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Neuronal apoptosis inhibitory protein (NAIP)-like immunoreactivity in brains of adult patients with Down syndrome
Seidl R, Bajo M, Böhm K, LaCasse EC, MacKenzie AE, Cairns N, Lubec G.. Journal of neural transmission. Supplementum, 1999-01-01
Topic: Brain proteins, microglia and lab models
In Down syndrome (DS), enhanced apoptosis (programmed cell death) may play a role in the pathogenesis of characteristic early mental retardation and precocious neurodegeneration of Alzheimer-type. The human IAP (inhibitor of apoptosis proteins) genes (NAIP, c-IAP-2/HIAP-1, c-IAP-1/Hiap-2, XIAP, survivin) are an evolutionary conserved family of proteins which prevent cell death across species, implying that they act at a central, highly conserved point in the cell death cascade. Evidence for downregulation of NAIP-mRNA in fetal DS (23rd week of gestation), as found by subtractive hybridization technique challenged studies at the protein level in adult DS brain specimen. NAIP-like immunoreactivity was determined in four different regions of cerebral cortex and cerebellum in 9 adult DS patients with Alzheimer-like neuropathologic lesions, 9 Alzheimer disease (AD) patients as compared to 9 controls. For the first time, NAIP-IR could be demonstrated in different cortical regions of the human brain. Compared to control subjects, western blotting demonstrated significantly decreased levels in parietal and occipital cortex in DS and in frontal and occipital cortex in AD. While the mode of NAIP action is unknown, inhibition of certain caspases has already been demonstrated for other IAP-family members (c-IAP1, c-IAP2 and XIAP). Although decreased NAIP-IR of certain brain regions in DS and AD awaits further confirmation, the results suggest that alterations of apoptosis regulatory (inhibitory) proteins may be another feature of neurodegeneration in DS and AD.
Key findings
- NAIP-like immunoreactivity was determined in four different regions of cerebral cortex and cerebellum in 9 adult DS patients with Alzheimer-like neuropathologic lesions, 9 Alzheimer disease (AD) patients as compared to 9 controls.
- For the first time, NAIP-IR could be demonstrated in different cortical regions of the human brain.
- Compared to control subjects, western blotting demonstrated significantly decreased levels in parietal and occipital cortex in DS and in frontal and occipital cortex in AD.
- While the mode of NAIP action is unknown, inhibition of certain caspases has already been demonstrated for other IAP-family members (c-IAP1, c-IAP2 and XIAP).
- Although decreased NAIP-IR of certain brain regions in DS and AD awaits further confirmation, the results suggest that alterations of apoptosis regulatory (inhibitory) proteins may be another feature of neurodegeneration in DS and AD.
Why it matters
In brain tissue from 9 adults with Down syndrome and Alzheimer-like lesions, 9 with Alzheimer disease and 9 controls, NAIP-like immunoreactivity was significantly decreased in some cortical regions in the Down syndrome and Alzheimer disease groups. The authors state the mode of NAIP action is unknown, and this is tissue research, not a treatment or cure.
Study details
- Evidence strengthLow
How this study scored 34/100
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, so that was left out: it earned 33 of the 96 points we could judge it on, which is 34 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Journal of neural transmission. Supplementum) |
| 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 | 1999 — 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 | 3 / 7 | Cited 17 times (OpenAlex, 2026-10-10) |
| Citations per year | 0 / 5 | 0.6 citations a year over 29 year(s) since 1999 |
| Impact for its field and year | 3 / 6 | Cited 6.9× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 0 / 4 | Cited 0 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Gert Lübec: h-index 70 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of Vienna: institution h-index 851 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 5 institution(s) in 4 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 10666683) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 33 / 96 | Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 33 of the 96 points we could judge it on is 34 out of 100. |
| Total | 34 / 100 | — |
What each of these 20 components measures, and what this score is not →
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. The record names 7 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.
APA 7th
Seidl, R., Bajo, M., Böhm, K., LaCasse, E. C., MacKenzie, A. E., Cairns, N., et al. (1999). Neuronal apoptosis inhibitory protein (NAIP)-like immunoreactivity in brains of adult patients with Down syndrome. Journal of neural transmission. Supplementum. https://doi.org/10.1007/978-3-7091-6380-1_19
Vancouver
Seidl R, Bajo M, Böhm K, LaCasse EC, MacKenzie AE, Cairns N, et al. Neuronal apoptosis inhibitory protein (NAIP)-like immunoreactivity in brains of adult patients with Down syndrome. Journal of neural transmission. Supplementum. 1999. doi:10.1007/978-3-7091-6380-1_19. PMID: 10666683.
BibTeX
@article{seidl1999-10666683,
author = {Seidl, R. and Bajo, M. and Böhm, K. and LaCasse, E. C. and MacKenzie, A. E. and Cairns, N. and Lubec, G.},
title = {{Neuronal apoptosis inhibitory protein (NAIP)-like immunoreactivity in brains of adult patients with Down syndrome}},
journal = {Journal of neural transmission. Supplementum},
year = {1999},
doi = {10.1007/978-3-7091-6380-1_19},
pmid = {10666683},
url = {https://doi.org/10.1007/978-3-7091-6380-1_19}
}
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