Home › Research › Biomarkers
Glutamate Transporter GLT1 Expression in Alzheimer Disease and Dementia With Lewy Bodies
Garcia-Esparcia P, Diaz-Lucena D, Ainciburu M, Torrejón-Escribano B, Carmona M, Llorens F, Ferrer I.. Frontiers in aging neuroscience, 2018-04-26
Topic: Brain proteins, microglia and lab models
Glutamate transporter solute carrier family 1, member 2 (GLT1/EAAT2), a major modulator of glutamate homeostasis in astrocytes, is assessed in post-mortem human brain samples of frontal cortex area 8 in advanced stages of Alzheimer disease (AD) and terminal stages of dementia with Lewy bodies (DLB) in order to gain understanding of astrogliopathy in diseases manifested by dementia. Glial fibrillary acidic protein (GFAP) mRNA expression is significantly increased in AD but not in DLB, whereas GLT1 , vesicular glutamate transporter 1 ( vGLUT1 ) and aldehyde dehydrogenase 1 family member 1 ( ALDH1L1 ) are not modified in AD and DLB when compared with controls. GLT1 protein levels are not altered in AD and DLB but GFAP and ALDH1L1 are significantly increased in AD, and GFAP in DLB. As a result, a non-significant decrease in the ratio between GLT1 and GFAP, and between GLT1 and ALDH1L1, is found in both AD and DLB. Double-labeling immunofluorescence and confocal microscopy revealed no visible reduction of GLT1 immunoreactivity in relation to β-amyloid plaques in AD. These data suggest a subtle imbalance between GLT1, and GFAP and ALDH1L1 expression, with limited consequences in glutamate transport.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Garcia-Esparcia, P., Diaz-Lucena, D., Ainciburu, M., Torrejón-Escribano, B., Carmona, M., Llorens, F., et al. (2018). Glutamate Transporter GLT1 Expression in Alzheimer Disease and Dementia With Lewy Bodies. Frontiers in aging neuroscience. https://doi.org/10.3389/fnagi.2018.00122
Vancouver
Garcia-Esparcia P, Diaz-Lucena D, Ainciburu M, Torrejón-Escribano B, Carmona M, Llorens F, et al. Glutamate Transporter GLT1 Expression in Alzheimer Disease and Dementia With Lewy Bodies. Frontiers in aging neuroscience. 2018. doi:10.3389/fnagi.2018.00122. PMID: 29755340.
BibTeX
@article{garciaesparcia2018-29755340,
author = {Garcia-Esparcia, P. and Diaz-Lucena, D. and Ainciburu, M. and Torrejón-Escribano, B. and Carmona, M. and Llorens, F. and Ferrer, I.},
title = {{Glutamate Transporter GLT1 Expression in Alzheimer Disease and Dementia With Lewy Bodies}},
journal = {Frontiers in aging neuroscience},
year = {2018},
doi = {10.3389/fnagi.2018.00122},
pmid = {29755340},
url = {https://doi.org/10.3389/fnagi.2018.00122}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record names 7 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.
Key findings
- Glial fibrillary acidic protein (GFAP) mRNA expression is significantly increased in AD but not in DLB, whereas GLT1 , vesicular glutamate transporter 1 ( vGLUT1 ) and aldehyde dehydrogenase 1 family member 1 ( ALDH1L1 ) are not modified in AD and DLB when compared with controls.
- GLT1 protein levels are not altered in AD and DLB but GFAP and ALDH1L1 are significantly increased in AD, and GFAP in DLB.
- As a result, a non-significant decrease in the ratio between GLT1 and GFAP, and between GLT1 and ALDH1L1, is found in both AD and DLB.
- Double-labeling immunofluorescence and confocal microscopy revealed no visible reduction of GLT1 immunoreactivity in relation to β-amyloid plaques in AD.
Why it matters
In postmortem frontal cortex, GLT1 protein levels were not altered in Alzheimer disease or dementia with Lewy bodies, while GFAP was increased in both and ALDH1L1 in Alzheimer disease. The study found only a non-significant decrease in GLT1-to-GFAP and GLT1-to-ALDH1L1 ratios and reports no treatment or prevention effect.
New to this subject? Start with our plain-English guide: Blood tests & biomarkers →
Study details
- Evidence strengthLow
How this study scored 44/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Frontiers in aging neuroscience) |
| Journal's citation record | 2 / 4 | Frontiers in Aging Neuroscience: journal h-index 174 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 2 / 5 | 2018 — within 10 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 4 / 7 | Cited 56 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 5.6 citations a year over 10 year(s) since 2018 |
| Impact for its field and year | 3 / 6 | Cited 3.1× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 2 / 4 | Cited 16 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Isidró Ferrer: h-index 120 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Universitat de Barcelona: institution h-index 1,049 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 5 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 29755340) |
| Free to read | 2 / 2 | Free to read |
| Total | 44 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
Full text: free to read — PubMed Central lists this copy as free to read: the link above (checked 10 Oct 2026).
Related
Studies in the library that share something with this one. The line above each title says what.
Studies this one cites
Referenced by this study and also in the alzhub library, so you can read them here.
Related studies in Biomarkers
Also tagged “precursor”
1,337 studies in the library carry the topic tag “precursor”; these are this study's neighbours in a fixed, alphabetical-by-hash tour of them, not the closest in content. All 1,337 tagged studies.