Evidence map›Paper›PMID 15181253›Full record

ReviewJournal of molecular neuroscience : MN2004

In vivo effects of ApoE and clusterin on amyloid-beta metabolism and neuropathology.

David M Holtzman

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of molecular neuroscience : MN, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
5.7field-weighted citation impact, top 4% 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

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 140 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Alterations in the inflammatory homeostasis of aging-related cardiac dysfunction and Alzheimer's diseases.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

6 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

1 author at 1 institution in 1 country.

David M HoltzmanCenter for the Study of Nervous System Injury, Alzheimer's Disease Research Center, Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA. holtzman@neuro.wustl.edu
Washington University in St. Louis · US

Funding

WASHINGTON UNIVERSITY ALZHEIMERS DISEASE RESEARCH CENTERP50AG005681 · NIA · WASHINGTON UNIVERSITY · PI MORRIS, JOHN · 1985 to 2019
$52.1M
Alzheimer's Abeta, Tau, Apolipoproteins and Blood-brain barrierR01NS034467 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI YASSINE, HUSSEIN N · 1995 to 2024
$9.1M
SENSITIVITY OF AGED RATS TO NRHYPO NEURODEGENERATIONP01AG011355 · NIA · WASHINGTON UNIVERSITY · PI OLNEY, JOHN W · 1995 to 2004
$7.0M
Effect of apoE on CNS neurons: Role of LRPR37AG013956 · NIA · WASHINGTON UNIVERSITY · PI HOLTZMAN, DAVID M. · 2004 to 2013
$3.8M
Alzheimer's Abeta, apolipoproteins and blood-brain barrierR37NS034467 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ZLOKOVIC, BERISLAV V · 2007 to 2013
$3.4M
APOE EFFECT ON CNS NEURONS--ROLE OF LRPR01AG013956 · NIA · WASHINGTON UNIVERSITY · PI HOLTZMAN, DAVID M · 1996 to 2003
$1.2M
NIA NIH HHS AG11355NIA NIH HHS AG13956NIA NIH HHS P50-AG05681NINDS NIH HHS NS034467
6 · The paper itself

Abstract

The epsilon4 allele of apolipoprotein E APOE is a risk factor for Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA), and the epsilon2 allele is associated with a decreased risk for AD. There is strong evidence to suggest that a major, if not the main, mechanism underlying the link between apoE and both AD and CAA is related to the ability of apoE to interact with the amyloid-beta (Abeta) peptide and influence its clearance, aggregation, and conformation. In addition to a number of in vitro studies supporting this concept, in vivo studies with amyloid precursor protein (APP) transgenic mice indicate that apoE and a related molecule, clusterin (also called apolipoprotein J), have profound effects on the onset of Abeta deposition, as well as the local toxicity associated with Abeta deposits both in the brain parenchyma and in cerebral blood vessels. Taken together, these studies suggest that altering the expression of apoE and clusterin in the brain or the interactions between these molecules and Abeta would alter AD pathogenesis and provide new therapeutic avenues for prevention or treatment of CAA and AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsApolipoproteins EClusterinGlycoproteinsHumansMiceMice, TransgenicMolecular ChaperonesRisk FactorsAmyloid beta-PeptidesApolipoproteins ECLU protein, humanClu protein, mouseClusterinGlycoproteinsMolecular Chaperones

Identifiers

PMID15181253
OpenAlexW2032452147

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.