Objectives: The aim of the study was to create a local normal database brain template of Thai individuals for C-Pittsburgh compound B (C-PiB) and F-THK 5351 depositions using statistical parametric mapping (SPM) software, and to validate and optimize the established specific brain template for use in clinical practice with a highly reliability and reproducibility.
Methods: This prospective study was conducted in 24 healthy right-handed volunteers (13 men, 11 women; aged: 42-79 years) who underwent F-THK 5351 and C-PiB PET/CT scans. SPM was used for the F-THK 5351 and C-PiB PET/CT image analysis. All PET images were processed individually using Diffusion Tensor Image -Magnetic Resonance Imaging-weighted images (DTI-MRI images), which involved: (1) conversion of Digital Imaging and Communications in Medicine (DICOM) files into an analyzable file extension (.NIFTI) for statistical parametric mapping, (2) setting of the origin (the anterior commissure was used as the anatomical landmark), (3) re-alignment, (4) co-registration of PET with B0 (T1W) and DTI-MRI images, (5) normalization, and (6) normal verification using the Thai MRI standard. We then compared the normal PET template with the abnormal deposition area of different dementia syndromes, including Alzheimer's disease and progressive supranuclear palsy.
Results: This method was able to differentiate cognitively normal from Alzheimer's disease and progressive supranuclear palsy subjects.
Conclusions: This normal brain template was able to be integrated into clinical practice and research using PET analyses at our center.
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http://dx.doi.org/10.22038/AOJNMB.2020.49623.1338 | DOI Listing |
Nihon Yakurigaku Zasshi
November 2022
Department of Pharmacology, Tohoku University Graduate School of Medicine.
Alzheimer's disease (AD) is one of the most common causes of dementia in the world. Neurodegeneration, gliosis, and misfolded proteins such as amyloid plaques and tau tangles are neuropathological hallmarks in AD. In vivo imaging of these neuropathological lesions would be good biomarkers to understand pathophysiology as well as surrogate markers for clinical trials.
View Article and Find Full Text PDFJ Clin Neurol
July 2022
Department of Nuclear Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Background And Purpose: Alzheimer's disease (AD) does not always mean amyloid positivity. [F]THK-5351 has been shown to be able to detect reactive astrogliosis as well as tau accompanied by neurodegenerative changes. We evaluated the [F]THK-5351 retention patterns in positron-emission tomography (PET) and the clinical characteristics of patients clinically diagnosed with AD dementia who had negative amyloid PET findings.
View Article and Find Full Text PDFFront Neurosci
February 2022
Division of Pharmacology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, Sendai, Japan.
Many neurodegenerative diseases are neuropathologically characterized by neuronal loss, gliosis, and the deposition of misfolded proteins such as β-amyloid (Aβ) plaques and tau tangles in Alzheimer's disease (AD). In postmortem AD brains, reactive astrocytes and activated microglia are observed surrounding Aβ plaques and tau tangles. These activated glial cells secrete pro-inflammatory cytokines and reactive oxygen species, which may contribute to neurodegeneration.
View Article and Find Full Text PDFWorld J Nucl Med
June 2020
National Cyclotron and PET Centre, Chulabhorn Hospital, Chulabhorn Royal Academy, Bangkok, Thailand.
Abnormal beta-amyloid plaques and tau protein accumulation are the core pathologic features of Alzheimer's disease. However, the accumulation of these proteins is also common in cognitively normal elderly people. Therefore, this study is aimed to evaluate the amyloid and tau accumulation in the cognitively normal population.
View Article and Find Full Text PDFFront Neurol
July 2021
Department of Neurology, Gunma University Graduate School of Medicine, Maebashi, Japan.
In Alzheimer's disease, the apolipoprotein E gene ε2 allele is a protective genetic factor, whereas the ε4 allele is a genetic risk factor. However, both the ε2 and the ε4 alleles are genetic risk factors for lobar intracerebral hemorrhage. The reasons for the high prevalence of lobar intracerebral hemorrhage and the low prevalence of Alzheimer's disease with the ε2 allele remains unknown.
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