Evidence map›Paper›PMID 28902142›Full record

ReviewInternational journal of molecular sciences2017

Blood-Brain Barrier Dysfunction and the Pathogenesis of Alzheimer's Disease.

Yu Yamazaki, Takahisa Kanekiyo

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 236 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
236citing papers in PubMed, 5 pooled it
16.8field-weighted citation impact, top 1% 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

236 citing papers in PubMed, 5 syntheses or guidelines pooled it, 427 citations in OpenAlex.

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  9. Blood-Based Biomarkers for Post-Stroke Cognitive Impairment.Current issues in molecular biology · 2026
    Review
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176 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

2 authors at 1 institution in 1 country.

Yu YamazakiDepartment of Neuroscience, Mayo Clinic, 4500 San Pablo Road, Jacksonville, FL 32224, USA. yamazaki.yu@mayo.edu.ORCID 0000-0002-0806-4960
Takahisa KanekiyoDepartment of Neuroscience, Mayo Clinic, 4500 San Pablo Road, Jacksonville, FL 32224, USA. kanekiyo.takahisa@mayo.edu.
Mayo Clinic in Florida · US

Funding

Brain Neurotropic Growth Factor Delivery to Prevent and Treat Alzheimer’s DiseaseR01AG051574 · NIA · NORTH DAKOTA STATE UNIVERSITY · PI KANEKIYO, TAKAHISA, SINGH, JAGDISH · 2016 to 2020
$2.0M
NIA NIH HHS R01 AG051574
6 · The paper itself

Abstract

Brain capillary endothelial cells form the blood-brain barrier (BBB), which is covered with basement membranes and is also surrounded by pericytes and astrocyte end-feet in the neurovascular unit. The BBB tightly regulates the molecular exchange between the blood flow and brain parenchyma, thereby regulating the homeostasis of the central nervous system (CNS). Thus, dysfunction of the BBB is likely involved in the pathogenesis of several neurological diseases, including Alzheimer's disease (AD). While amyloid-β (Aβ) deposition and neurofibrillary tangle formation in the brain are central pathological hallmarks in AD, cerebrovascular lesions and BBB alteration have also been shown to frequently coexist. Although further clinical studies should clarify whether BBB disruption is a specific feature of AD pathogenesis, increasing evidence indicates that each component of the neurovascular unit is significantly affected in the presence of AD-related pathologies in animal models and human patients. Conversely, since some portions of Aβ are eliminated along the neurovascular unit and across the BBB, disturbing the pathways may result in exacerbated Aβ accumulation in the brain. Thus, current evidence suggests that BBB dysfunction may causatively and consequently contribute to AD pathogenesis, forming a vicious cycle between brain Aβ accumulation and neurovascular unit impairments during disease progression.

Indexed as

AlbuminsAlzheimer DiseaseAmyloid beta-PeptidesAnimalsAstrocytesBasement MembraneBiological TransportBlood-Brain BarrierBrainCentral Nervous SystemCerebral Amyloid AngiopathyCerebrovascular DisordersDisease ProgressionEndothelial CellsHomeostasisHumansAlbuminsAmyloid beta-PeptidesPeptide FragmentsSerum Albuminamyloid-βastrocytesbasement membranecerebral amyloid angiopathyendothelial cellsneurovascular unitpericytestight junctions

Identifiers

PMID28902142
PMCPMC5618614
OpenAlexW2756319919

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.