Background: Histopathological evidence of cerebral vascular amyloid β accumulation is the gold standard to diagnose cerebral amyloid angiopathy (CAA). Neuroimaging findings obtained with CT and MRI can suggest the presence of CAA when histopathology is lacking. We explored the role of amyloid PET in patients with lobar intracerebral hemorrhage (ICH) as this may provide molecular evidence for CAA as well.
Methods: In this retrospective, monocenter analysis, we included consecutive patients with non-traumatic lobar ICH who had undergone amyloid PET. We categorized patients according to amyloid PET status and compared demographics and neuroimaging findings. We calculated sensitivity and specificity of the simplified Edinburgh criteria and amyloid PET with probable modified Boston criteria as reference standard, as well as sensitivity and specificity of the simplified Edinburgh and modified Boston criteria with amyloid PET status as molecular marker for presence or absence of CAA.
Results: We included 38 patients of whom 24 (63%) were amyloid PET positive. Amyloid PET positive patients were older at presentation (p = 0.004). We observed no difference in prevalence of subarachnoid hemorrhages, fingerlike projections or microbleeds between both groups, but cortical superficial siderosis (p = 0.003) was more frequent in the amyloid PET positive group. In 5 out of 38 patients (13%), the modified Boston criteria were not fulfilled due to young age or concomitant vitamin K antagonist use with INR > 3.0. With the modified Boston criteria as reference standard, there was no difference in sensitivity nor specificity between the simplified Edinburgh criteria and amyloid PET status. With amyloid PET status as reference standard, there was also no difference in sensitivity nor specificity between the simplified Edinburgh and modified Boston criteria.
Conclusions: Amyloid PET was positive in 63% of lobar ICH patients. Under certain circumstances, patients might not be diagnosed with probable CAA according to the modified Boston criteria and in these cases, amyloid PET may be useful. Accuracy to predict CAA based on amyloid PET status did not differ between the simplified Edinburgh and modified Boston criteria.
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http://dx.doi.org/10.1016/j.nicl.2022.103107 | DOI Listing |
Alzheimers Res Ther
January 2025
Functional Imaging Unit, Department of Clinical Physiology and Nuclear Medicine, Copenhagen University Hospital Rigshospitalet, Valdemar Hansens Vej 1-23, Glostrup, 2600, Denmark.
Background: Accumulation of β-amyloid (Aβ) in the brain is a hallmark of Alzheimer's Disease (AD). Cerebral deposition of Aβ initiates deteriorating pathways which eventually can lead to AD. However, the exact mechanisms are not known.
View Article and Find Full Text PDFAlzheimers Dement (N Y)
October 2024
Eli Lilly and Company Indianapolis Indiana USA.
Introduction: Alzheimer's disease is partially characterized by the progressive accumulation of aggregated tau-containing neurofibrillary tangles. Although the association between accumulated tau, neurodegeneration, and cognitive decline is critical for disease understanding and clinical trial design, we still lack robust tools to predict individualized trajectories of tau accumulation. Our objective was to assess whether brain imaging biomarkers of flortaucipir-positron emission tomography (PET), in combination with clinical and genomic measures, could predict future pathological tau accumulation.
View Article and Find Full Text PDFParkinsonism Relat Disord
December 2024
Department of Psychiatry, University of Cambridge School of Clinical Medicine, Cambridge, UK.
Co-morbid Alzheimer's disease (AD) pathology (amyloid-beta and tau) is commonly observed in Lewy body dementia (LBD), and this may affect clinical outcomes. A systematic review of the effect of AD co-pathology on longitudinal clinical outcomes in LBD was conducted. A search of MEDLINE and EMBASE (October 2024) yielded n = 3558 records that were screened by two independent reviewers.
View Article and Find Full Text PDFBrain Commun
December 2024
Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94304, USA.
Co-pathology is frequent in Lewy body disease, which includes clinical diagnoses of both Parkinson's disease and dementia with Lewy bodies. Measuring concomitant pathology can improve clinical and research diagnoses and prediction of cognitive trajectories. Tau PET imaging may serve a dual role in Lewy body disease by measuring cortical tau aggregation as well as assessing dopaminergic loss attributed to binding to neuromelanin within substantia nigra.
View Article and Find Full Text PDFEJNMMI Phys
December 2024
Department of Nuclear Medicine, State Key Laboratory of Complex Severe and Rare Diseases, Center for Rare Diseases Research, Beijing Key Laboratory of Molecular Targeted Diagnosis and Therapy in Nuclear Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, 1# Shuaifuyuan, Dongcheng District, Beijing, 100730, China.
Background: There is a need for faster amyloid PET scans to reduce patients' discomfort, minimize movement artifacts, and increase throughput. The recently introduced uMI Panorama PET/CT system featuring enhanced spatial resolution and sub-200ps TOF offers the potential for shorter scan duration without sacrificing image quality or efficacy to detect Aβ deposition. The study aims to establish a faster acquisition protocol for [F]florbetapir PET imaging using digital PET/CT scanner uMI Panorama, while ensuring adequate image quality and amyloid-β (Aβ) detectability comparable to the standard 10-minute scan.
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