Evidence map›Paper›PMID 9122249›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1997

Transcription factor NF-kappaB is activated in primary neurons by amyloid beta peptides and in neurons surrounding early plaques from patients with Alzheimer disease.

B Kaltschmidt, M Uherek, B Volk, P A Baeuerle, C Kaltschmidt

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 191 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
191citing papers in PubMed, 2 pooled it
16.7field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

191 citing papers in PubMed, 2 syntheses or guidelines pooled it, 618 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. IMD-1 Protects SH-SY5Y Cells Against HNeurochemical research · 2026
    Article
  6. Article
  7. Beyond Neuroinflammation: Microglia at the Crossroads of Amyloid, Tau, and Neurodegeneration in Alzheimer's Disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Rationally Designed Peptoid Inhibitors of Amyloid-β Oligomerization.Chembiochem : a European journal of chemical biology · 2024
    Article
  19. Review
  20. Urolithin A improves Alzheimer's disease cognition and restores mitophagy and lysosomal functions.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article

131 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

B KaltschmidtInstitute of Biochemistry and Molecular Biology, Albert-Ludwigs-University, Freiburg, Germany. kaltschm@ruf.uni-freiburg.de
M Uherek
B Volk
P A Baeuerle
C Kaltschmidt
University of Freiburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyloid beta peptide (A beta)-containing plaques are a hallmark of Alzheimer disease. Here, we show that the neurotoxic A beta, a major plaque component, is a potent activator of the transcription factor NF-kappaB in primary neurons. This activation required reactive oxygen intermediates as messengers because an antioxidant prevented A beta-induced NF-kappaB activation. Maximal activation of NF-kappaB was found with 0.1 microM A beta-(1-40) and 0.1 microM A beta-(25-35) fragments, making a role for NF-kappaB in neuroprotection feasible. Using an activity-specific mAb for the p65 NF-kappaB subunit, activation of NF-kappaB also was observed in neurons and astroglia of brain sections from Alzheimer disease patients. Activated NF-kappaB was restricted to cells in the close vicinity of early plaques. Our data suggest that the aberrant gene expression in diseased nervous tissue is at least in part due to A beta-induced activation of NF-kappaB, a potent immediate-early transcriptional regulator of numerous proinflammatory genes.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsAntioxidantsAstrocytesCatalaseCells, CulturedCerebellumHumansNeuronsNF-kappa BPeptide FragmentsProlineRatsRats, WistarThiocarbamatesAmyloid beta-Peptidesamyloid beta-protein (1-40)amyloid beta-protein (25-35)AntioxidantsCatalaseNF-kappa BPeptide FragmentsProlineprolinedithiocarbamateThiocarbamates

Identifiers

PMID9122249
PMCPMC20142
OpenAlexW1968786165

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.