Evidence map›Paper›PMID 29361890›Full record

ArticleTissue engineering. Part A2018

Modeling Neurodegenerative Microenvironment Using Cortical Organoids Derived from Human Stem Cells.

Yuanwei Yan, Liqing Song, Julie Bejoy, Jing Zhao, Takahisa Kanekiyo, Guojun Bu, Yi Zhou, Yan Li

Open access · greenAbstract read
In one paragraph

Article in Tissue engineering. Part A, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 2 pooled it
4.4field-weighted citation impact, top 4% 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

52 citing papers in PubMed, 2 syntheses or guidelines pooled it, 79 citations in OpenAlex.

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  19. Lamin B1 as a key modulator of the developing and aging brain.Frontiers in cellular neuroscience · 2023
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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

8 authors at 2 institutions in 1 country.

Yuanwei Yan1 Department of Chemical and Biomedical Engineering, FAMU-FSU College of Engineering, Florida State University , Tallahassee, Florida.
Liqing Song1 Department of Chemical and Biomedical Engineering, FAMU-FSU College of Engineering, Florida State University , Tallahassee, Florida.
Julie Bejoy1 Department of Chemical and Biomedical Engineering, FAMU-FSU College of Engineering, Florida State University , Tallahassee, Florida.
Jing Zhao2 Department of Neuroscience, Alzheimer's Disease Research Center , Mayo Clinic, Jacksonville, Florida.
Takahisa Kanekiyo2 Department of Neuroscience, Alzheimer's Disease Research Center , Mayo Clinic, Jacksonville, Florida.
Guojun Bu2 Department of Neuroscience, Alzheimer's Disease Research Center , Mayo Clinic, Jacksonville, Florida.
Yi Zhou3 Department of Biomedical Sciences, College of Medicine, Florida State University , Tallahassee, Florida.
Yan Li1 Department of Chemical and Biomedical Engineering, FAMU-FSU College of Engineering, Florida State University , Tallahassee, Florida.
Florida A&M University - Florida State University College of Engineering · USFlorida State University · US

Funding

Viral Vectors CoreP01NS074969 · NINDS · WASHINGTON UNIVERSITY · PI SNIDER, BARBARA JOY · 2012 to 2021
$13.0M
Integrative translational discovery of vascular risk factors in aging and dementiaRF1AG051504 · NIA · MAYO CLINIC JACKSONVILLE · PI BU, GUOJUN, ERTEKIN-TANER, NILUFER · 2015 to 2019
$9.8M
ApoE Receptor Pathways to Intraneuronal AbetaR01AG027924 · NIA · WASHINGTON UNIVERSITY · PI LI, YONGHE · 2006 to 2021
$3.7M
BRAIN LIPID METABOLISM, DENDRITES AND SYNAPSES IN AGING AND ALZHEIMER'S DISEASER01AG035355 · NIA · MAYO CLINIC JACKSONVILLE · PI BU, GUOJUN · 2010 to 2019
$3.1M
ApoE isoform-specific therapy for Alzheimer diseaseRF1AG046205 · NIA · MAYO CLINIC JACKSONVILLE · PI ZHAO, NA · 2019 to 2019
$3.1M
ApoE pathway in cerebrovascular Aβ clearance in Alzheimer’s diseaseR37AG027924 · NIA · MAYO CLINIC JACKSONVILLE · PI BU, GUOJUN · 2017 to 2020
$2.4M
Molecular, synaptic and circuit basis for 14-3-3 dysfunction-induced behavioral deficitsR01MH115188 · NIMH · FLORIDA STATE UNIVERSITY · PI ZHOU, YI · 2017 to 2021
$1.9M
ApoE isoform-specific therapy for Alzheimer diseaseR01AG046205 · NIA · MAYO CLINIC JACKSONVILLE · PI BU, GUOJUN · 2013 to 2017
$1.6M
Engineering Extracellular Matrices in Forebrain Organoids for Studying Neural DegenerationR03NS102640 · NINDS · FLORIDA STATE UNIVERSITY · PI LI, YAN · 2017 to 2018
$143k
NIA NIH HHS R01 AG027924NIA NIH HHS R01 AG035355NIA NIH HHS RF1 AG046205NIA NIH HHS RF1 AG051504NIMH NIH HHS R01 MH115188NINDS NIH HHS P01 NS074969NINDS NIH HHS R03 NS102640
6 · The paper itself

Abstract

Alzheimer's disease (AD) is one of the most common neurodegenerative disorders and causes cognitive impairment and memory deficits of the patients. The mechanism of AD is not well known, due to lack of human brain models. Recently, mini-brain tissues called organoids have been derived from human induced pluripotent stem cells (hiPSCs) for modeling human brain development and neurological diseases. Thus, the objective of this research is to model and characterize neural degeneration microenvironment using three-dimensional (3D) forebrain cortical organoids derived from hiPSCs and study the response to the drug treatment. It is hypothesized that the 3D forebrain organoids derived from hiPSCs with AD-associated genetic background may partially recapitulate the extracellular microenvironment in neural degeneration. To test this hypothesis, AD-patient derived hiPSCs with presenilin-1 mutation were used for cortical organoid generation. AD-related inflammatory responses, matrix remodeling and the responses to DAPT, heparin (completes with heparan sulfate proteoglycans [HSPGs] to bind Aβ42), and heparinase (digests HSPGs) treatments were investigated. The results indicate that the cortical organoids derived from AD-associated hiPSCs exhibit a high level of Aβ42 comparing with healthy control. In addition, the AD-derived organoids result in an elevated gene expression of proinflammatory cytokines interleukin-6 and tumor necrosis factor-α, upregulate syndecan-3, and alter matrix remodeling protein expression. Our study demonstrates the capacity of hiPSC-derived organoids for modeling the changes of extracellular microenvironment and provides a potential approach for AD-related drug screening.

Indexed as

Cellular MicroenvironmentModels, BiologicalAlzheimer DiseaseAmyloid beta-PeptidesBiomarkersCell DeathCell SurvivalCerebral CortexGene Expression RegulationHumansNerve DegenerationOrganoidsPhenotypeSpheroids, CellularStem Cellstau ProteinsAmyloid beta-PeptidesBiomarkerstau Proteinsdegenerationhuman induced pluripotent stem cellsneural differentiationorganoidsthree-dimensional

Identifiers

PMID29361890
PMCPMC6033307
OpenAlexW2784614257

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.