Evidence map›Paper›PMID 19705461›Full record

ArticleGlia2010

Overexpression of human S100B exacerbates cerebral amyloidosis and gliosis in the Tg2576 mouse model of Alzheimer's disease.

Takashi Mori, Naoki Koyama, Gary W Arendash, Yuko Horikoshi-Sakuraba, Jun Tan, Terrence Town

Open access · greenAbstract read
In one paragraph

Article in Glia, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed, 3 pooled it
5.8field-weighted citation impact, top 3% 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

96 citing papers in PubMed, 3 syntheses or guidelines pooled it, 200 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. S100B Serum Levels Predict Treatment Response in Patients with Melancholic Depression.The international journal of neuropsychopharmacology · 2015
    Trial
  5. Article
  6. Article
  7. Review
  8. Early microglial and astrocyte reactivity in preclinical Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  9. Association between oxytocin and S100B in community-dwelling older adults.PCN reports : psychiatry and clinical neurosciences · 2025
    Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. The S100B Protein: A Multifaceted Pathogenic Factor More Than a Biomarker.International journal of molecular sciences · 2023
    Review
  18. Article
  19. Article
  20. Article

36 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

6 authors at 4 institutions in 2 countries.

Takashi MoriDepartment of Medical Science, Saitama Medical Center and University, Kawagoe, Saitama, Japan. t_mori@saitama-med.ac.jp
Naoki Koyama
Gary W Arendash
Yuko Horikoshi-Sakuraba
Jun Tan
Terrence Town
Social Insurance Saitama Chuo Hospital · JPUniversity of South Florida · USMedical & Biological Laboratories (Japan) · JPSaitama Medical University · JP

Funding

Blocking TGF-Beta immune signaling as a therapeutic target for Alzheimer's diseasR00AG029726 · NIA · CEDARS-SINAI MEDICAL CENTER · PI TOWN, TERRENCE C · 2008 to 2010
$790k
NIA NIH HHS R00 AG029726
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common progressive dementia and is pathologically characterized by brain deposition of amyloid-beta (Abeta) peptide as senile plaques. Inflammatory and immune response pathways are chronically activated in AD patient brains at low levels, and likely play a role in disease progression. Like microglia, activated astrocytes produce numerous acute-phase reactants and proinflammatory molecules in the AD brain. One such molecule, S100B, is highly expressed by reactive astrocytes in close vicinity of beta-amyloid deposits. We have previously shown that augmented and prolonged activation of astrocytes has a detrimental impact on neuronal survival. Furthermore, we have implicated astrocyte-derived S100B as a candidate molecule responsible for this deleterious effect. To evaluate a putative relationship between S100B and AD pathogenesis, we crossed transgenic mice overexpressing human S100B (TghuS100B mice) with the Tg2576 mouse model of AD, and examined AD-like pathology. Brain parenchymal and cerebral vascular beta-amyloid deposits and Abeta levels were increased in bigenic Tg2576-huS100B mice. These effects were associated with increased cleavage of the beta-C-terminal fragment of amyloid precursor protein (APP), elevation of the N-terminal APP cleavage product (soluble APPbeta), and activation of beta-site APP cleaving enzyme 1. In addition, double transgenic mice showed augmented reactive astrocytosis and microgliosis, high levels of S100 expression, and increased levels of proinflammatory cytokines as early as 7-9 months of age. These results provide evidence that (over)-expression of S100B acts to accelerate AD-like pathology, and suggest that inhibiting astrocytic activation by blocking S100B biosynthesis may be a promising therapeutic strategy to delay AD progression..

Indexed as

Alzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsAstrocytesCerebral Amyloid AngiopathyCerebral CortexCytokinesDisease Models, AnimalFemaleGene Expression RegulationGliosisHumansMaleMiceMice, Inbred C57BLMice, TransgenicAmyloid beta-Protein PrecursorCytokinesNerve Growth FactorsPeptide FragmentsS100B protein, humanS100b protein, mouseS100 Calcium Binding Protein beta SubunitS100 Proteins

Identifiers

PMID19705461
PMCPMC2795105
OpenAlexW1972637602

What OpenQuestion holds

Textmetadata
LicenceTDM
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.