scholarly journals 18F-THK5351 Positron Emission Tomography Imaging in Neurodegenerative Tauopathies

2021 ◽  
Vol 13 ◽  
Author(s):  
Michinori Ezura ◽  
Akio Kikuchi ◽  
Nobuyuki Okamura ◽  
Aiko Ishiki ◽  
Takafumi Hasegawa ◽  
...  

Introduction: We aimed to determine whether in vivo tau deposits and monoamine oxidase B (MAO-B) detection using 18F-THK5351 positron emission tomography (PET) can assist in the differential distribution in patients with corticobasal syndrome (CBS), progressive supranuclear palsy (PSP), and Alzheimer’s disease (AD) and whether 18F-THK5351 retention of lesion sites in CBS and PSP can correlate with clinical parameters.Methods:18F-THK5351 PET was performed in 35 participants, including 7, 9, and 10 patients with CBS, PSP, and AD, respectively, and 9 age-matched normal controls. In CBS and PSP, cognitive and motor functions were assessed using the Montreal Cognitive Assessment, Addenbrooke’s Cognitive Examination–Revised, and Frontal Assessment Battery, Unified Parkinson’s Disease Rating Scale Motor Score, and PSP Rating Scale.Results:18F-THK5351 retention was observed in sites susceptible to disease-related pathologies in CBS, PSP, and AD. 18F-THK5351 uptake in the precentral gyrus clearly differentiated patients with CBS from those with PSP and AD. Furthermore, 18F-THK5351 uptake in the inferior temporal gyrus clearly differentiated patients with AD from those with CBS and PSP. Regional 18F-THK5351 retention was associated with the cognitive function in CBS and PSP.Conclusion: Measurement of the tau deposits and MAO-B density in the brain using 18F-THK5351 may be helpful for the differential diagnosis of tauopathies and for understanding disease stages.

2015 ◽  
Vol 58 (14) ◽  
pp. 5538-5547 ◽  
Author(s):  
Nikolai M. Evdokimov ◽  
Peter M. Clark ◽  
Graciela Flores ◽  
Timothy Chai ◽  
Kym F. Faull ◽  
...  

2017 ◽  
Vol 39 (3) ◽  
pp. 439-453 ◽  
Author(s):  
Paula Kopschina Feltes ◽  
Erik FJ de Vries ◽  
Luis E Juarez-Orozco ◽  
Ewelina Kurtys ◽  
Rudi AJO Dierckx ◽  
...  

Psychosocial stress is a risk factor for the development of depression. Recent evidence suggests that glial activation could contribute to the development of depressive-like behaviour. This study aimed to evaluate in vivo whether repeated social defeat (RSD) induces short- and long-term inflammatory and metabolic alterations in the brain through positron emission tomography (PET). Male Wistar rats ( n = 40) were exposed to RSD by dominant Long-Evans rats on five consecutive days. Behavioural and biochemical alterations were assessed at baseline, day 5/6 and day 24/25 after the RSD protocol. Glial activation (11C-PK11195 PET) and changes in brain metabolism (18F-FDG PET) were evaluated on day 6, 11 and 25 (short-term), and at 3 and 6 months (long-term). Defeated rats showed transient depressive- and anxiety-like behaviour, increased corticosterone and brain IL-1β levels, as well as glial activation and brain hypometabolism in the first month after RSD. During the third- and six-month follow-up, no between-group differences in any investigated parameter were found. Therefore, non-invasive PET imaging demonstrated that RSD induces transient glial activation and reduces brain glucose metabolism in rats. These imaging findings were associated with stress-induced behavioural changes and support the hypothesis that neuroinflammation could be a contributing factor in the development of depression.


Biomaterials ◽  
2012 ◽  
Vol 33 (16) ◽  
pp. 4147-4156 ◽  
Author(s):  
Hao Hong ◽  
Yin Zhang ◽  
Jonathan W. Engle ◽  
Tapas R. Nayak ◽  
Charles P. Theuer ◽  
...  

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