Evidence map›Paper›PMID 34331941›Full record

ReviewThe American journal of pathology2021

Cerebral Small Vessel Disease in Sporadic and Familial Alzheimer Disease.

Rajesh N Kalaria, Diego Sepulveda-Falla

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in The American journal of pathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
6.0field-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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Association between blood pressure and risk of ischemic stroke among individuals with dementia: A nationwide cohort study.Hypertension research : official journal of the Japanese Society of Hypertension · 2026
    Article
  5. Article
  6. Observational
  7. How does type 2 diabetes modify the risk of Alzheimer's disease?Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Advancements in investigating the role of cerebral small vein loss in Alzheimer's disease-related pathological changes.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024
    Review
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

2 authors at 2 institutions in 3 countries.

Rajesh N KalariaNeurovascular Research Group, Translational and Clinical Research Institute, Newcastle University, Newcastle upon Tyne, United Kingdom; Department of Human Anatomy, College of Health Sciences, University of Nairobi, Nairobi, Kenya. Electronic address: raj.kalaria@ncl.ac.uk.
Diego Sepulveda-FallaInstitute of Neuropathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Universität Hamburg · DEUniversity of Nairobi · KE

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
Medical Research Council G0400074Medical Research Council G0500247Medical Research Council G0502157Medical Research Council G0900652Medical Research Council G1100540NINDS NIH HHS RF1 NS110048
6 · The paper itself

Abstract

Alzheimer disease (AD) is the most common cause of dementia. Biological definitions of AD are limited to the cerebral burden of amyloid β plaques, neurofibrillary pathology, and neurodegeneration. However, current evidence suggests that various features of small vessel disease (SVD) are part of and covertly modify both sporadic and familial AD. Neuroimaging studies suggest that white matter hyperintensities explained by vascular mechanisms occurs frequently in the AD spectrum. Recent advances have further emphasized that frontal periventricular and posterior white matter hyperintensities are associated with cerebral amyloid angiopathy in familial AD. Although whether SVD markers precede the classically recognized biomarkers of disease is debatable, post-mortem studies show that SVD pathology incorporating small cortical and subcortical infarcts, microinfarcts, microbleeds, perivascular spacing, and white matter attenuation is commonly found in sporadic as well as in mutation carriers with confirmed familial AD. Age-related cerebral vessel pathologies such as arteriolosclerosis and cerebral amyloid angiopathy modify progression or worsen risk by shifting the threshold for cognitive impairment and AD dementia. The incorporation of SVD as a biomarker is warranted in the biological definition of AD. Therapeutic interventions directly reducing the burden of brain amyloid β have had no major impact on the disease or delaying cognitive deterioration, but lowering the risk of vascular disease seems the only rational approach to tackle both early- and late-onset AD dementia.

Indexed as

Alzheimer DiseaseCerebral Small Vessel DiseasesHumans

Identifiers

PMID34331941
PMCPMC8573679
OpenAlexW3186926754

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.