Vascular Considerations for Amyloid Immunotherapy

Kate E. Foley, Donna M. Wilcock

Research output: Contribution to journalReview articlepeer-review

3 Scopus citations

Abstract

Purpose of Review: Amyloid beta (Aβ) plaque accumulation is a hallmark pathology contributing to Alzheimer’s disease (AD) and is widely hypothesized to lead to cognitive decline. Decades of research into anti-Aβ immunotherapies provide evidence for increased Aβ clearance from the brain; however, this is frequently accompanied by complicated vascular deficits. This article reviews the history of anti-Aβ immunotherapies and clinical findings and provides recommendations moving forward. Recent Findings: In 20 years of both animal and human studies, anti-Aβ immunotherapies have been a prevalent avenue of reducing hallmark Aβ plaques. In both models and with different anti-Aβ antibody designs, amyloid-related imaging abnormalities (ARIA) indicating severe cerebrovascular compromise have been common and concerning occurrence. Summary: ARIA caused by anti-Aβ immunotherapy has been noted since the early 2000s, and the mechanisms driving it are still unknown. Recent approval of aducanumab comes with renewed urgency to consider vascular deficits caused by anti-Aβ immunotherapy.

Original languageEnglish
Pages (from-to)709-719
Number of pages11
JournalCurrent Neurology and Neuroscience Reports
Volume22
Issue number11
DOIs
StatePublished - Nov 2022

Bibliographical note

Publisher Copyright:
© 2022, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

Keywords

  • Aducanumab
  • Alzheimer’s disease
  • Amyloid
  • Biomarkers
  • Immunotherapy
  • Vascular

ASJC Scopus subject areas

  • General Neuroscience
  • Clinical Neurology

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