Cited by 186Alzheimer's disease research and treatmentsNeuroscience and Neuropharmacology ResearchAmino Acid Enzymes and Metabolism

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Amyloid-β 1–42 Slows Clearance of Synaptically Released Glutamate by Mislocalizing Astrocytic GLT-1

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Scimemi, Annalisa, Meabon, James S., Woltjer, Randall L., Sullivan, Jane M., Diamond, Jeffrey S., Cook, David G.·2013·The Journal of Neuroscience

DOI 10.1523/jneurosci.5274-12.2013PMC PMC3866500

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Abstract

GLT-1, the major glutamate transporter in the adult brain, is abundantly expressed in astrocytic processes enveloping synapses. By limiting glutamate escape into the surrounding neuropil, GLT-1 preserves the spatial specificity of synaptic signaling. Here we show that the amyloid-β peptide Aβ 1–42 markedly prolongs the extracellular lifetime of synaptically released glutamate by reducing GLT-1 surface expression in mouse astrocytes and that this effect is prevented by the vitamin E derivative Trolox. These findings indicate that astrocytic glutamate transporter dysfunction may play an important role in the pathogenesis of Alzheimer's disease and suggest possible mechanisms by which several current treatment strategies could protect against the disease.

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Authors: Scimemi, A., Meabon, J. S., Woltjer, R. L., Sullivan, J. M., Diamond, J. S., & Cook, D. G.
Affiliations: National Institutes of Health (US)
VA Puget Sound Health Care System (US)
Oregon Health & Science University (US)
University of Washington (US)
ORCID: Scimemi, Annalisa
Meabon, James S.
Woltjer, Randall L.
Sullivan, Jane M.
Diamond, Jeffrey S.
Cook, David G.
Venue: The Journal of Neuroscience
Publisher: Society for Neuroscience
Published: 2013-03-20
Volume: 33
Issue: 12
Pages: 5312-5318
ISSN: 0270-6474 (ISSN-L)
1529-2401
DOI: 10.1523/jneurosci.5274-12.2013
PMC: PMC3866500
OpenAlex: W1979889191
Cited by: 185
References: 28
Citations by year: 2026: 8 · 2025: 16 · 2024: 23 · 2023: 9 · 2022: 22 · 2021: 15 · 2020: 18 · 2019: 12 · 2018: 11 · 2017: 19 · 2016: 7 · 2015: 13 · 2014: 11 · 2013: 1
FWCI: 7.43
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc-sa
creativecommons.org/licenses/by-nc-sa/4.0/ (vor, 184 d)
Locations: Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health
National Institute on Aging (T32AG000258)
National Institute of Diabetes and Digestive and Kidney Diseases (P30DK017047)
National Institute of Neurological Disorders and Stroke (R01NS055804, ZIANS002986, Z01NS002986)
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
Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Amino Acid Enzymes and Metabolism
Keywords: amyloid-beta 42, GLT-1, glutamate transporters, astrocytes, glutamate clearance, Alzheimer's disease, Trolox, vitamin E, extracellular glutamate
MeSH terms: Alzheimer Disease, Animals, Antioxidants, Astrocytes, Chromans, Drug Interactions, Extracellular Space, Female, Hippocampus, Male, Mice, Inbred C57BL, Models, Neurological, Neurons, Organ Culture Techniques, Peptide Fragments, Synapses, Amyloid beta-Peptides, Glutamic Acid, Excitatory Amino Acid Transporter 2, Mice

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Amyloid-β 1–42 Slows Clearance of Synaptically Released Glutamate by Mislocalizing Astrocytic GLT-1

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