Evidence map›Paper›PMID 36564356›Full record

ReviewNeuropathology and applied neurobiology2023

Arteriolar neuropathology in cerebral microvascular disease.

Chuo Fang, Shino D Magaki, Ronald C Kim, Raj N Kalaria, Harry V Vinters, Mark Fisher

Open access · hybridAbstract readReview
In one paragraph

Review in Neuropathology and applied neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
5.6field-weighted citation impact, top 3% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. The role of vascular risk factors in white matter tract microstructure: a multi-cohort study in older adults.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
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  11. Blended Phenotype ofNeurology. Genetics · 2024
    Article
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  14. Review
  15. Observational
  16. Article
  17. Arteriolar neuropathology in cerebral microvascular disease.Neuropathology and applied neurobiology · 2023
    Review
  18. Review
  19. Article
  20. Article
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 4 institutions in 2 countries.

Chuo FangDepartment of Neurology, University of California, Irvine Medical Center, 101 The City Drive South Shanbrom Hall (Building 55), Room 121, Orange, 92868, California, USA.
Shino D MagakiDepartment of Pathology & Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California, USA.
Ronald C KimDepartment of Pathology & Laboratory Medicine, University of California, Irvine, Orange, California, USA.
Raj N KalariaTranslational and Clinical Research Institute, Newcastle University, Campus for Ageing and Vitality, Newcastle upon Tyne, NE4 5PL, UK.ORCID 0000-0001-7907-4923
Harry V VintersDepartment of Pathology & Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California, USA.ORCID 0000-0002-2965-1240
Mark FisherDepartment of Neurology, University of California, Irvine Medical Center, 101 The City Drive South Shanbrom Hall (Building 55), Room 121, Orange, 92868, California, USA.
University of California, Irvine · USUniversity of California, Los Angeles · USNewcastle Hospitals - Campus for Ageing and Vitality · GBUniversity of California, Irvine Medical Center · US

Funding

HEMORHOLOGICAL FACTORS IN CEREBRAL ISCHEMIAR01NS020989 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CRIBBS, DAVID HASTINGS, FISHER, MARK J · 1985 to 2022
$9.1M
Medical Research Council G0500247NINDS NIH HHS R01 NS020989
6 · The paper itself

Abstract

Cerebral microvascular disease (MVD) is an important cause of vascular cognitive impairment. MVD is heterogeneous in aetiology, ranging from universal ageing to the sporadic (hypertension, sporadic cerebral amyloid angiopathy [CAA] and chronic kidney disease) and the genetic (e.g., familial CAA, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy [CADASIL] and cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy [CARASIL]). The brain parenchymal consequences of MVD predominantly consist of lacunar infarcts (lacunes), microinfarcts, white matter disease of ageing and microhaemorrhages. MVD is characterised by substantial arteriolar neuropathology involving ubiquitous vascular smooth muscle cell (SMC) abnormalities. Cerebral MVD is characterised by a wide variety of arteriolar injuries but only a limited number of parenchymal manifestations. We reason that the cerebral arteriole plays a dominant role in the pathogenesis of each type of MVD. Perturbations in signalling and function (i.e., changes in proliferation, apoptosis, phenotypic switch and migration of SMC) are prominent in the pathogenesis of cerebral MVD, making 'cerebral angiomyopathy' an appropriate term to describe the spectrum of pathologic abnormalities. The evidence suggests that the cerebral arteriole acts as both source and mediator of parenchymal injury in MVD.

Indexed as

CADASILCerebral Amyloid AngiopathyNeuromuscular DiseasesArteriolesBrainCerebral InfarctionHumanscerebral angiomyopathycerebral arteriolescerebral microvascular diseaseneuropathologysmooth muscle cells

Identifiers

PMID36564356
PMCPMC10350910
OpenAlexW4312115755

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.