Evidence map›Paper›PMID 21904637›Full record

ArticleInternational journal of clinical and experimental pathology2011

Brain microvasculature and hypoxia-related proteins in Alzheimer's disease.

Paula Grammas, Debjani Tripathy, Alma Sanchez, Xiangling Yin, Jinhua Luo

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

38 citing papers in PubMed, 61 citations in OpenAlex.

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  4. Evidence of cortical vascular impairments in early stage of Alzheimer's transgenic mice: Optical imaging.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2025
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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.

Paula GrammasGarrison Institute on Aging and Department of Neurology, Texas Tech University Health Sciences Center Lubbock, TX 79430, USA. paula.grammas@ttuhsc.edu
Debjani Tripathy
Alma Sanchez
Xiangling Yin
Jinhua Luo
Texas Tech University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive, neurodegenerative disease of increasing incidence. The pathologic processes that underlie this disorder are incompletely understood, however, hypoperfusion/hypoxia is thought to contribute to disease pathogenesis. Hypoxia inducible factor 1-alpha (HIF-1α), a key regulator of cellular responses to hypoxia, is elevated in the microcirculation of AD patients. Cerebral hypoxia is a potent stimulus for vascular activation and angiogenesis. Microvessels isolated from the brains of AD patients express a large number of angiogenic proteins. Despite considerable data in human tissues regarding vascular expression of hypoxia-related angiogenic proteins, there is little information regarding these proteins in the brain vasculature of transgenic AD mice. The objectives of this study were to determine expression of HIF-1α, angiogenic proteins, angiopoietin-2 (Ang-2), and matrix metalloproteinase 2 (MMP2), and survival/apoptotic proteins (Bcl-xL, caspase 3) in the cerebromicrovasculature of AD transgenic mice and to determine the direct effect of hypoxia on cerebral endothelial expression of these proteins in vitro. Cultured brain endothelial cells were subjected to hypoxia for 4-6 h and analyzed by western blot and immunofluorescence. Our results demonstrated that HIF-1α is induced in cultured brain endothelial cells exposed to hypoxia and that expression of Ang-2, MMP2 and caspase 3 was elevated and the anti-apoptotic protein Bcl-xL decreased. Brain sections from AD and control mice showed that HIF-1α, Ang-2, MMP2 and caspase 3 are elevated and Bcl-xL decreased in the microvasculature of AD mice. These data suggest the cerebromicrovasculature is an important target for the effects of hypoxia in the AD brain.

Indexed as

Alzheimer DiseaseAngiopoietin-2Animalsbcl-X ProteinBrainCaspase 3Cell HypoxiaCells, CulturedDisease Models, AnimalEndothelial CellsHypoxia-Inducible Factor 1, alpha SubunitMatrix Metalloproteinase 2MiceMice, TransgenicMicrocirculationRatsAngiopoietin-2Bcl2l1 protein, mousebcl-X ProteinCasp3 protein, mouseCaspase 3Hif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitMatrix Metalloproteinase 2von Willebrand FactorAD miceangiogenesisapoptosisbrain microvesselsHypoxia

Identifiers

PMID21904637
PMCPMC3160613
OpenAlexW76306425

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.