Evidence map›Paper›PMID 39794509›Full record

ReviewNature reviews. Neurology2025

Amyloid-related imaging abnormalities: manifestations, metrics and mechanisms.

Steven M Greenberg, Francesco Bax, Susanne J van Veluw

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing 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

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

  1. Guideline
  2. Volume change with gantenerumab: Impact of amyloid-related imaging abnormalities and amyloid removal.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Trial
  3. Trial
  4. Trial
  5. Trial
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Beyond the Cochrane review: Re-evaluating anti-amyloid therapy in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  15. Article
  16. Review
  17. Article
  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

3 authors.

Steven M GreenbergJ. Philip Kistler Stroke Research Center, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. sgreenberg@mgh.harvard.edu.ORCID 0000-0003-1792-8887
Francesco BaxJ. Philip Kistler Stroke Research Center, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.ORCID 0000-0003-1725-1175
Susanne J van VeluwJ. Philip Kistler Stroke Research Center, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.ORCID 0000-0002-7957-8643

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Three monoclonal antibodies directed against specific forms of the amyloid-β (Aβ) peptide have been granted accelerated or traditional approval by the FDA as treatments for Alzheimer disease, representing the first step towards bringing disease-modifying treatments for this disease into clinical practice. Here, we review the detection, underlying pathophysiological mechanisms and clinical implications of amyloid-related imaging abnormalities (ARIA), the most impactful adverse effect of anti-Aβ immunotherapy. ARIA appears as regions of oedema or effusions (ARIA-E) in brain parenchyma or sulci or as haemorrhagic lesions (ARIA-H) in the form of cerebral microbleeds, convexity subarachnoid haemorrhage, cortical superficial siderosis or intracerebral haemorrhage. Analysis of the radiographic appearance of ARIA, its clinical risk factors and underlying neuropathology, and results from animal models point to a central role for cerebral amyloid angiopathy - a condition characterized by cerebrovascular Aβ deposits - as a key component, either as a direct target for antibody-mediated inflammation or as recipient of Aβ mobilized from plaques in the Alzheimer brain parenchyma. The great majority of ARIA occurrences are associated with mild or no clinical symptoms. However, ~5% of all ARIA events are severe enough to result in hospitalization, permanent disability or death and thus raise challenging clinical questions regarding patient selection and use of concomitant agents. Therefore, identifying novel approaches to predicting, modelling, preventing and treating ARIA remains a key step towards allowing safe use of anti-Aβ immunotherapy for the world's rapidly ageing population.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesBrainCerebral Amyloid AngiopathyNeuroimagingAnimalsHumansAmyloid beta-Peptides

Identifiers

PMID39794509

What OpenQuestion holds

Textmetadata
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.