ArticleAlzheimer's research & therapy2023
Plasma amyloid beta 42 is a biomarker for patients with hereditary, but not sporadic, cerebral amyloid angiopathy.
Article in Alzheimer's research & therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Plasma Amyloid Beta and Tau Associations with Cerebral Amyloid Angiopathy Presence and Severity.Annals of neurology · 2026Article
- A plasma protein signature for cerebral amyloid angiopathy.Acta neuropathologica · 2026Article
- Weekly fluctuations of plasma amyloid-beta in Alzheimer's disease: implications for biomarker reliability.Alzheimer's research & therapy · 2026Article
- An Automated Micro-Immunobeads-Based Electromagnetic Operation System (MEMOs) for Blood Testing of Alzheimer's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Plasma biomarkers distinguish Boston Criteria 2.0 cerebral amyloid angiopathy from healthy controls.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Circulating proteomic biomarkers for cerebral amyloid angiopathy screening and risk stratification.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Fluid biomarkers in cerebral amyloid angiopathy.Frontiers in neuroscience · 2024Review
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundThe diagnosis of probable cerebral amyloid angiopathy (CAA) is currently mostly based on characteristics of brain MRI. Blood biomarkers would be a cost-effective, easily accessible diagnostic method that may complement diagnosis by MRI and aid in monitoring disease progression. We studied the diagnostic potential of plasma Aβ38, Aβ40, and Aβ42 in patients with hereditary Dutch-type CAA (D-CAA) and sporadic CAA (sCAA).
methodsAll Aβ peptides were quantified in the plasma by immunoassays in a discovery cohort (11 patients with presymptomatic D-CAA and 24 patients with symptomatic D-CAA, and 16 and 24 matched controls, respectively) and an independent validation cohort (54 patients with D-CAA, 26 presymptomatic and 28 symptomatic, and 39 and 46 matched controls, respectively). In addition, peptides were quantified in the plasma in a group of 61 patients with sCAA and 42 matched controls. We compared Aβ peptide levels between patients and controls using linear regression adjusting for age and sex.
resultsIn the discovery cohort, we found significantly decreased levels of all Aβ peptides in patients with presymptomatic D-CAA (Aβ38: p < 0.001; Aβ40: p = 0.009; Aβ42: p < 0.001) and patients with symptomatic D-CAA (Aβ38: p < 0.001; Aβ40: p = 0.01; Aβ42: p < 0.001) compared with controls. In contrast, in the validation cohort, plasma Aβ38, Aβ40, and Aβ42 were similar in patients with presymptomatic D-CAA and controls (Aβ38: p = 0.18; Aβ40: p = 0.28; Aβ42: p = 0.63). In patients with symptomatic D-CAA and controls, plasma Aβ38 and Aβ40 were similar (Aβ38: p = 0.14; Aβ40: p = 0.38), whereas plasma Aβ42 was significantly decreased in patients with symptomatic D-CAA (p = 0.033). Plasma Aβ38, Aβ40, and Aβ42 levels were similar in patients with sCAA and controls (Aβ38: p = 0.092; Aβ40: p = 0.64. Aβ42: p = 0.68).
conclusionsPlasma Aβ42 levels, but not plasma Aβ38 and Aβ40, may be used as a biomarker for patients with symptomatic D-CAA. In contrast, plasma Aβ38, Aβ40, and Aβ42 levels do not appear to be applicable as a biomarker in patients with sCAA.
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