Evidence map›Paper›PMID 37158955›Full record

ArticleActa neuropathologica communications2023

ER stress induced immunopathology involving complement in CADASIL: implications for therapeutics.

Mahmod Panahi, Yoshiki Hase, Xavier Gallart-Palau, Sumonto Mitra, Atsushi Watanabe, Roger C Low, Yumi Yamamoto, Diego Sepulveda-Falla, Atticus H Hainsworth, Masafumi Ihara and 4 more

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

14 citing papers in PubMed, 17 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

14 authors at 10 institutions in 7 countries.

Mahmod Panahi *Department of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Clinical Geriatrics, Karolinska Institutet, BioClinicum J9:20 Visionsgatan 4, Solna, 171 64, Sweden.
Yoshiki Hase *Translational and Clinical Research Institute, Campus for Ageing and Vitality, Newcastle University, Newcastle upon Tyne, NE4 5PL, UK.
Xavier Gallart-Palau *Biomedical Research Institute of Lleida (IRBLLEIDA) - +Pec Proteomics Research Group (+PPRG) - Neuroscience Area, University Hospital Arnau de Vilanova (HUAV) - Department of Psychology, University of Lleida (UdL), Lleida, Spain.
Sumonto MitraDepartment of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Clinical Geriatrics, Karolinska Institutet, BioClinicum J9:20 Visionsgatan 4, Solna, 171 64, Sweden.
Atsushi WatanabeEquipment Management Division, Center for Core Facility Administration, Research Institute, National Center for Geriatrics and Gerontology (NCGG), 7-430, Morioka-cho, Obu-shi, 474-8511, Aichi, Japan.
Roger C LowTranslational and Clinical Research Institute, Campus for Ageing and Vitality, Newcastle University, Newcastle upon Tyne, NE4 5PL, UK.
Yumi YamamotoDepartment of Molecular Innovation in Lipidemiology and Department of Neurology, National Cerebral and Cardiovascular Center, 6-1 Kishibeshinmachi, Suita, 564-8565, Osaka, Japan.
Diego Sepulveda-FallaMolecular Neuropathology of Alzheimer's Disease, Institute of Neuropathology, University Medical Center Hamburg-Eppendorf, 20246, Hamburg, Germany.
Atticus H HainsworthMolecular and Clinical Sciences, St George's University of London, Cranmer Terrace, London, SW17 0RE, UK.
Masafumi IharaDepartment of Molecular Innovation in Lipidemiology and Department of Neurology, National Cerebral and Cardiovascular Center, 6-1 Kishibeshinmachi, Suita, 564-8565, Osaka, Japan.
Siu Kwan SzeFaculty of Applied Health Sciences, Brock University, St. Catharines, ON, L2S 3A1, Canada.
Matti ViitanenDepartment of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Clinical Geriatrics, Karolinska Institutet, BioClinicum J9:20 Visionsgatan 4, Solna, 171 64, Sweden.
Homira Behbahani *Department of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Clinical Geriatrics, Karolinska Institutet, BioClinicum J9:20 Visionsgatan 4, Solna, 171 64, Sweden.
Raj N Kalaria *Translational and Clinical Research Institute, Campus for Ageing and Vitality, Newcastle University, Newcastle upon Tyne, NE4 5PL, UK. raj.kalaria@newcastle.ac.uk.
Karolinska Institutet · SENational Cerebral and Cardiovascular Center · JPNewcastle Hospitals - Campus for Ageing and Vitality · GBBrock University · CAHospital Universitari Arnau de Vilanova · ESNational Center for Geriatrics and Gerontology · JPNewcastle University · GBSt George's, University of London · GBTurku City Hospital · FIUniversität Hamburg · DE

Funding

Charting vascular contributions to white matter disease in familial Alzheimer's disease and CADASILRF1NS110048 · NINDS · SCHEPENS EYE RESEARCH INSTITUTE · PI ARBOLEDA-VELASQUEZ, JOSEPH, SEPULVEDA-FALLA, DIEGO · 2018 to 2019
$3.6M
Department of HealthMedical Research Council G0400074Medical Research Council G0500247National Centre for the Replacement, Refinement and Reduction of Animals in Research G0800701/1NIA NIH HHS RF1NS110048NINDS NIH HHS RF1 NS110048
6 · The paper itself

Abstract

Cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is caused by NOTCH3 mutations. Typical CADASIL is characterised by subcortical ischemic strokes due to severe arteriopathy and fibrotic thickening of small arteries. Arteriolar vascular smooth muscle cells (VSMCs) are the key target in CADASIL, but the potential mechanisms involved in their degeneration are still unclear. Focusing on cerebral microvessels in the frontal and anterior temporal lobes and the basal ganglia, we used advanced proteomic and immunohistochemical methods to explore the extent of inflammatory and immune responses in CADASIL subjects compared to similar age normal and other disease controls. There was variable loss of VSMC in medial layers of arteries in white matter as well as the cortex, that could not be distinguished whether NOTCH3 mutations were in the epidermal growth factor (EGFr) domains 1-6 or EGFr7-34. Proteomics of isolated cerebral microvessels showed alterations in several proteins, many associated with endoplasmic reticulum (ER) stress including heat shock proteins. Cerebral vessels with sparsely populated VSMCs also attracted robust accrual of perivascular microglia/macrophages in order CD45

Indexed as

CADASILCerebral InfarctionComplement System ProteinsHumansIntercellular Adhesion Molecule-1ProteomicsComplement System ProteinsIntercellular Adhesion Molecule-1CADASILComplementInterleukin 6Intracellular adhesion moleculeStrokeVascular smooth muscle cells

Identifiers

PMID37158955
PMCPMC10169505
OpenAlexW4375860850

What OpenQuestion holds

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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.