Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
Proteomic dysregulation associated with cerebral amyloid angiopathy.
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Han Sang-Won, Park Young Ho, Pyun Jung-Min, Bice Paula J, Bennett David A, Oveisgharan Shahram, Saykin Andrew J, Kim SangYun, Nho Kwangsik
Аннотация
INTRODUCTION: Cerebral amyloid angiopathy (CAA) is characterized by impaired vascular amyloid-β clearance, distinct from Alzheimer's disease (AD), underscoring the need to clarify its molecular basis for predicting therapy-related amyloid-related imaging abnormalities.
METHODS: We analyzed post-mortem brain proteomics from Religious Orders Study and Rush Memory and Aging Project (ROS/MAP) and cerebrospinal fluid (CSF) proteomics from Alzheimer's Disease Neuroimaging Initiative (ADNI) to identify CAA-associated proteins and network modules, delineate their biological processes and cellular origins, and determine their diagnostic performance.
RESULTS: Proteomics analysis identified 30 proteins as associated with CAA severity, enriched in pathways distinct from AD pathology, with 11 replicated in ADNI. Two CAA-associated modules were enriched for microglial vesicle transport and astrocytic potassium-ion homeostasis. Pseudotime analysis demonstrated a molecular trajectory aligned with increasing CAA severity. Three proteins (RCSD1, FRZB, AKAP6) improved CAA classification beyond demographics and APOE ε4.
DISCUSSION: This integrative proteomics analysis identifies distinct, reproducible molecular signatures of CAA, revealing glia-mediated pathways and promising biomarkers for CAA detection and therapy-related risk assessment.
METHODS: We analyzed post-mortem brain proteomics from Religious Orders Study and Rush Memory and Aging Project (ROS/MAP) and cerebrospinal fluid (CSF) proteomics from Alzheimer's Disease Neuroimaging Initiative (ADNI) to identify CAA-associated proteins and network modules, delineate their biological processes and cellular origins, and determine their diagnostic performance.
RESULTS: Proteomics analysis identified 30 proteins as associated with CAA severity, enriched in pathways distinct from AD pathology, with 11 replicated in ADNI. Two CAA-associated modules were enriched for microglial vesicle transport and astrocytic potassium-ion homeostasis. Pseudotime analysis demonstrated a molecular trajectory aligned with increasing CAA severity. Three proteins (RCSD1, FRZB, AKAP6) improved CAA classification beyond demographics and APOE ε4.
DISCUSSION: This integrative proteomics analysis identifies distinct, reproducible molecular signatures of CAA, revealing glia-mediated pathways and promising biomarkers for CAA detection and therapy-related risk assessment.