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Aberrant expression of the glutamate transporter excitatory amino acid transporter 1 (EAAT1) in Alzheimer's disease
Scott, H. L., Pow, D. V., Tannenberg, A. E. G. and Dodd, P. R. (2002-02) Aberrant expression of the glutamate transporter excitatory amino acid transporter 1 (EAAT1) in Alzheimer's disease. Journal of Neuroscience, 22 3: RC206: 1-5.
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| Author(s) |
Scott, H. L.
Pow, D. V.
Tannenberg, A. E. G.
Dodd, P. R.
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| Title |
Aberrant expression of the glutamate transporter excitatory amino acid transporter 1 (EAAT1) in Alzheimer's disease
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| Journal name |
Journal of Neuroscience
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| Publication date |
2002-02
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| Volume number |
22
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| Issue number |
3
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| ISSN |
0270-6474; 1529-2401
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| Start page |
RC206: 1
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| End page |
5
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| Total pages |
5
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| Place of publication |
New York
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| Publisher |
Society for Neuroscience
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| Language |
eng
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| Subject |
110906 Sensory Systems
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| Abstract |
Glutamate-mediated toxicity has been implicated in the neurodegeneration observed in Alzheimer's disease. In particular, glutamate transport dysfunction may increase susceptibility to glutamate toxicity, thereby contributing to neuronal cell injury and death. In this study, we examined the cellular localization of the glial glutamate transporter excitatory amino acid transporter 1 (EAAT1) in the cerebral cortex of control, Alzheimer's disease, and non-Alzheimer dementia cases. We found that EAAT1 was strongly expressed in a subset of cortical pyramidal neurons in dementia cases showing Alzheimer-type pathology. In addition, tau (which is a marker of neurofibrillary pathology) colocalized to those same pyramidal cells that expressed EAAT1. These findings suggest that EAAT1 changes are related to tau expression (and hence neurofibrillary tangle formation) in dementia cases showing Alzheimer-type pathology. This study implicates aberrant glutamate transporter expression as a mechanism involved in neurodegeneration in Alzheimer's disease.
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| Keyword(s) |
Neurosciences
Alzheimer's disease
glutamate transporter
EAAT1
tau
immunocytochemistry
human cortex
Amyotrophic-lateral-sclerosis
Cerebral-cortex
Protein
Glast
Brain
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| Additional Notes |
Our 1995 paper [42 cites] used classical pharmacological methods; here, we followed up with immunocytochemistry. ‘Hot topic’ in AD.
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