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24. Plasma phosphorylated-tau181 as a predictive biomarker for Alzheimer’s amyloid, tau and FDG PET status

Author

Shen, Xue-Ning, Huang, Yu-Yuan, Chen, Shi-Dong, Guo, Yu, Tan, Lan, Dong, Qiang, and Yu, Jin-Tai

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Biomedical Imaging, Dementia, Neurodegenerative, Acquired Cognitive Impairment, Alzheimer's Disease, Aging, Neurosciences, Brain Disorders, Clinical Research, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), 4.2 Evaluation of markers and technologies, 4.1 Discovery and preclinical testing of markers and technologies, Detection, screening and diagnosis, Neurological, Alzheimer Disease, Amyloid beta-Peptides, Biomarkers, Fluorodeoxyglucose F18, Humans, tau Proteins, Alzheimer’s Disease Neuroimaging Initiative, Public Health and Health Services, Psychology, Clinical sciences, Biological psychology
Abstract

Plasma phosphorylated-tau181 (p-tau181) showed the potential for Alzheimer's diagnosis and prognosis, but its role in detecting cerebral pathologies is unclear. We aimed to evaluate whether it could serve as a marker for Alzheimer's pathology in the brain. A total of 1189 participants with plasma p-tau181 and PET data of amyloid, tau or FDG PET were included from ADNI. Cross-sectional relationships of plasma p-tau181 with PET biomarkers were tested. Longitudinally, we further investigated whether different p-tau181 levels at baseline predicted different progression of Alzheimer's pathological changes in the brain. We found plasma p-tau181 significantly correlated with brain amyloid (Spearman ρ = 0.45, P 18.85 pg/ml) at baseline had a higher risk of pathological progression in brain amyloid (HR: 2.32, 95%CI 1.32-4.08) and FDG PET (3.21, 95%CI 2.06-5.01) status. Plasma p-tau181 may be a sensitive screening test for detecting brain pathologies, and serve as a predictive biomarker for Alzheimer's pathophysiology.

Published
2021

25. Staging tau pathology with tau PET in Alzheimer’s disease: a longitudinal study

Author

Chen, Shi-Dong, Lu, Jia-Ying, Li, Hong-Qi, Yang, Yu-Xiang, Jiang, Jie-Hui, Cui, Mei, Zuo, Chuan-Tao, Tan, Lan, Dong, Qiang, and Yu, Jin-Tai

Subjects
Biomedical and Clinical Sciences, Biological Psychology, Clinical Sciences, Neurosciences, Psychology, Acquired Cognitive Impairment, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Brain Disorders, Biomedical Imaging, Dementia, Neurodegenerative, Alzheimer's Disease, Clinical Research, Aging, 4.2 Evaluation of markers and technologies, Aetiology, 4.1 Discovery and preclinical testing of markers and technologies, Detection, screening and diagnosis, 2.1 Biological and endogenous factors, Neurological, Aged, Aged, 80 and over, Alzheimer Disease, Amyloid beta-Peptides, Biomarkers, Cognitive Dysfunction, Female, Humans, Longitudinal Studies, Male, Positron-Emission Tomography, tau Proteins, Alzheimer’s Disease Neuroimaging Initiative, Public Health and Health Services, Clinical sciences, Biological psychology
Abstract

A biological research framework to define Alzheimer' disease with dichotomized biomarker measurement was proposed by National Institute on Aging-Alzheimer's Association (NIA-AA). However, it cannot characterize the hierarchy spreading pattern of tau pathology. To reflect in vivo tau progression using biomarker, we constructed a refined topographic 18F-AV-1451 tau PET staging scheme with longitudinal clinical validation. Seven hundred and thirty-four participants with baseline 18F-AV-1451 tau PET (baseline age 73.9 ± 7.7 years, 375 female) were stratified into five stages by a topographic PET staging scheme. Cognitive trajectories and clinical progression were compared across stages with or without further dichotomy of amyloid status, using linear mixed-effect models and Cox proportional hazard models. Significant cognitive decline was first observed in stage 1 when tau levels only increased in transentorhinal regions. Rates of cognitive decline and clinical progression accelerated from stage 2 to stage 3 and stage 4. Higher stages were also associated with greater CSF phosphorylated tau and total tau concentrations from stage 1. Abnormal tau accumulation did not appear with normal β-amyloid in neocortical regions but prompt cognitive decline by interacting with β-amyloid in temporal regions. Highly accumulated tau in temporal regions independently led to cognitive deterioration. Topographic PET staging scheme have potentials in early diagnosis, predicting disease progression, and studying disease mechanism. Characteristic tau spreading pattern in Alzheimer's disease could be illustrated with biomarker measurement under NIA-AA framework. Clinical-neuroimaging-neuropathological studies in other cohorts are needed to validate these findings.

Published
2021

31. MAPT rs242557 variant is associated with hippocampus tau uptake on 18F-AV-1451 PET in non-demented elders

Author

Shen, Xue-Ning, Miao, Dan, Li, Jie-Qiong, Tan, Chen-Chen, Cao, Xi-Peng, Tan, Lan, and Yu, Jin-Tai

Subjects
Biochemistry and Cell Biology, Biological Sciences, Aging, Neurosciences, Brain Disorders, Alzheimer's Disease, Acquired Cognitive Impairment, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Neurodegenerative, Dementia, Neurological, Aged, Aged, 80 and over, Amyloid beta-Peptides, Apolipoprotein E4, Carbolines, Case-Control Studies, Cognitive Dysfunction, Female, Heterozygote, Hippocampus, Humans, Male, Middle Aged, Polymorphism, Single Nucleotide, Positron-Emission Tomography, tau Proteins, tauopathy, MAPT, hippocampus, F-18-AV-1451 PET, non-demented, Alzheimer's disease, Alzheimer’s disease, F-AV-1451 PET 18, Physiology, Oncology and Carcinogenesis, Developmental Biology
Abstract

The microtubule-associated protein tau gene (MAPT) rs242557 variant is associated with multiple tauopathies and dementia. This study investigated whether it was correlated with brain tau-PET uptake in non-demented elders. Ninety non-demented elders were identified from the Alzheimer's Disease Neuroimaging Initiative cohort. We compared standardized uptake value ratios (SUVRs) of tau-PET tracer 18F-AV-1451 between rs242557 variant carriers and non-carriers in 25 regions of interest (ROIs). The minor allele A was associated with increased hippocampus 18F-AV-1451 uptake in non-demented elders (left: β = 0.111, Bonferroni corrected p = 0.035; right: β = 0.103, Bonferroni corrected p = 0.031). Aβ-positive participants (left: β = 0.206, Bonferroni corrected p = 0.029; right: β = 0.198, Bonferroni corrected p = 0.035) and APOE ε4 non-carriers (left: β = 0.140, Bonferroni corrected p = 0.006; right: β = 0.134, Bonferroni corrected p = 0.004) exhibited approximately the same findings in hippocampus. Considering no obvious associations in other regions, we confirmed the significant correlation of MAPT rs242557 risk variant with increased hippocampus tau deposition in non-demented elders. With higher magnitude signals in the hippocampus that is more likely to be uniquely affected in AD, the tau PET ligand 18F-AV-1451 seemed to possess a specific binding property for AD-like tau pathology.

Published
2019

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