Evidence map›Paper›PMID 20684749›Full record

ReviewClinical science (London, England : 1979)2010

The vascular contribution to Alzheimer's disease.

Robin Altman, John C Rutledge

Open access · greenAbstract readReview
In one paragraph

Review in Clinical science (London, England : 1979), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
7.0field-weighted citation impact, top 2% 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

54 citing papers in PubMed, 117 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Review
  5. Cerebrovascular phenotypes in mouse models of Alzheimer's disease.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
    Review
  6. Perspectives on the Role ofJournal of Alzheimer's disease reports · 2021
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Molecular Insight into the Therapeutic Promise of TargetingOxidative medicine and cellular longevity · 2020
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Metabolic Syndrome and Amyloid Accumulation in the Aging Brain.Journal of Alzheimer's disease : JAD · 2018
    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.

Robin AltmanDepartment of Internal Medicine, University of California-Davis, 451 East Health Sciences Drive, Davis, CA 95616, U.S.A. raltman@ucdavis.edu
John C Rutledge
University of California, Davis · US

Funding

UC Davis Alzheimer's Disease Core CenterP30AG010129 · NIA · UNIVERSITY OF CALIFORNIA DAVIS · PI DECARLI, CHARLES · 1991 to 2020
$28.3M
UC DAVIS CLINICAL AND TRANSLATIONAL SCIENCE CENTER: BPCAUL1RR024146 · NCRR · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BERGLUND, LARS F · 2006 to 2011
$27.0M
Interactions of Lipoproteins with the Vascular WallR01HL055667 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI RUTLEDGE, JOHN CALVERT · 1996 to 2010
$2.8M
Brain Microvascular Determinants of Alzheimers DiseaseR01AG039094 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI RUTLEDGE, JOHN CALVERT · 2010 to 2014
$2.1M
NCRR NIH HHS UL1 RR024146NHLBI NIH HHS R01 HL055667NHLBI NIH HHS R01 HL55667NIA NIH HHS P30 AG010129NIA NIH HHS P30 AG10129-15NIA NIH HHS R01 AG039094
6 · The paper itself

Abstract

AD (Alzheimer's disease) is a progressive neurodegenerative disease of unknown origin. Despite questions as to the underlying cause(s) of this disease, shared risk factors for both AD and atherosclerotic cardiovascular disease indicate that vascular mechanisms may critically contribute to the development and progression of both AD and atherosclerosis. An increased risk of developing AD is linked to the presence of the apoE4 (apolipoprotein E4) allele, which is also strongly associated with increased risk of developing atherosclerotic cardiovascular disease. Recent studies also indicate that cardiovascular risk factors, including elevated blood cholesterol and triacylglycerol (triglyceride), increase the likelihood of AD and vascular dementia. Lipids and lipoproteins in the circulation interact intimately with the cerebrovasculature, and may have important effects on its constituent brain microvascular endothelial cells and the adjoining astrocytes, which are components of the neurovascular unit. The present review will examine the potential mechanisms for understanding the contributions of vascular factors, including lipids, lipoproteins and cerebrovascular Abeta (amyloid beta), to AD, and suggest therapeutic strategies for the attenuation of this devastating disease process. Specifically, we will focus on the actions of apoE, TGRLs (triacylglycerol-rich lipoproteins) and TGRL lipolysis products on injury of the neurovascular unit and increases in blood-brain barrier permeability.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesApolipoprotein E4BrainDisease ProgressionHumansLipidsLipolysisLipoproteinsProtein ConformationRisk FactorsVascular DiseasesAmyloid beta-PeptidesApolipoprotein E4LipidsLipoproteins

Identifiers

PMID20684749
PMCPMC2950620
OpenAlexW2045562899

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.