Evidence map›Paper›PMID 21385309›Full record

ArticleAging cell2011

Phenotypic and gene expression modification with normal brain aging in GFAP-positive astrocytes and neural stem cells.

Giovanna M Bernal, Daniel A Peterson

Open access · bronzeAbstract read
In one paragraph

Article in Aging cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 5% 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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Entwined processes in Alzheimer's disease: Brain cellular senescence and Alzheimer's disease pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Nutrients · 2023
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Astrocyte Senescence and Alzheimer's Disease: A Review.Frontiers in aging neuroscience · 2020
    Review
  18. Article
  19. Article
  20. Review
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

2 authors at 1 institution in 1 country.

Giovanna M BernalDepartment of Neuroscience, The Chicago Medical School, Rosalind Franklin University of Medicine and Science, IL 60647, USA.
Daniel A Peterson
Rosalind Franklin University of Medicine and Science · US

Funding

Stem Cells for Brain RepairR01AG020047 · NIA · ROSALIND FRANKLIN UNIV OF MEDICINE &SCI · PI PETERSON, DANIEL ALAN · 2001 to 2013
$2.5M
Neurogenesis in the Aging BrainR01AG022555 · NIA · ROSALIND FRANKLIN UNIV OF MEDICINE &SCI · PI PETERSON, DANIEL ALAN · 2003 to 2007
$1.8M
NIA NIH HHS AG20047NIA NIH HHS AG22555NIA NIH HHS R01 AG020047NIA NIH HHS R01 AG022555
6 · The paper itself

Abstract

Astrocytes secrete growth factors that are both neuroprotective and supportive for the local environment. Identified by glial fibrillary acidic protein (GFAP) expression, astrocytes exhibit heterogeneity in morphology and in the expression of phenotypic markers and growth factors throughout different adult brain regions. In adult neurogenic niches, astrocytes secrete vascular endothelial growth factor (VEGF) and fibroblast growth factor-2 (FGF-2) within the neurogenic niche and are also a source of special GFAP-positive multipotent neural stem cells (NSCs). Normal aging is accompanied by a decline in CNS function and reduced neurogenesis. We asked whether a decreased availability of astrocyte-derived factors may contribute to the age-related decline in neurogenesis. Determining alterations of astrocytic activity in the aging brain is crucial for understanding CNS homeostasis in aging and for assessing appropriate therapeutic targets for an aging population. We found region-specific alterations in the gene expression of GFAP, VEGF, and FGF-2 and their receptors in the aged brain corresponding to changes in astrocytic reactivity, supporting astrocytic heterogeneity and demonstrating a differential aging effect. We found that GFAP-positive NSCs uniquely coexpress both VEGF and its key mitotic receptor Flk-1 in both young and aged hippocampus, indicating a possible autocrine/paracrine signaling mechanism. VEGF expression is lost once NSCs commit to a neuronal fate, but Flk-1-mediated sensitivity to VEGF signaling is maintained. We propose that age-related astrocytic changes result in reduced VEGF and FGF-2 signaling, which in turn limits NSC and progenitor cell maintenance and contributes to decreased neurogenesis.

Indexed as

AgingGlial Fibrillary Acidic ProteinAdultAnimalsAstrocytesCell ProliferationFibroblast Growth Factor 2Gene Expression RegulationGenetic VariationHippocampusHumansImmunohistochemistryIntermediate FilamentsNeural Stem CellsNeuronsRatsFibroblast Growth Factor 2Glial Fibrillary Acidic ProteinVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2

Identifiers

PMID21385309
PMCPMC3094510
OpenAlexW1807507622

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.