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Background: Alzheimer's disease (AD) is the most common cause of dementia worldwide. In AD, abnormal tau accumulates within neurons of the brain, facilitated by extracellular β-amyloid deposition, leading to neurodegeneration, and eventually, cognitive impairment. As this process is thought to be irreversible, early identification of abnormal tau in the brain is crucial for the development of new therapeutic interventions.
Aims: F-PI-2620 is one of the second-generation tau PET tracers with presumably less off-target binding than its predecessors. Although a few clinical studies have recently reported the use of F-PI-2620 tau PET in patients with AD, its applicability to AD is yet to be thoroughly examined.
Methods: In the present pilot study, we performed F-PI-2620 tau PET in seven cases of probable AD (AD group) and seven healthy controls (HC group). Standardized uptake value ratios (SUVR) in regions of interest (ROIs) in the medial temporal region and neocortex were compared between the AD and HC groups. Furthermore, correlations between regional SUVR and plasma p-tau181 as well as cognitive test scores were also analyzed.
Results: The uptake of F-PI-2620 was distinctly increased in the AD group across all the ROIs. SUVR in all the target ROIs were significantly correlated with plasma p-tau181 levels, as well as with MMSE and ADAS-cog scores.
Discussion & Conclusion: Our results add to accumulating evidence suggesting that F-PI-2620 is a promising tau PET tracer that allows patients with AD to be distinguished from healthy controls, although a study with a larger sample size is warranted.
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http://dx.doi.org/10.1002/npr2.12281 | DOI Listing |
Ann Neurol
September 2025
Department of Radiology, Mayo Clinic, Rochester, MN, USA.
Objective: The objective of this study was to determine the predictive value of amyloid-positron emission tomography (PET) versus the plasma ratio of phosphorylated tau at threonine 217 (p-tau217) to non-phosphorylated tau217 (%p-tau217) for tau-PET transitions (T- to T+). The added value of combining plasma amyloid-β 42 and amyloid-β 40 (Aβ42/40) and %p-tau217 into an amyloid probability score (APS2) was also assessed.
Methods: Mayo Clinic Study of Aging (MCSA) participants had plasma markers measured at via mass spectrometry (MS), an amyloid-PET scan, and a tau-PET (meta-temporal region of interest [ROI]) negative scan (standardized uptake value ratio [SUVR] <1.
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.
Alzheimers 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 PDFParkinsonism Relat Disord
September 2025
Translational and Clinical Research Institute, Newcastle University, UK.
Introduction: Dysfunction of the glymphatic system is thought to lead to build up of toxic proteins including β-amyloid and α-synuclein, and thus may be involved in dementia with Lewy bodies (DLB) and Alzheimer's disease (AD). The Diffusion Tensor Image Analysis Along the Perivascular Space (DTI-ALPS) index has been proposed as a marker of glymphatic function.
Aims: To investigate DTI-ALPS in mild cognitive impairment (MCI) and dementia, and determine its relationship with cognitive decline, and biomarkers of neurodegeneration.