Evidence map›Paper›PMID 37986739›Full record

ArticlebioRxiv : the preprint server for biology2023

A novel mouse model of cerebral adrenoleukodystrophy highlights NLRP3 activity in lesion pathogenesis.

Ezzat Hashemi, Isha Narain Srivastava, Alejandro Aguirre, Ezra Tilahan Yoseph, Esha Kaushal, Avni Awani, Jae Kyu Ryu, Katerina Akassoglou, Shahrzad Talebian, Pauline Chu and 14 more

Open access · greenAbstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed, 3 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

24 authors at 7 institutions in 2 countries.

Ezzat HashemiDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0003-0868-4331
Isha Narain SrivastavaDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
Alejandro AguirreDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
Ezra Tilahan YosephDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
Esha KaushalDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
Avni AwaniDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
Jae Kyu RyuGladstone Institute for Neurological Disease; San Francisco, CA, USA.
Katerina AkassoglouGladstone Institute for Neurological Disease; San Francisco, CA, USA.ORCID 0000-0002-2632-1465
Shahrzad TalebianDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0003-4470-2170
Pauline ChuStanford Human Research Histology Core, Stanford University School of Medicine, Stanford, CA, USA.
Laura PisaniDepartment of Radiology, Stanford University School of Medicine Stanford, CA, USA.
Patricia MusolinoDepartment of Neurology, Massachusetts General Hospital, Boston, MA, USA.ORCID 0000-0001-8724-5649
Lawrence SteinmanDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
Kristian DoyleDepartment of Immunobiology, University of Arizona, Tucson, AZ, USA.ORCID 0000-0003-2788-7038
William H RobinsonDepartment of Immunology & Rheumatology, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0003-4385-704X
Orr SharpeDepartment of Immunology & Rheumatology, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0003-1986-7555
Romain CayrolDepartment of Pathology, Clinical Department of Laboratory Medicine, University of Montreal, Quebec, Canada.ORCID 0000-0003-2745-2704
Paul OrchardDivision of Pediatric Blood & Marrow Transplantation, University of Minnesota, Minneapolis, MN, USA.ORCID 0000-0001-9426-1292
Troy LundDivision of Pediatric Blood & Marrow Transplantation, University of Minnesota, Minneapolis, MN, USA.ORCID 0000-0001-9174-8919
Hannes VogelDepartments of Pathology, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0002-0960-3508
Max LenailDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
May Htwe HanDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
Joshua Leith BonkowskyDivision of Pediatric Neurology, Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, Utah.ORCID 0000-0001-8775-147X
Keith P Van HarenDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0002-0233-9361
Stanford University · USGladstone Institutes · USUniversity of Minnesota · USMassachusetts General Hospital · USPrimary Children's Hospital · USUniversité de Montréal · CAUniversity of Arizona · US

Funding

Neurovascular Interactions: Mechanisms, imaging, therapeutic potentialR35NS097976 · NINDS · J. DAVID GLADSTONE INSTITUTES · PI AKASSOGLOU, KATERINA · 2016 to 2023
$11.1M
Training Program in Adult and Pediatric RheumatologyT32AR050942 · NIAMS · STANFORD UNIVERSITY · PI LEWIS, DAVID BRAM, ROBINSON, WILLIAM H · 2005 to 2025
$6.6M
Effects of ABCD1 Deficiency on Endothelial Function and Permeability to Leukocytes in Cerebral X-linked AdrenoleukodystrophyR01NS117575 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI MUSOLINO, PATRICIA L · 2020 to 2024
$2.0M
NIAMS NIH HHS T32 AR050942NINDS NIH HHS R01 NS117575NINDS NIH HHS R35 NS097976
6 · The paper itself

Abstract

Objective: We sought to create and characterize a mouse model of the inflammatory, cerebral demyelinating phenotype of X-linked adrenoleukodystrophy (ALD) that would facilitate the study of disease pathogenesis and therapy development. We also sought to cross-validate potential therapeutic targets such as fibrin, oxidative stress, and the NLRP3 inflammasome, in post-mortem human and murine brain tissues. Background: ALD is caused by mutations in the gene Methods: We generated a cALD phenotype in 8-week-old, male Results: MRI studies revealed T2 hyperintensities and post-gadolinium enhancement in the medial corpus callosum of cALD mice, similar to human cALD lesions. Both human and mouse cALD lesions shared common histologic features of myelin phagocytosis, myelin loss, abundant microglial activation, T and B-cell infiltration, and astrogliosis. Compared to wild-type controls, Interpretation: This novel mouse model of cALD suggests loss of

Identifiers

PMID37986739
PMCPMC10659266
OpenAlexW4388582781

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.