Evidence map›Paper›PMID 37051650›Full record

ReviewJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2023

CD31 as a probable responding and gate-keeping protein of the blood-brain barrier and the risk of Alzheimer's disease.

Zhengrong Zhang, Qini Gan, Jingyan Han, Qiushan Tao, Wei Qiao Qiu, Joseph A Madri

Open access · greenAbstract readReview
In one paragraph

Review in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed, 29 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Zhengrong ZhangDepartments of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Boston, MA, USA.ORCID 0000-0002-0608-8520
Qini GanDepartments of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Boston, MA, USA.
Jingyan HanWhitaker Cardiovascular Research Institute, Boston University School of Medicine, Boston, MA, USA.
Qiushan TaoDepartments of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Boston, MA, USA.
Wei Qiao QiuDepartments of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Boston, MA, USA.
Joseph A MadriDepartment of Pathology, Yale University School of Medicine, New Haven, CT, USA.
Boston University · USYale University · US

Funding

CD14 AND THE IMMUNOPATHOGENESIS OF CHRONIC LYME DISEASER01AI054546 · NIAID · ALBANY MEDICAL COLLEGE · PI SELLATI, TIMOTHY J · 2004 to 2008
$1.7M
NIAID NIH HHS R01 AI054546
6 · The paper itself

Abstract

Several studies have shown that an abnormal vascular-immunity link could increase Alzheimer's disease (AD) risk; however, the mechanism is unclear. CD31, also named platelet endothelial cell adhesion molecule (PECAM), is a surface membrane protein of both endothelial and immune cells and plays important roles in the interaction between the vascular and immune systems. In this review, we focus on research regarding CD31 biological actions in the pathological process that may contribute to AD based on the following rationales. First, endothelial, leukocyte and soluble forms of CD31 play multi-roles in regulating transendothelial migration, increasing blood-brain barrier (BBB) permeability and resulting in neuroinflammation. Second, CD31 expressed by endothelial and immune cells dynamically modulates numbers of signaling pathways, including Src family kinases, selected G proteins, and β-catenin which in turn affect cell-matrix and cell-cell attachment, activation, permeability, survival, and ultimately neuronal cell injury. In endothelia and immune cells, these diverse CD31-mediated pathways act as a critical regulator in the immunity-endothelia-brain axis, thereby mediating AD pathogenesis in ApoE4 carriers, which is the major genetic risk factor for AD. This evidence suggests a novel mechanism and potential drug target for CD31 in the background of genetic vulnerabilities and peripheral inflammation for AD development and progression.

Indexed as

Alzheimer DiseaseBlood-Brain BarrierHumansPlatelet Endothelial Cell Adhesion Molecule-1Signal TransductionTransendothelial and Transepithelial MigrationPECAM1 protein, humanPlatelet Endothelial Cell Adhesion Molecule-1Alzheimer's disease (AD)blood–brain barrier (BBB)CD31neuroinflammationtrans-endothelia

Identifiers

PMID37051650
PMCPMC10291450
OpenAlexW4365444147

What Socratic 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 Socratic graph.