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Caspase dependent DNA fragmentation might be associated with excitotoxicity in Alzheimer disease
Masliah E, Mallory M, Alford M, Tanaka S, Hansen LA.. Journal of neuropathology and experimental neurology, 1998-11-01
Topic: Brain proteins, microglia and lab models
Recent studies have shown that deficient functioning of glutamate transporters (GTs) in Alzheimer disease (AD) might lead to neurodegeneration via excitotoxicity; however, the characteristics of cell death and pathways involved are not yet clear. The main objective of the present study was to determine if deficient GT functioning in AD could be associated with cell damage and caspase activation. For this purpose, we analyzed the levels of caspase-1 and 3 immunoreactivity in AD and control brains and correlated this data with the numbers of cells displaying DNA fragmentation, GT activity, and amyloid precursor protein (APP) mRNA expression.
Key findings
- The main objective of the present study was to determine if deficient GT functioning in AD could be associated with cell damage and caspase activation.
- For this purpose, we analyzed the levels of caspase-1 and 3 immunoreactivity in AD and control brains and correlated this data with the numbers of cells displaying DNA fragmentation, GT activity, and amyloid precursor protein (APP) mRNA expression.
- Compared to controls, AD cases showed extensive positive labeling of neurons and glial cells with an assay for DNA fragmentation suggestive of cell damage, as well as increased neuronal caspase-3 and Bcl-2 immunoreactivity.
- Linear regression analysis showed a strong negative correlation between GT activity and apoptosis, and between deficient GT functioning and caspase-3 immunoreactivity.
Why it matters
This study examined whether poor glutamate transporter function in Alzheimer's disease is linked to cell damage and activation of caspase enzymes. It reports an association between these processes, but the work is descriptive and does not test any treatment or show that blocking caspases would help patients.
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Study details
- Evidence strengthLow
How this study scored 43/100
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 (Journal of neuropathology and experimental neurology) |
| Journal's citation record | 2 / 4 | Journal of Neuropathology & Experimental Neurology: journal h-index 239 (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 | 1 / 5 | 1998 — older than 20 years, still counted |
| 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 | 5 / 7 | Cited 151 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 5.0 citations a year over 30 year(s) since 1998 |
| Impact for its field and year | 4 / 6 | Cited 10.2× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 4 other studies in this library |
| Still being cited | 1 / 4 | Cited 4 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Lawrence A. Hansen: h-index 79 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of California San Diego: institution h-index 1,852 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 9825941) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 43 / 100 | — |
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Read the original
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Cite this study APA, Vancouver, BibTeX · download .bib or .ris
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
APA 7th
Masliah, E., Mallory, M., Alford, M., Tanaka, S., & Hansen, L. A. (1998). Caspase dependent DNA fragmentation might be associated with excitotoxicity in Alzheimer disease. Journal of neuropathology and experimental neurology. https://doi.org/10.1097/00005072-199811000-00007
Vancouver
Masliah E, Mallory M, Alford M, Tanaka S, Hansen LA. Caspase dependent DNA fragmentation might be associated with excitotoxicity in Alzheimer disease. Journal of neuropathology and experimental neurology. 1998. doi:10.1097/00005072-199811000-00007. PMID: 9825941.
BibTeX
@article{masliah1998-9825941,
author = {Masliah, E. and Mallory, M. and Alford, M. and Tanaka, S. and Hansen, L. A.},
title = {{Caspase dependent DNA fragmentation might be associated with excitotoxicity in Alzheimer disease}},
journal = {Journal of neuropathology and experimental neurology},
year = {1998},
doi = {10.1097/00005072-199811000-00007},
pmid = {9825941},
url = {https://doi.org/10.1097/00005072-199811000-00007}
}
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