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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 53 out of 100. Prevention and risk

Topic: Risk, prevention and care in population studies

The notion of what qualifies as vascular dementia has varied greatly since the first mention of dementia after apoplexy in ancient literature. Current insight points towards a multifactorial cause of cognitive decline at old age, in which vascular components like atherosclerosis, arterio(lo)sclerosis, (micro)infarcts, and amyloid angiopathy play an important role alongside other markers of neurodegeneration. Cerebrovascular disease will be present in most individuals with dementia, but-just like other causes-rarely a cause on its own. The consequent limitations of nosology may be alleviated by addition of a vascular component to the recently introduced amyloid/tau/neurodegeneration etiological classification system for dementia. Meanwhile, risk of dementia is increased about 2-fold after stroke, and the prevention of (recurrent) stroke remains a cornerstone in the prevention of vascular dementia. Similarly, control of cardiovascular risk factors from middle age onwards is likely to have contributed to the reported decline in the age-specific incidence of dementia over the past decades. In conjunction with experimental studies, large-scale observational evidence from imaging, genomics, metabolomics, and alike will continue to improve our understanding of the underlying pathophysiological processes. To prevent ecological fallacies, such etiological studies in patients with dementia are best served by inclusion of subjects regardless of the presumed (single) cause of their disease.

Key findings

Why it matters

This review describes vascular dementia as usually having multiple contributing causes, with cerebrovascular disease present in most people with dementia but rarely a cause on its own. It states that dementia risk is about doubled after stroke and that preventing stroke and controlling cardiovascular risk factors from middle age remain cornerstones of prevention.

Study details

How this study scored 53/100
How this study's score is builtJournal tier 7 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 6 of 7; Citations per year 4 of 5; Impact for its field and year 5 of 6; Cited by studies here 3 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 1 of 3; Indexed in PubMed 2 of 2; Free to read 0 of 2. Total 53 of 100.53 of 100 points earned47 not earned

Published in a peer-reviewed 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 7 / 10 Tier 3 — peer-reviewed journal (Arteriosclerosis, thrombosis, and vascular biology)
Journal's citation record 3 / 4 Arteriosclerosis Thrombosis and Vascular Biology: journal h-index 340 (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 6 / 7 Cited 404 times (OpenAlex, 2026-10-10)
Citations per year 4 / 5 44.9 citations a year over 9 year(s) since 2019
Impact for its field and year 5 / 6 Cited 21.8× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 3 / 6 Cited by 15 other studies in this library
Still being cited 4 / 4 Cited 211 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record 4 / 4 Last-listed author M. Arfan Ikram: h-index 167 (OpenAlex, whole career)
Institution's track record 1 / 3 Erasmus MC: institution h-index 1,321 (OpenAlex)
Multi-centre collaboration 1 / 3 OpenAlex lists 2 institution(s) in 1 country
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 31294622)
Free to read 0 / 2 Behind a paywall — scores zero
Total 53 / 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

Wolters, F. J., & Ikram, M. A. (2019). Epidemiology of Vascular Dementia. Arteriosclerosis, thrombosis, and vascular biology. https://doi.org/10.1161/atvbaha.119.311908

Vancouver

Wolters FJ, Ikram MA. Epidemiology of Vascular Dementia. Arteriosclerosis, thrombosis, and vascular biology. 2019. doi:10.1161/atvbaha.119.311908. PMID: 31294622.

BibTeX

@article{wolters2019-31294622,
  author  = {Wolters, F. J. and Ikram, M. A.},
  title   = {{Epidemiology of Vascular Dementia}},
  journal = {Arteriosclerosis, thrombosis, and vascular biology},
  year    = {2019},
  doi     = {10.1161/atvbaha.119.311908},
  pmid    = {31294622},
  url     = {https://doi.org/10.1161/atvbaha.119.311908}
}

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