scholarly journals Positron emission tomography imaging of tau pathology in progressive supranuclear palsy

2016 ◽  
Vol 37 (9) ◽  
pp. 3150-3160 ◽  
Author(s):  
Sarah Coakeley ◽  
Sang Soo Cho ◽  
Yuko Koshimori ◽  
Pablo Rusjan ◽  
Madeleine Harris ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Positron Emission Tomography ◽  
Progressive Supranuclear Palsy ◽  
Standardized Uptake Value ◽  
Paired Helical Filaments ◽  
Emission Tomography ◽  
Positron Emission ◽  
Parkinsonian Disorders

Progressive supranuclear palsy is a rare form of atypical Parkinsonism that differs neuropathologically from other parkinsonian disorders. While many parkinsonian disorders such as Parkinson’s disease, Lewy body dementia, and multiple system atrophy are classified as synucleinopathies, progressive supranuclear palsy is coined a tauopathy due to the aggregation of pathological tau in the brain. [18F]AV-1451 (also known as [18F]-T807) is a positron emission tomography radiotracer that binds to paired helical filaments of tau in Alzheimer’s disease. We investigated whether [18F]AV-1451 could be used as biomarker for the diagnosis and disease progression monitoring in progressive supranuclear palsy. Six progressive supranuclear palsy, six Parkinson’s disease, and 10 age-matched healthy controls were recruited. An anatomical MRI and a 90-min PET scan, using [18F]AV-1451, were acquired from all participants. The standardized uptake value ratio from 60 to 90 min post-injection was calculated in each region of interest, using the cerebellar cortex as a reference region. No significant differences in standardized uptake value ratios were detected in our progressive supranuclear palsy group compared to the two control groups. [18F]AV-1451 may bind selectivity to the paired helical filaments in Alzheimer’s disease, which differ from the straight conformation of tau filaments in progressive supranuclear palsy.

Therapeutic effect of mesenchymal stem cells in an animal model of Alzheimer’s disease evaluated by β-amyloid positron emission tomography imaging

2020 ◽  
Vol 54 (9) ◽  
pp. 883-891
Author(s):  
Bok-Nam Park ◽  
Jang-Hee Kim ◽  
Tae Sung Lim ◽  
So Hyun Park ◽  
Tae-Gyu Kim ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Positron Emission Tomography ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Standardized Uptake Value ◽  
Emission Tomography ◽  
Positron Emission ◽  
Β Amyloid

Objective: We evaluated the effects of bone marrow–derived mesenchymal stem cells in a model of Alzheimer’s disease using serial [18F]Florbetaben positron emission tomography. Methods: 3xTg Alzheimer’s disease mice were treated with intravenously injected bone marrow–derived mesenchymal stem cells, and animals without stem cell therapy were used as controls. Serial [18F]Florbetaben positron emission tomography was performed after therapy. The standardized uptake value ratio was measured as the cortex standardized uptake value divided by the cerebellum standardized uptake value. Memory function and histological changes were observed using the Barnes maze test and β-amyloid-reactive cells. Results: Standardized uptake value ratio decreased significantly from day 14 after stem cell administration in the bone marrow–derived mesenchymal stem cells–treated group ( n = 28). In contrast, there was no change in the ratio in control mice ( n = 25) at any time point. In addition, mice that received bone marrow–derived mesenchymal stem cell therapy also exhibited significantly better memory function and less β-amyloid-immunopositive plaques compared to controls. Conclusion: The therapeutic effect of intravenously injected bone marrow–derived mesenchymal stem cells in a mouse model of Alzheimer’s disease was confirmed by β-amyloid positron emission tomography imaging, memory functional studies and histopathological evaluation.

scholarly journals 18F-AV-1451 positron emission tomography in Alzheimer’s disease and progressive supranuclear palsy

Brain ◽  
2017 ◽  
pp. aww340 ◽  
Author(s):  
Luca Passamonti ◽  
Patricia Vázquez Rodríguez ◽  
Young T. Hong ◽  
Kieren S. J. Allinson ◽  
David Williamson ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Positron Emission Tomography ◽  
Progressive Supranuclear Palsy ◽  
Emission Tomography ◽  
Positron Emission

Season of Birth and Vulnerability to the Pathology of Alzheimer’s Disease: an in Vivo Positron Emission Tomography Study

2021 ◽  
Author(s):  
Fumihiko Yasuno ◽  
Hiroyuki Minami
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Positron Emission Tomography ◽  
Amyloid Β ◽  
Standardized Uptake Value ◽  
Analysis Of Covariance ◽  
Emission Tomography ◽  
Disease Assessment ◽  
Positron Emission

Abstract This study used positron emission tomography to examine whether the seasonal birth effect as an exogenic indicator of early life environmental factors influenced vulnerability to Alzheimer’s disease (AD) pathology in the elderly. We analyzed datasets from the Alzheimer’s Disease Neuroimaging Initiative, which included the data for 234 cognitively normal individuals and patients with mild cognitive impairment (n = 115) and AD dementia (n = 38). As an index of amyloid β (Aβ)/tau accumulation, the AV-45/AV-1451-standardized uptake value ratios (SUVRs) were compared between groups of spring-to-summer births and fall-to-winter births by analysis of covariance. Seasonal birth difference was a good predictor of AV-1451 SUVR. We found that participants with a fall-to-winter birth showed lower AV-1451 SUVRs than those with a spring-to-summer birth, after accounting for the Alzheimer’s Disease Assessment Scale-cognitive subscale (ADAS) score and other factors that could possibly affect tau accumulation. Our findings showed a vulnerability to tau pathology in participants with a fall-to-winter birth, which may be caused by perinatal or postnatal brain damage due to the risk factors associated with the cold season.

scholarly journals Recent Developments in Positron Emission Tomography Tracers for Proteinopathies Imaging in Dementia

2022 ◽  
Vol 13 ◽  
Author(s):  
Ruiqing Ni ◽  
Roger M. Nitsch
Keyword(s):  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Positron Emission Tomography ◽  
Parkinson's Disease ◽  
Amyloid Β ◽  
Emission Tomography ◽  
Imaging Biomarkers ◽  
Positron Emission ◽  
Imaging Probes

An early detection and intervention for dementia represent tremendous unmet clinical needs and priorities in society. A shared feature of neurodegenerative diseases causing dementia is the abnormal accumulation and spreading of pathological protein aggregates, which affect the selective vulnerable circuit in a disease-specific pattern. The advancement in positron emission tomography (PET) biomarkers has accelerated the understanding of the disease mechanism and development of therapeutics for Alzheimer’s disease and Parkinson’s disease. The clinical utility of amyloid-β PET and the clinical validity of tau PET as diagnostic biomarker for Alzheimer’s disease continuum have been demonstrated. The inclusion of biomarkers in the diagnostic criteria has introduced a paradigm shift that facilitated the early and differential disease diagnosis and impacted on the clinical management. Application of disease-modifying therapy likely requires screening of patients with molecular evidence of pathological accumulation and monitoring of treatment effect assisted with biomarkers. There is currently still a gap in specific 4-repeat tau imaging probes for 4-repeat tauopathies and α-synuclein imaging probes for Parkinson’s disease and dementia with Lewy body. In this review, we focused on recent development in molecular imaging biomarkers for assisting the early diagnosis of proteinopathies (i.e., amyloid-β, tau, and α-synuclein) in dementia and discussed future perspectives.

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