scholarly journals Blood phosphorylated tau 181 predicts early, preclinical brain amyloid deposition

2021 ◽  
Vol 17 (S5) ◽  
Author(s):  
Emer R. McGrath ◽  
Alexa S. Beiser ◽  
Qiong Yang ◽  
Saptaparni Ghosh ◽  
Charles S. DeCarli ◽  
...  
Keyword(s):  
Amyloid Deposition ◽  
Phosphorylated Tau ◽  
Phosphorylated Tau 181 ◽  
Brain Amyloid Deposition

scholarly journals Insulin resistance predicts brain amyloid deposition in late middle-aged adults

2014 ◽  
Vol 11 (5) ◽  
pp. 504-510.e1 ◽  
Author(s):  
Auriel A. Willette ◽  
Sterling C. Johnson ◽  
Alex C. Birdsill ◽  
Mark A. Sager ◽  
Bradley Christian ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Amyloid Deposition ◽  
Middle Aged ◽  
Middle Aged Adults ◽  
Brain Amyloid Deposition

scholarly journals Relationship of amyloid-β1–42 in blood and brain amyloid: Ginkgo Evaluation of Memory Study

2019 ◽  
Vol 2 (1) ◽  
Author(s):  
Oscar L Lopez ◽  
William E Klunk ◽  
Chester A Mathis ◽  
Beth E Snitz ◽  
Yuefang Chang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Pet Imaging ◽  
Standardized Uptake Value ◽  
Amyloid Plaques ◽  
Amyloid Deposition ◽  
Pittsburgh Compound B ◽  
Blood Samples ◽  
Apolipoprotein E4 ◽  
The Brain ◽  
Brain Amyloid Deposition

Abstract A blood test that predicts the extent of amyloid plaques in the brain and risk of Alzheimer’s disease would have important benefits for the early identification of higher risk of dementia and Alzheimer’s disease and the evaluation of new preventative therapies. The goal of this study was to determine whether plasma levels of amyloid-β1–42, 1–40 and the amyloid-β1–42/1–40 ratio among participants in the Pittsburgh centre of the Ginkgo Evaluation of Memory Study were related to the extent of brain fibrillar amyloid plaques measured in 2009 using Pittsburgh compound-B PET imaging, hippocampal volume, cortical thickness in the temporal lobe and white matter lesions. There were 194 participants who had Pittsburgh compound-B measurements in 2009 with the mean age of 85 years; 96% were white and 60% men. Pittsburgh compound-B positivity was defined as a standardized uptake value ratio of ≥1.57. Amyloid-β in blood was measured using a sandwich enzyme-linked immunosorbent assay developed by Eli Lilly and modified at the University of Vermont. All participants were nondemented as of 2008 at the time of study close out. The study sample included 160 with blood samples drawn in 2000–02 and 133 from 2009 and also had brain amyloid measured in 2009. All blood samples were analysed at the same time in 2009. Plasma amyloid-β1–42 was inversely related to the percent Pittsburgh compound-B positive (standardized uptake value ratio ≥1.57), β −0.04, P = 0.005. Practically all participants who were apolipoprotein-E4 positive at older ages were also Pittsburgh compound-B positive for fibrillar amyloid. Among apolipoprotein-E4-negative participants, quartiles of amyloid-β1–42 were inversely related to Pittsburgh compound-B positivity. In multiple regression models, plasma amyloid-β1–42 measured in 2000–02 or 2009 were significantly and inversely related to Pittsburgh compound-B positivity as was the amyloid-β1–42/1–40 ratio. There was a 4-fold increase in the odds ratio for the presence of Pittsburgh compound-B positivity in the brain in 2009 for the first quartile of amyloid-β1–42 as compared with the fourth quartile in the multiple logistic model. This is one of the first longitudinal studies to evaluate the relationship between amyloid-β1–42 in the blood and the extent of brain amyloid deposition measured by PET imaging using Pittsburgh compound-B. Our findings showed that remote and recent low plasma amyloid-β1–42 levels were inversely associated with brain amyloid deposition in cognitively normal individuals. However, changes in plasma amyloid-β1–42 over time (8 years) were small and not related to the amount of Pittsburgh compound-B.

scholarly journals ATN profiles among cognitively normal individuals and longitudinal cognitive outcomes

Neurology ◽  
2019 ◽  
Vol 92 (14) ◽  
pp. e1567-e1579 ◽  
Author(s):  
Anja Soldan ◽  
Corinne Pettigrew ◽  
Anne M. Fagan ◽  
Suzanne E. Schindler ◽  
Abhay Moghekar ◽  
...  
Keyword(s):  
Cognitive Decline ◽  
Cognitive Outcomes ◽  
Phosphorylated Tau ◽  
Cognitively Normal ◽  
Growth Curve Models ◽  
Amyloid A ◽  
Total Tau ◽  
Global Factor ◽  
Normal Individuals ◽  
Phosphorylated Tau 181

ObjectiveTo examine the long-term cognitive trajectories of individuals with normal cognition at baseline and distinct amyloid/tau/neurodegeneration (ATN) profiles.MethodsPooling data across 4 cohort studies, 814 cognitively normal participants (mean baseline age = 59.6 years) were classified into 8 ATN groups using baseline CSF levels of β-amyloid 1–42 as a measure of amyloid (A), phosphorylated tau 181 as a measure of tau (T), and total tau as a measure of neurodegeneration (N). Cognitive performance was measured using a previously validated global factor score and with the Mini-Mental State Examination. We compared the cognitive trajectories across groups using growth curve models (mean follow-up time = 7 years).ResultsUsing different model formulations and cut points for determining biomarker abnormality, only the group with abnormal levels of amyloid, tau, and neurodegeneration (A+T+N+) showed consistently greater cognitive decline than the group with normal levels of all biomarkers (A−T−N−). Replicating prior findings using the 2011 National Institute on Aging–Alzheimer's Association/suspected non–Alzheimer disease pathophysiology schema, only individuals with abnormal levels of both amyloid and phosphorylated tau 181 or total tau (stage 2) showed greater cognitive decline than those with normal biomarker levels (stage 0).ConclusionThe results are consistent with the hypothesis that both elevated brain amyloid and neurofibrillary tangles are necessary to observe accelerated neurodegeneration, which in turn leads to cognitive decline.

scholarly journals Total tau and Phosphorylated tau 181 Levels in the Cerebrospinal Fluid of Patients With Frontotemporal Dementia Due to P301L and G272V tau Mutations

2003 ◽  
Vol 60 (9) ◽  
Author(s):  
Sonia M. Rosso ◽  
Esther van Herpen ◽  
Yolande A. L. Pijnenburg ◽  
Niki S. M. Schoonenboom ◽  
Philip Scheltens ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Frontotemporal Dementia ◽  
Phosphorylated Tau ◽  
Total Tau ◽  
Phosphorylated Tau 181
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