期刊
ALZHEIMERS RESEARCH & THERAPY
卷 6, 期 1, 页码 -出版社
BMC
DOI: 10.1186/alzrt240
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资金
- Florey Institute of Neuroscience and Mental Health
- Alfred and the Victorian Forensic Institute of Medicine
- Australia's National Health & Medical Research Council (NHMRC)
- Parkinson's Victoria
- Alzheimer's Drug Discovery Foundation [20101208 AFTD]
- NHMRC [1044361]
Introduction: The introduction of tau imaging agents such as F-18-THK523 offers new hope for the in vivo assessment of tau deposition in tauopathies such as Alzheimer's disease (AD), where preliminary F-18-THK523-PET studies have demonstrated significantly higher cortical retention of F-18-THK523 in AD compared to age-matched healthy individuals. In addition to AD, tau imaging with PET may also be of value in assessing non-AD tauopathies, such as corticobasal degeneration (CBD), progressive supranuclear palsy (PSP) and Pick's disease (PiD). Methods: To further investigate the ability of THK523 to recognize tau lesions, we undertook immunohistochemical and fluorescence studies in serial brain sections taken from individuals with AD (n = 3), CBD (n = 2), PSP (n = 1), PiD (n = 2) and Parkinson's disease (PD; n = 2). In addition to the neuropathological analysis, one PSP patient had undergone a F-18-THK523 PET scan 5 months before death. Results: Although THK523 labelled tau-containing lesions such as neurofibrillary tangles and neuropil threads in the hippocampus and frontal regions of AD brains, it failed to label tau-containing lesions in non-AD tauopathies. Furthermore, though THK523 faintly labelled dense-cored amyloid-beta plaques in the AD frontal cortex, it failed to label a-synuclein-containing Lewy bodies in PD brain sections. Conclusion: The results of this study suggest that F-18-THK523 selectively binds to paired helical filament tau in AD brains but does not bind to tau lesions in non-AD tauopathies, or to a-synuclein in PD brains.
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