Evidence map›Paper›PMID 37280119›Full record

ReviewBrain : a journal of neurology2023

Clinical considerations in early-onset cerebral amyloid angiopathy.

Gargi Banerjee, John Collinge, Nick C Fox, Tammaryn Lashley, Simon Mead, Jonathan M Schott, David J Werring, Natalie S Ryan

Abstract readReview
In one paragraph

Review in Brain : a journal of neurology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

31 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Headache Attributed to Genetic Vasculopathies.Current pain and headache reports · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Observational
  8. Article
  9. Ethical considerations of disclosure of iatrogenic cerebral amyloid angiopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  10. Article
  11. Clinical Management of Cerebral Amyloid Angiopathy.Journal of clinical medicine · 2025
    Review
  12. Gustav Oppenheim (1882-1937) and the Discovery of Cerebral Amyloid Angiopathy.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2025
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

8 authors.

Gargi BanerjeeMRC Prion Unit at University College London (UCL), Institute of Prion Diseases, UCL, London, W1W 7FF, UK.ORCID 0000-0003-0190-7782
John CollingeMRC Prion Unit at University College London (UCL), Institute of Prion Diseases, UCL, London, W1W 7FF, UK.
Nick C FoxDementia Research Centre, Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, London, WC1N 3BG, UK.
Tammaryn LashleyThe Queen Square Brain Bank for Neurological Disorders, Department of Clinical and Movement Disorders, UCL Queen Square Institute of Neurology, London, W1 1PJ, UK.
Simon MeadMRC Prion Unit at University College London (UCL), Institute of Prion Diseases, UCL, London, W1W 7FF, UK.
Jonathan M SchottDementia Research Centre, Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, London, WC1N 3BG, UK.ORCID 0000-0003-2059-024X
David J WerringStroke Research Centre, Department of Brain Repair and Rehabilitation, UCL Queen Square Institute of Neurology, London, WC1N 3BG, UK.
Natalie S RyanDementia Research Centre, Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, London, WC1N 3BG, UK.

Funding

British Heart FoundationDepartment of HealthMedical Research Council
6 · The paper itself

Abstract

Cerebral amyloid angiopathy (CAA) is an important cerebral small vessel disease associated with brain haemorrhage and cognitive change. The commonest form, sporadic amyloid-β CAA, usually affects people in mid- to later life. However, early-onset forms, though uncommon, are increasingly recognized and may result from genetic or iatrogenic causes that warrant specific and focused investigation and management. In this review, we firstly describe the causes of early-onset CAA, including monogenic causes of amyloid-β CAA (APP missense mutations and copy number variants; mutations of PSEN1 and PSEN2) and non-amyloid-β CAA (associated with ITM2B, CST3, GSN, PRNP and TTR mutations), and other unusual sporadic and acquired causes including the newly-recognized iatrogenic subtype. We then provide a structured approach for investigating early-onset CAA, and highlight important management considerations. Improving awareness of these unusual forms of CAA amongst healthcare professionals is essential for facilitating their prompt diagnosis, and an understanding of their underlying pathophysiology may have implications for more common, late-onset, forms of the disease.

Indexed as

Alzheimer DiseaseCerebral Amyloid AngiopathyAmyloid beta-PeptidesHumansIatrogenic DiseaseMutationMutation, MissenseAmyloid beta-PeptidesAlzheimer’s diseasecerebral amyloid angiopathydementiaearly-onsetstroke

Identifiers

PMID37280119
PMCPMC10545523

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.