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A Metadata Extraction Approach for Clinical Case Reports to Enable Advanced Understanding of Biomedical Concepts
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Clinical Manifestations.

Natalie S Ryan1,2, Clíona Farrell1,3, Moneeb Nasir1,2

  • 1UK Dementia Research Institute at UCL, London, United Kingdom.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 25, 2025
PubMed
Summary
This summary is machine-generated.

Autosomal dominant Alzheimer's disease (ADAD) shows varied amyloid-β pathology and cerebral amyloid angiopathy (CAA) severity. Lecanemab-BS binds to plaques and CAA, with increased binding correlating to more severe CAA.

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Area of Science:

  • Neuropathology
  • Neurodegenerative Diseases
  • Genetics

Background:

  • Autosomal dominant Alzheimer's disease (ADAD) is linked to mutations in APP, PSEN1, and PSEN2, affecting amyloid-β processing and leading to plaque and cerebral amyloid angiopathy (CAA) deposition.
  • Variations in mutations influence amyloid-β isoforms, plaque/CAA type and severity, and clinical presentation.
  • CAA is a risk factor for amyloid-related imaging abnormalities (ARIA) during anti-amyloid-β immunotherapy.

Purpose of the Study:

  • To investigate the neuropathological heterogeneity in ADAD.
  • To explore relationships between genetic mutations, clinical phenotypes, and amyloid-β deposition, including CAA.
  • To assess the binding of a lecanemab-biosimilar antibody (lecanemab-BS) to amyloid-β plaques and CAA in ADAD.

Main Methods:

  • Post-mortem brain donation from 50 ADAD individuals (37 PSEN1, 13 APP mutations).
  • Immunohistochemical staining with pan-amyloid-β and lecanemab-BS antibodies.
  • Assessment of CAA frequency and severity in leptomeninges and parenchyma.
  • Immunofluorescence co-staining for amyloid-β isoforms and lecanemab-BS.
  • Correlation with clinical data and in-vivo MRI (SWI) in 10 cases.

Main Results:

  • Non-amnestic and atypical clinical features were more common in PSEN1 than APP mutations.
  • All cases showed end-stage AD pathology, with variable CAA frequency and severity.
  • Lecanemab-BS bound to amyloid-β plaques and CAA; binding was more extensive in cases with severe CAA.
  • Microbleeds on SWI MRI were observed in 4/10 individuals, all with moderate-severe CAA, but also present in 5/10 without microbleeds.

Conclusions:

  • Lecanemab-BS effectively binds to amyloid-β plaques and CAA across diverse ADAD mutations and clinical presentations.
  • Increased lecanemab-BS binding in cerebral blood vessels with severe CAA underscores the need for in-vivo CAA biomarkers.
  • Findings support early therapeutic intervention in ADAD and highlight the importance of understanding CAA in treatment response.