Evidence map›Paper›PMID 34416494›Full record

ArticleNeurobiology of aging2021

Vascular endothelial growth factor associated dissimilar cerebrovascular phenotypes in two different mouse models of Alzheimer's Disease.

Nicholas M Tataryn, Vishal Singh, Jonathan P Dyke, Hanna E Berk-Rauch, Dana M Clausen, Eric Aronowitz, Erin H Norris, Sidney Strickland, Hyung Jin Ahn

Abstract read
In one paragraph

Article in Neurobiology of aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Review
  2. Article
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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

9 authors.

Nicholas M TatarynTri-Institutional Training Program in Laboratory Animal Medicine and Science, Memorial Sloan Kettering Cancer Center, Weill Cornell Medicine, and The Rockefeller University, New York, New York, USA and Center for Comparative Medicine and Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA; Patricia and John Rosenwald Laboratory of Neurobiology and Genetics, Rockefeller University, New York, NY, USA; Division of Comparative Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
Vishal SinghDepartment of Pharmacology, Physiology and Neurosciences, Rutgers-New Jersey Medical School, Newark, NJ, USA.
Jonathan P DykeCitigroup Biomedical Imaging Center, Department of Radiology, Weill Cornell Medicine, New York, NY, USA.
Hanna E Berk-RauchPatricia and John Rosenwald Laboratory of Neurobiology and Genetics, Rockefeller University, New York, NY, USA.
Dana M ClausenDepartment of Pharmacology, Physiology and Neurosciences, Rutgers-New Jersey Medical School, Newark, NJ, USA.
Eric AronowitzCitigroup Biomedical Imaging Center, Department of Radiology, Weill Cornell Medicine, New York, NY, USA.
Erin H NorrisPatricia and John Rosenwald Laboratory of Neurobiology and Genetics, Rockefeller University, New York, NY, USA.
Sidney StricklandPatricia and John Rosenwald Laboratory of Neurobiology and Genetics, Rockefeller University, New York, NY, USA.
Hyung Jin AhnDepartment of Pharmacology, Physiology and Neurosciences, Rutgers-New Jersey Medical School, Newark, NJ, USA; Brain Health Institute, Rutgers University, Piscataway, NJ, USA. Electronic address: hyungjin.ahn@rutgers.edu.

Funding

Role of Fibrinogen in Alzheimer's DiseaseR01NS106668 · NINDS · ROCKEFELLER UNIVERSITY · PI Erin H. Norris, SIDNEY STRICKLAND · 2018 to 2026
$5.8M
Studying Pathogenic Mechanism of Hereditary Cerebral Amyloid AngiopathyR01NS104386 · NINDS · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI AHN, HYUNG JIN · 2018 to 2023
$2.1M
HIGH POTASSIUM INDUCED NEURONAL DEATH--IN VIVO MECHANICSF05NS010668 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ZHANG, JIANJUN · 1998 to 1998
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NINDS NIH HHS F05 NS010668NINDS NIH HHS R01 NS104386NINDS NIH HHS R01 NS106668
6 · The paper itself

Abstract

Vascular perturbations and cerebral hypometabolism are emerging as important components of Alzheimer's disease (AD). While various in vivo imaging modalities have been designed to detect changes of cerebral perfusion and metabolism in AD patients and animal models, study results were often heterogenous with respect to imaging techniques and animal models. We therefore evaluated cerebral perfusion and glucose metabolism of two popular transgenic AD mouse strains, TgCRND8 and 5xFAD, at 7 and 12 months-of-age under identical conditions and analyzed possible molecular mechanisms underlying heterogeneous cerebrovascular phenotypes. Results revealed disparate findings in these two strains, displaying important aspects of AD progression. TgCRND8 mice showed significantly decreased cerebral blood flow and glucose metabolism with unchanged cerebral blood volume (CBV) at 12 months-of-age whereas 5xFAD mice showed unaltered glucose metabolism with significant increase in CBV at 12 months-of-age and a biphasic pattern of early hypoperfusion followed by a rebound to normal cerebral blood flow in late disease. Finally, immunoblotting assays suggested that VEGF dependent vascular tone change may restore normoperfusion and increase CBV in 5xFAD.

Indexed as

Alzheimer DiseaseAnimalsBrainCerebrovascular CirculationDisease Models, AnimalGlucoseHumansMice, TransgenicVascular Endothelial Growth Factor AGlucoseVascular Endothelial Growth Factor AAlzheimer diseaseArterial spin labeling (ASL)Cerebral blood flowCerebral blood volumeCerebral metabolismDynamic susceptibility contrast-enhanced magnetic resonance imagingVascular endothelial growth factor

Identifiers

PMID34416494
PMCPMC8595520

What OpenQuestion holds

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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.