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This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

✓ Peer-reviewed alzhub usefulness score 60 out of 100. Lewy body dementia

Topic: Brain proteins, microglia and lab models

Small vessel disease is a disorder of cerebral microvessels that causes white matter hyperintensities and several other common abnormalities (eg, recent small subcortical infarcts and lacunes) seen on brain imaging. Despite being a common cause of stroke and vascular dementia, the underlying pathogenesis is poorly understood. Research in humans has identified several manifestations of cerebral microvessel endothelial dysfunction including blood-brain barrier dysfunction, impaired vasodilation, vessel stiffening, dysfunctional blood flow and interstitial fluid drainage, white matter rarefaction, ischaemia, inflammation, myelin damage, and secondary neurodegeneration. These brain abnormalities are more dynamic and widespread than previously thought. Relationships between lesions and symptoms are highly variable but poorly understood. Major challenges are the determination of which vascular dysfunctions are most important in pathogenesis, which abnormalities are reversible, and why lesion progression and symptomatology are so variable. This knowledge will help to identify potential targets for intervention and improve risk prediction for individuals with small vessel disease.

Key findings

Why it matters

This review describes cerebral small vessel disease, which shows up on brain scans as white matter hyperintensities, small subcortical infarcts and lacunes, as a common cause of stroke and vascular dementia whose underlying cause is still "poorly understood". It summarises human research linking the disease to blood vessel lining (endothelial) problems such as blood-brain barrier dysfunction, impaired blood flow and fluid drainage, inflammation and myelin damage, and says the link between these lesions and symptoms is "highly variable". It reports no new data and names no treatment; which abnormalities can be reversed is listed as an open question.

Study details

How this study scored 60/100
How this study's score is builtJournal tier 9 of 10; Journal's citation record 3 of 4; Study design 0 of 12; Strength of evidence 1 of 5; Peer-review validation 10 of 10; How recent 2 of 5; Sample size 0 of 4; Effect reported 0 of 3; Studied in people 0 of 3; Randomised / blinded 0 of 2; Times cited 7 of 7; Citations per year 5 of 5; Impact for its field and year 6 of 6; Cited by studies here 4 of 6; Still being cited 4 of 4; Senior author's track record 4 of 4; Institution's track record 1 of 3; Multi-centre collaboration 2 of 3; Indexed in PubMed 2 of 2; Free to read 0 of 2. Total 60 of 100.60 of 100 points earned40 not earned

Published in a leading specialty journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.

ComponentPointsWhy
Journal tier 9 / 10 Tier 2 — leading specialty journal (The Lancet. Neurology)
Journal's citation record 3 / 4 The Lancet Neurology: journal h-index 457 (OpenAlex, 2026-10-29)
Study design 0 / 12 No study design recorded — scores zero, not guessed (not stated in the record — scored 0)
Strength of evidence 1 / 5 Rated “low” in our summary
Peer-review validation 10 / 10 Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent 2 / 5 2019 — within 10 year(s) of the newest study here
Sample size 0 / 4 Participant count not stated — scores zero (not stated in the record — scored 0)
Effect reported 0 / 3 No effect size reported — scores zero (not stated in the record — scored 0)
Studied in people 0 / 3 Not stated whether this was studied in people — scores zero (not stated in the record — scored 0)
Randomised / blinded 0 / 2 No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited 7 / 7 Cited 1,767 times (OpenAlex, 2026-10-10)
Citations per year 5 / 5 196.3 citations a year over 9 year(s) since 2019
Impact for its field and year 6 / 6 Cited 81.3× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 4 / 6 Cited by 59 other studies in this library
Still being cited 4 / 4 Cited 944 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record 4 / 4 Last-listed author Martin Dichgans: h-index 146 (OpenAlex, whole career)
Institution's track record 1 / 3 University of Edinburgh: institution h-index 1,378 (OpenAlex)
Multi-centre collaboration 2 / 3 OpenAlex lists 7 institution(s) in 2 countries
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 31097385)
Free to read 0 / 2 Behind a paywall — scores zero
Total 60 / 100 —

What each of these 20 components measures, and what this score is not →

Read the original

Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.

APA 7th

Wardlaw, J. M., Smith, C., & Dichgans, M. (2019). Small vessel disease: mechanisms and clinical implications. The Lancet. Neurology. https://doi.org/10.1016/s1474-4422(19)30079-1

Vancouver

Wardlaw JM, Smith C, Dichgans M. Small vessel disease: mechanisms and clinical implications. The Lancet. Neurology. 2019. doi:10.1016/s1474-4422(19)30079-1. PMID: 31097385.

BibTeX

@article{wardlaw2019-31097385,
  author  = {Wardlaw, J. M. and Smith, C. and Dichgans, M.},
  title   = {{Small vessel disease: mechanisms and clinical implications}},
  journal = {The Lancet. Neurology},
  year    = {2019},
  doi     = {10.1016/s1474-4422(19)30079-1},
  pmid    = {31097385},
  url     = {https://doi.org/10.1016/s1474-4422(19)30079-1}
}

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