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Cytosolic phospholipase A2 (cPLA2) immunoreactivity is elevated in Alzheimer's disease brain
Stephenson DT, Lemere CA, Selkoe DJ, Clemens JA.. Neurobiology of disease, 1996-02-01
Topic: Inflammation, microglia and astrocytes
Phospholipase A2 (PLA2) is the key enzyme that initiates the arachidonic acid cascade, which leads to the generation of multiple eicosanoid products. Many of these products are believed to play an important role in the inflammatory process. Activation of PLA2 is observed under pathological conditions where inflammation is present. Cytosolic PLA2 (cPLA2) is activated by very low levels of calcium and is thought to control receptor-mediated eicosanoid production and to participate in intracellular signal transduction processes. In view of the presence of numerous inflammatory mediators and acute phase proteins in the Alzheimer's disease (AD) brain, localization of cPLA2 in AD brain was evaluated and compared to that observed in nonneurologically diseased controls. In this study, a monoclonal antibody raised against cPLA2 was used to immunostain tissue sections of human cerebral cortex. Five AD cases and six neurologically normal cases were evaluated in the occipital cortex and the cerebellum. Two of the AD cases were also examined in other cortical regions. Granular-like staining with anti-cPLA2 was found to be associated with astrocytes in the cortex of both control and AD cases. Colocalization with GFAP confirmed that cPLA2 immunoreactivity is associated almost exclusively with protoplasmic astrocytes. Staining was abolished when sections were labeled with antibody that had been preadsorbed with purified cPLA2. In AD brain, cPLA2 immunoreactive astrocytes were greater in number and more intensely stained than those in control cases. cPLA2 immunoreactivity was virtually absent in the cerebelium of AD and control cases, despite the presence in this region of diffuse amyloid in two AD cases and amyloid angiopathy in a third case. In the cortex, cPLA2 immunoreactive astrocytes were detected in regions that contained numerous A beta deposits. The finding of elevated levels of cPLA2 immunoreactivity in AD brain supports the hypothesis that there is an active inflammatory process occurring in AD.
Key findings
- In view of the presence of numerous inflammatory mediators and acute phase proteins in the Alzheimer's disease (AD) brain, localization of cPLA2 in AD brain was evaluated and compared to that observed in nonneurologically diseased controls.
- Granular-like staining with anti-cPLA2 was found to be associated with astrocytes in the cortex of both control and AD cases.
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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 (Neurobiology of disease) |
| 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 | 1996 — 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 | — / 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 9173912) |
| 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 | — |
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APA 7th
Stephenson, D. T., Lemere, C. A., Selkoe, D. J., & Clemens, J. A. (1996). Cytosolic phospholipase A2 (cPLA2) immunoreactivity is elevated in Alzheimer's disease brain. Neurobiology of disease. https://doi.org/10.1006/nbdi.1996.0005
Vancouver
Stephenson DT, Lemere CA, Selkoe DJ, Clemens JA. Cytosolic phospholipase A2 (cPLA2) immunoreactivity is elevated in Alzheimer's disease brain. Neurobiology of disease. 1996. doi:10.1006/nbdi.1996.0005. PMID: 9173912.
BibTeX
@article{stephenson1996-9173912,
author = {Stephenson, D. T. and Lemere, C. A. and Selkoe, D. J. and Clemens, J. A.},
title = {{Cytosolic phospholipase A2 (cPLA2) immunoreactivity is elevated in Alzheimer's disease brain}},
journal = {Neurobiology of disease},
year = {1996},
doi = {10.1006/nbdi.1996.0005},
pmid = {9173912},
url = {https://doi.org/10.1006/nbdi.1996.0005}
}