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Neuronal and glial gene expression in neocortex of Down's syndrome and Alzheimer's disease
Goodison KL, Parhad IM, White CL, Sima AA, Clark AW.. Journal of neuropathology and experimental neurology, 1993-05-01
Topic: Brain proteins, microglia and lab models
The association cortex of Down's syndrome (DS) predictably and prematurely undergoes neurofibrillary degeneration of Alzheimer type. Hence studies of DS are potentially useful in defining the earliest pathogenetic events in Alzheimer's disease (AD). Previous reports have described altered expression of several mRNAs in AD cortex; but the pathogenetic stage at which expression of these mRNAs begins to deviate from the norm has not been defined. We have examined this issue in neocortex of DS. Expression of mRNAs, known to be altered in AD cortex, was studied by Northern analysis, comparing frontal cortex of DS (15-45 years) with age-matched controls and with AD. Chromosome 21- and non-21-encoded mRNAs were studied, including transcripts expressed preferentially in neurons (neurofilament light subunit and amyloid precursor transcripts) and in glia (glial fibrillary acidic protein [GFAP] and S100 beta). Chromosome 21-encoded mRNAs were increased in DS cortex as expected. Except in the DS case with extensive neurofibrillary degeneration, GFAP was expressed at levels significantly below the control, suggesting that trisomy 21 exerts a suppressive effect on GFAP gene expression. We found no instance in which AD-type changes of transcript expression preceded the appearance of neurofibrillary degeneration. The findings indicate that in trisomy 21, certain changes of mRNA prevalence previously described for AD neocortex are not a necessary antecedent to neurofibrillary degeneration.
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APA 7th
Goodison, K. L., Parhad, I. M., White, C. L., Sima, A. A., & Clark, A. W. (1993). Neuronal and glial gene expression in neocortex of Down's syndrome and Alzheimer's disease. Journal of neuropathology and experimental neurology. https://doi.org/10.1097/00005072-199305000-00002
Vancouver
Goodison KL, Parhad IM, White CL, Sima AA, Clark AW. Neuronal and glial gene expression in neocortex of Down's syndrome and Alzheimer's disease. Journal of neuropathology and experimental neurology. 1993. doi:10.1097/00005072-199305000-00002. PMID: 8492138.
BibTeX
@article{goodison1993-8492138,
author = {Goodison, K. L. and Parhad, I. M. and White, C. L. and Sima, A. A. and Clark, A. W.},
title = {{Neuronal and glial gene expression in neocortex of Down's syndrome and Alzheimer's disease}},
journal = {Journal of neuropathology and experimental neurology},
year = {1993},
doi = {10.1097/00005072-199305000-00002},
pmid = {8492138},
url = {https://doi.org/10.1097/00005072-199305000-00002}
}
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Key findings
- Except in the DS case with extensive neurofibrillary degeneration, GFAP was expressed at levels significantly below the control, suggesting that trisomy 21 exerts a suppressive effect on GFAP gene expression.
- We found no instance in which AD-type changes of transcript expression preceded the appearance of neurofibrillary degeneration.
- The findings indicate that in trisomy 21, certain changes of mRNA prevalence previously described for AD neocortex are not a necessary antecedent to neurofibrillary degeneration.
Why it matters
In Down's syndrome cortex, GFAP expression was lower than in controls except in one case with extensive neurofibrillary degeneration, and no Alzheimer-type mRNA changes appeared before neurofibrillary degeneration. This provides clues about the sequence of early changes in Down's syndrome and Alzheimer disease but does not test any treatment.
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Study details
- Evidence strengthLow
How this study scored 37/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / 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 | 1993 — 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) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 4 / 7 | Cited 43 times (OpenAlex, 2026-10-10) |
| Citations per year | 1 / 5 | 1.2 citations a year over 35 year(s) since 1993 |
| Impact for its field and year | 2 / 6 | Cited 1.5× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 2 other studies in this library |
| Still being cited | 0 / 4 | Cited 1 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Arthur W. Clark: h-index 34 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of Michigan: institution h-index 2,240 (OpenAlex) |
| Multicenter collaboration | 2 / 3 | OpenAlex lists 4 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 8492138) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 37 / 100 | — |
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