2026/11/15 12:00-13:30 Room Venue 301
- 午餐議程-台灣拜耳:
台灣拜耳股份有限公司
台灣拜耳股份有限公司
- Time
- Topic
- Speaker
- Moderator
- 12:05-12:40
- The First-in-Class nsMRA in DKD: A Deep Dive into the Clinical Evidence
- SPEAKER:
Hsin-Hsi Tsai
蔡欣熹
Taiwan (台灣)
- MODERATOR:
Lung Chan
陳龍
Taiwan (台灣)
- Hsin-Hsi Tsai
- MD, PhD
-
Clinical Associate Professor, Department of Neurology, National Taiwan University Hospital
Lecture Abstract：
Cerebral amyloid angiopathy (CAA) is defined by vascular β-amyloid deposition and is a major cause of lobar intracerebral hemorrhage and cognitive impairment. However, its biological overlap with Alzheimer disease (AD) complicates interpretation of amyloid biomarkers. Molecular imaging may characterize this CAA–AD spectrum by integrating the amount, distribution, and downstream consequences of amyloid and tau pathology.
In this presentation, we summarize our multimodal imaging studies of CAA. Amyloid positron emission tomography (PET) identifies increased cortical amyloid burden in CAA, which predicts long-term cognitive decline after hemorrhagic small-vessel disease. Although the overall amyloid distribution resembles AD, CAA shows relatively occipital-predominant uptake. An occipital-to-whole-cortex uptake ratio >0.98 differentiated CAA from AD with an area under the curve of 0.762. Amyloid PET burden is also associated with lobar cerebral microbleeds and other CAA-related MRI markers, linking molecular pathology to vascular injury.
Tau PET demonstrates that concomitant tau pathology is present in a clinically relevant subset of patients with CAA. Greater tau burden is associated with cortical superficial siderosis and memory impairment, supporting an overlapping CAA–AD phenotype. Nevertheless, compared with AD, CAA has a lower overall tau burden but relatively greater pericentral tau deposition. Spatial analyses further demonstrate regional colocalization between amyloid and tau signals, consistent with neuropathological observations of perivascular phosphorylated tau. Early-phase amyloid PET may additionally provide a surrogate marker of neurodegeneration and help identify tau-positive CAA, extending the information obtained from a single tracer.
Together, these findings define a multidimensional molecular imaging signature of CAA. Combining amyloid and tau imaging with clinical and hemorrhagic MRI phenotypes may improve differentiation from AD, clarify mechanisms of cognitive decline, and support patient stratification for future therapeutic trials.
Cerebral amyloid angiopathy (CAA) is defined by vascular β-amyloid deposition and is a major cause of lobar intracerebral hemorrhage and cognitive impairment. However, its biological overlap with Alzheimer disease (AD) complicates interpretation of amyloid biomarkers. Molecular imaging may characterize this CAA–AD spectrum by integrating the amount, distribution, and downstream consequences of amyloid and tau pathology.
In this presentation, we summarize our multimodal imaging studies of CAA. Amyloid positron emission tomography (PET) identifies increased cortical amyloid burden in CAA, which predicts long-term cognitive decline after hemorrhagic small-vessel disease. Although the overall amyloid distribution resembles AD, CAA shows relatively occipital-predominant uptake. An occipital-to-whole-cortex uptake ratio >0.98 differentiated CAA from AD with an area under the curve of 0.762. Amyloid PET burden is also associated with lobar cerebral microbleeds and other CAA-related MRI markers, linking molecular pathology to vascular injury.
Tau PET demonstrates that concomitant tau pathology is present in a clinically relevant subset of patients with CAA. Greater tau burden is associated with cortical superficial siderosis and memory impairment, supporting an overlapping CAA–AD phenotype. Nevertheless, compared with AD, CAA has a lower overall tau burden but relatively greater pericentral tau deposition. Spatial analyses further demonstrate regional colocalization between amyloid and tau signals, consistent with neuropathological observations of perivascular phosphorylated tau. Early-phase amyloid PET may additionally provide a surrogate marker of neurodegeneration and help identify tau-positive CAA, extending the information obtained from a single tracer.
Together, these findings define a multidimensional molecular imaging signature of CAA. Combining amyloid and tau imaging with clinical and hemorrhagic MRI phenotypes may improve differentiation from AD, clarify mechanisms of cognitive decline, and support patient stratification for future therapeutic trials.
