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Targeting excitotoxic/free radical signaling pathways for therapeutic intervention in glaucoma
Seki M, Lipton SA.. Progress in brain research, 2008-01-01
Topic: Brain proteins, microglia and lab models
Glaucoma is a visual disorder characterized by progressive loss of retinal ganglion cells (RGCs), which is often associated with high intraocular pressure. However, mechanisms of RGC death in glaucoma still remain a mystery. Two theories have been proposed as pathogeneses of glaucoma: mechanical and vascular. We demonstrate that glutamate excitotoxicity triggered by overactivation of the N-methyl-D-aspartate (NMDA)-type glutamate receptors may contribute according to both theories to RGC death in glaucoma and other retinal diseases such as ischemia. From a therapeutic standpoint, NMDA receptors and downstream signaling pathways, triggered by p38 mitogen-activated protein kinase (MAPK) and caspases, are potential targets of intervention to prevent RGC death. Glutamate, however, mediates synaptic transmission essential for normal function of the nervous system. Hence, complete blockade of NMDA receptor activity causes unacceptable side effects. Studies in our laboratory have shown that an open-channel blocker of the NMDA receptors, memantine, blocks only excessive NMDA receptor activity while leaving normal function relatively intact. This characteristic endows memantine with clinical tolerability, as demonstrated by its approval for treatment of Alzheimer's disease and vascular dementia, and clinical trials for glaucoma. In this review, we discuss improved memantine derivatives, p38 MAPK, and caspase inhibitors as plausible therapeutics to prevent RGC death.
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APA 7th
Seki, M., & Lipton, S. A. (2008). Targeting excitotoxic/free radical signaling pathways for therapeutic intervention in glaucoma. Progress in brain research. https://doi.org/10.1016/s0079-6123(08)01134-5
Vancouver
Seki M, Lipton SA. Targeting excitotoxic/free radical signaling pathways for therapeutic intervention in glaucoma. Progress in brain research. 2008. doi:10.1016/s0079-6123(08)01134-5. PMID: 18929130.
BibTeX
@article{seki2008-18929130,
author = {Seki, M. and Lipton, S. A.},
title = {{Targeting excitotoxic/free radical signaling pathways for therapeutic intervention in glaucoma}},
journal = {Progress in brain research},
year = {2008},
doi = {10.1016/s0079-6123(08)01134-5},
pmid = {18929130},
url = {https://doi.org/10.1016/s0079-6123(08)01134-5}
}
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Key findings
- Glaucoma is a visual disorder characterized by progressive loss of retinal ganglion cells (RGCs), which is often associated with high intraocular pressure.
- Studies in our laboratory have shown that an open-channel blocker of the NMDA receptors, memantine, blocks only excessive NMDA receptor activity while leaving normal function relatively intact.
- This characteristic endows memantine with clinical tolerability, as demonstrated by its approval for treatment of Alzheimer's disease and vascular dementia, and clinical trials for glaucoma.
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Study details
- Evidence strengthLow
How this study scored 36/100
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. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multi-centre collaboration, so those were left out: it earned 21 of the 58 points we could judge it on, which is 36 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Progress in brain research) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| 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 | 1 / 5 | 2008 — within 20 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 | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 18929130) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 21 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 21 of the 58 points we could judge it on is 36 out of 100. |
| Total | 36 / 100 | — |
What each of these 20 components measures, and what this score is not →
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