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Beta-amyloid-induced changes in cultured astrocytes parallel reactive astrocytosis associated with senile plaques in Alzheimer's disease
Pike CJ, Cummings BJ, Monzavi R, Cotman CW.. Neuroscience, 1994-11-01
Topic: Amyloid, tau and blood-test diagnosis
One neuropathological characteristic of Alzheimer's disease is an abundance of reactive astrocytes, particularly in association with senile plaques. Neither the factor(s) responsible for initiating the reactive astrocytosis nor the effects of this event on disease progression are known. We investigated the possibility that beta-amyloid protein, the primary constituent of plaques, contributes to reactive astrocytosis by comparing results derived from both culture studies and immunohistochemical analyses of Alzheimer brain tissue. We report that beta-amyloid peptides, in an aggregation-dependent manner, rapidly induce a reactive phenotype in cultured rat astrocytes. Reactive morphological changes are accompanied by increased immunoreactivities for glial fibrillary acidic protein and basic fibroblast growth factor. Although toxic to other types of central nervous system cells, aggregated beta-amyloid peptides do not significantly decrease astrocyte viability. Rather, the processes of cultured astrocytes envelop aggregated deposits of beta-amyloid peptide. In Alzheimer brain, the processes of reactive astrocytes were also observed to engulf beta-amyloid deposits. Similar to the in vitro findings, the astrocytic response was associated only with beta-amyloid plaques exhibiting an aggregated structure. Further, the plaque-associated reactive astrocytes showed enhanced immunoreactivities for glial fibrillary acidic protein and basic fibroblast growth factor. These data suggest that beta-amyloid which has assembled into beta-sheet fibrils significantly contributes to the reactive astrocytosis characteristic of Alzheimer's disease. Thus, in addition to its hypothesized direct effects on neuronal viability, beta-amyloid may also influence disease progression indirectly via reactive astrocytosis.
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APA 7th
Pike, C. J., Cummings, B. J., Monzavi, R., & Cotman, C. W. (1994). Beta-amyloid-induced changes in cultured astrocytes parallel reactive astrocytosis associated with senile plaques in Alzheimer's disease. Neuroscience. https://doi.org/10.1016/0306-4522(94)90547-9
Vancouver
Pike CJ, Cummings BJ, Monzavi R, Cotman CW. Beta-amyloid-induced changes in cultured astrocytes parallel reactive astrocytosis associated with senile plaques in Alzheimer's disease. Neuroscience. 1994. doi:10.1016/0306-4522(94)90547-9. PMID: 7891862.
BibTeX
@article{pike1994-7891862,
author = {Pike, C. J. and Cummings, B. J. and Monzavi, R. and Cotman, C. W.},
title = {{Beta-amyloid-induced changes in cultured astrocytes parallel reactive astrocytosis associated with senile plaques in Alzheimer's disease}},
journal = {Neuroscience},
year = {1994},
doi = {10.1016/0306-4522(94)90547-9},
pmid = {7891862},
url = {https://doi.org/10.1016/0306-4522(94)90547-9}
}
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Key findings
- We investigated the possibility that beta-amyloid protein, the primary constituent of plaques, contributes to reactive astrocytosis by comparing results derived from both culture studies and immunohistochemical analyses of Alzheimer brain tissue.
- Although toxic to other types of central nervous system cells, aggregated beta-amyloid peptides do not significantly decrease astrocyte viability.
- These data suggest that beta-amyloid which has assembled into beta-sheet fibrils significantly contributes to the reactive astrocytosis characteristic of Alzheimer's disease.
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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 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 (Neuroscience) |
| 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 | 1994 — 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 | Laboratory or animal study (title names “cultured”) — scores zero |
| 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 7891862) |
| 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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