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Alzheimer's disease is marked by accumulation of amyloid-β (Aβ) and abnormal tau, associated with subsequent neurodegeneration. Validated markers of neurodegeneration include brain glucose metabolism, perfusion and atrophy. Dual-phase amyloid PET imaging allows to assess both Aβ buildup and perfusion changes through a single tracer injection. Increasing evidence supports the comparability of early-phase amyloid PET scans and glucose metabolism changes assessed by F-FDG PET at group and individual levels, regardless of the amyloid tracers and the disease, emphasizing the added value of dual-phase amyloid PET imaging protocols for clinical and research settings.
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http://dx.doi.org/10.1177/13872877251366671 | DOI Listing |
JAMA Netw Open
September 2025
School of Medicine and Public Health, University of Wisconsin-Madison, Madison.
Importance: It is unclear whether the duration of amyloid-β (Aβ) pathology is associated with neurodegeneration and whether this depends on the presence of tau.
Objective: To examine the association of longitudinal atrophy with Aβ positron emission tomography (PET)-positivity (Aβ+) and the estimated duration of Aβ+ (Aβ+ duration), controlling for tau-positivity.
Design, Setting, And Participants: Data for this longitudinal cohort study were drawn from the Wisconsin Registry for Alzheimer Prevention and the Wisconsin Alzheimer Disease Research Center Clinical Core Study.
Radiology
September 2025
Department of Radiology and Radiological Sciences, Johns Hopkins University, Baltimore, Md.
Background Elevated brain iron is a potential marker for neurodegeneration, but its role in predicting onset of mild cognitive impairment (MCI) and prospective cognitive trajectories remains unclear. Purpose To investigate how brain iron and amyloid-β (Aβ) levels, measured using quantitative susceptibility mapping (QSM) MRI and PET, help predict MCI onset and cognitive decline. Materials and Methods In this prospective study conducted between January 2015 and November 2022, cognitively unimpaired older adults underwent baseline QSM MRI.
View Article and Find Full Text PDFAlzheimers Dement
September 2025
Boston University Alzheimer's Disease Research Center and BU CTE Center, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts, USA.
We describe the rationale, methodology, and design of the Boston University Alzheimer's Disease Research Center (BU ADRC) Clinical Core (CC). The CC characterizes a longitudinal cohort of participants with/without brain trauma to characterize the clinical presentation, biomarker profiles, and risk factors of post-traumatic Alzheimer's disease (AD) and AD-related dementias (ADRD), including chronic traumatic encephalopathy (CTE). Participants complete assessments of traumatic brain injury (TBI) and repetitive head impacts (RHIs); annual Uniform Data Set (UDS) and supplementary evaluations; digital phenotyping; annual blood draw; magnetic resonance imaging (MRI) and lumbar puncture every 3 years; electroencephalogram (EEG); and amyloid and/or tau positron emission tomography (PET) on a subset.
View Article and Find Full Text PDFAlzheimers Dement
September 2025
Wisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA.
This review covers recent advances (2023-2024) in neuroimaging research into the pathophysiology, progression, and treatment of Alzheimer's disease (AD) and related dementias (ADRD). Despite the rapid emergence of blood-based biomarkers, neuroimaging continues to be a vital area of research in ADRD. Here, we discuss neuroimaging as a powerful tool to topographically visualize and quantify amyloid, tau, neurodegeneration, inflammation, and vascular disease in the brain.
View Article and Find Full Text PDFEJNMMI Radiopharm Chem
September 2025
Department of Public Health and Caring Sciences, Uppsala University, Uppsala, 751 85, Sweden.
Background: Alzheimer's disease (AD) is increasingly recognized as a multifactorial disorder with vascular contributions, including a pro-coagulant state marked by fibrin deposition in the brain. Fibrin accumulation may exacerbate cerebral hypoperfusion and neuroinflammation, leading to neurodegeneration. Identifying patients with this pathology could enable targeted anticoagulant therapy.
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