and depicts the key aspects of GABAergic signal transduction. GABA is synthesized in the pre-synaptic terminal from glutamate by glutamic acid decarboxylase (GAD). GABA is then recruited into synaptic vesicles via the action of vesicular GABA transporter (vGAT). Following membrane depolarization, GABA is released into the synapse and can bind to either ionotropic GABAA receptors (GABAAR) or metabotropic GABAB receptors (GABABR) on the postsynaptic membrane, resulting in inhibition of the post-synaptic neuron. Released GABA is cleared from the synapse by membrane-bound GABA transporters (GATs), localized to neurons and astrocytes. In astrocytes, GABA is recycled into synaptic vesicles or taken up by mitochondria, where it is metabolized by GABA transaminase (GABA-T) to glutamine for neuronal uptake.
Figure 1 An overview of the γ-aminobutyric acid (GABA) signaling system. The schematic diagram represents a GABAergic synapse and depicts the key aspects of GABAergic signal transduction. GABA is synthesized in the pre-synaptic terminal from glutamate by glutamic acid decarboxylase (GAD). GABA is then recruited into synaptic vesicles via the action of vesicular GABA transporter (vGAT). Following membrane depolarization, GABA is released into the synapse and can bind to either ionotropic GABAA receptors (GABAAR) or metabotropic GABAB receptors (GABABR) on the postsynaptic membrane, resulting in inhibition of the post-synaptic neuron. Released GABA is cleared from the synapse by membrane-bound GABA transporters (GATs), localized to neurons and astrocytes. In astrocytes, GABA is recycled into synaptic vesicles or taken up by mitochondria, where it is metabolized by GABA transaminase (GABA-T) to glutamine for neuronal uptake.CC BY · PubMed Central

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  1. Wyper, 1998, Single photon emission computed tomography in Alzheimer’s disease: Cerebral perfusion and acetylcholine muscarinic receptor imaging and a novel study of the GABA/benzodiazepine system, Int. J. Geriatr. Psychopharmacol., 1, 126

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Metadata

Authors
Govindpani, K., Calvo-Flores Guzmán, B., Vinnakota, C., Waldvogel, H., Faull, R., & Kwakowsky, A.
Affiliations
  • University of Auckland (NZ)
  • Centre for Brain Research, Department of Anatomy and Medical Imaging, Faculty of Medical and Health Sciences, University of Auckland, Auckland 1023, New Zealand
Corresponding author
Kwakowsky, Andrea
ORCID
Venue
International Journal of Molecular Sciences
Publisher
MDPI AG
Published
2017-08-21
Volume
18
Issue
8
Pages
1813
ISSN
1422-0067 (ISSN-L)
DOI
10.3390/ijms18081813
PMC
PMC5578199
OpenAlex
W2746415584
Cited by
208
References
353
Citations by year
2026: 20 · 2025: 14 · 2024: 25 · 2023: 26 · 2022: 16 · 2021: 41 · 2020: 29 · 2019: 29 · 2018: 5 · 2017: 2
FWCI
2.18
Type
journal article
Language
en
Open access
Licence
Locations
  • International Journal of Molecular Sciences (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • ResearchSpace (University of Auckland) (submittedVersion, cc-by)
Funders
  • Aotearoa Foundation (3705579)
  • Brain Research New Zealand (3710638)
  • Health Research Council of New Zealand (3627373)
  • Maurice and Phyllis Paykel Trust (3713650)
  • Auckland Medical Research Foundation (3712563)
  • University of Otago (110089.01)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
Alzheimer's disease, GABAergic system, inhibitory neurotransmission, excitation-inhibition balance, neurodegeneration, AD pathogenesis, therapeutic target
MeSH terms
Alzheimer Disease, Brain, gamma-Aminobutyric Acid, Humans, Neurotransmitter Agents, GABAergic Neurons

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