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Alzheimer's disease (AD) exhibits spatially heterogeneous 3R/4R tau pathology distributions across participants, making it a challenge to quantify extent of tau deposition. Utilizing Tau-PET from three independent cohorts, we trained and validated a machine learning model to identify visually positive Tau-PET scans from regional SUVR values and developed a novel summary measure, THETA, that accounts for heterogeneity in tau deposition. The model for identification of tau positivity achieved a balanced test accuracy of 95% and accuracy of ≥87% on the validation datasets. THETA captured heterogeneity of tau deposition, had better association with clinical measures, and corresponded better with visual assessments in comparison with the temporal meta-region-of-interest Tau-PET quantification methods. Our novel approach aids in identification of positive Tau-PET scans and provides a quantitative summary measure, THETA, that effectively captures the heterogeneous tau deposition seen in AD. The application of THETA for quantifying Tau-PET in AD exhibits great potential.
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http://dx.doi.org/10.21203/rs.3.rs-3290598/v1 | DOI Listing |
Front Pharmacol
August 2025
Department of Physiology, Dongguk University College of Korean Medicine, Gyeongju, Republic of Korea.
Introduction: The development of new drugs for Alzheimer's disease (AD) remains a major challenge due to the disorder's complex and multifactorial nature. 2'-Fucosyllactose (2'-FL), a human milk oligosaccharide, has demonstrated promising neuroprotective properties. However, its effects on AD-related cognitive decline are not yet fully understood.
View Article and Find Full Text PDFJ Neurochem
September 2025
Division of Neurogeriatrics, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden.
Elucidating the earliest biological mechanisms underlying Alzheimer's disease (AD) is critical for advancing early detection strategies. While amyloid-β (Aβ) and tau pathologies have been central to preclinical AD research, the roles of peripheral biological processes in disease initiation remain underexplored. We investigated patterns of F-MK6240 tau positron emission tomography (PET) and peripheral inflammation across stages defined by Aβ burden and neuronal injury in n = 132 (64.
View Article and Find Full Text PDFACS Chem Neurosci
September 2025
Institute of Cell Engineering, School of Medicine, Johns Hopkins University, Baltimore, Maryland 21215, United States.
Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive cognitive impairment and neuronal loss, with pathological hallmarks including Aβ plaque deposition and tau tangles. At present, the early diagnosis and treatment of AD still face great challenges, such as limited diagnostic methods, difficulty in blood-brain barrier (BBB) penetration, complex disease mechanisms, and lack of highly effective targeted therapies. Antibody drugs have shown broad prospects in the field of AD due to their high specificity, engineering and multifunctional therapeutic potential, include targeted Aβ clearance, tau pathological regulation, imaging probes, and blood biomarkers.
View Article and Find Full Text PDFNat Commun
September 2025
Clinical Memory Research Unit, Department of Clinical Sciences Malmö, Faculty of Medicine, Lund University, Lund, Sweden.
The distribution of tau pathology in Alzheimer's disease (AD) shows remarkable inter-individual heterogeneity, including hemispheric asymmetry. However, the factors driving this asymmetry remain poorly understood. Here we explore whether tau asymmetry is linked to i) reduced inter-hemispheric brain connectivity (potentially restricting tau spread), or ii) asymmetry in amyloid-beta (Aβ) distribution (indicating greater hemisphere-specific vulnerability to AD pathology).
View Article and Find Full Text PDFCurrently, the causes for Alzheimer Disease (AD) are thought to lie in the formation of abnormal protein deposits including tau tangles and Amyloid ß (Aβ) plaques in the human cortex. These proteins are believed to accumulate in the brain due to impaired waste removal resulting in neurodegeneration. In an alternative hypothesis we have recently proposed the existence of an aquaporin4 aqua channel (AQP4)-expressing tanycyte-derived canal network that likely internalizes waste for removal from the brain.
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