Early Clinical PET Imaging Results with the Novel PHF-Tau Radioligand [F-18]-T807

Chien, David; Bahri, Shadfar; Szardenings, Anna Katrin; Walsh, Joseph C.; Mu, Fanrong; Su, Min‐Ying; Shankle, William R.; Elizarov, Arkadij M.; Kolb, Hartmuth C.

doi:10.3233/jad-122059

Cited by 606 publications

(579 citation statements)

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“…In the high-tau MCI, stage I commonly observes binding in the anterior, inferior, and lateral temporal lobes. In the dementia stages the tau deposition in the previously involved areas becomes denser and tau binding is also observed in the other associations fields like the parietal and frontal lobes as seen in the figure cingulate, and fusiform, entorhinal, and parahippocampal gyri [30,40,41,44]. As the MCI stage is quite heterogeneous, patients can demonstrate a full range of Braak stages, from I to VI [44].…”

Section: Tau Imaging Research Findingsmentioning

confidence: 99%

“…1). Specifically, patients with AD show significant tau PET tracer uptake in the temporal, parietal, and frontal lobes, while the primary sensory/motor cortices are relatively spared [30,[39][40][41][42][43][44]. Tau in the inferior temporal lobe is associated with increased amyloid deposition on PET, as well as greater cognitive impairment and disease severity in AD [41,44].…”

Section: Tau Imaging Research Findingsmentioning

confidence: 99%

“…The most used tracer to date is [ [29]. This benzimidazole-pyrimidine derivative has an approximately 29 times greater selectivity for PHF-tau over amyloid β and showed uptake in a pattern similar to that predicted by Braak staging in patients with AD [30]. The tracer also does not appear to bind with high affinity to the straight tau filaments seen in other tauopathies [31].…”

Section: Tau Imaging Approachesmentioning

confidence: 99%

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Tau Imaging in Alzheimer's Disease Diagnosis and Clinical Trials

et al. 2017

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In vivo imaging of the tau protein has the potential to aid in quantitative diagnosis of Alzheimer's disease, corroborate or dispute the amyloid hypothesis, and demonstrate biomarker engagement in clinical drug trials. A host of tau positron emission tomography agents have been designed, validated, and tested in humans. Several agents have characteristics approaching the ideal imaging tracer with some limitations, primarily regarding off-target binding. Dozens of clinical trials evaluating imaging techniques and several pharmaceutical trials have begun to integrate tau imaging into their protocols.

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Section: Tau Imaging Research Findingsmentioning

confidence: 99%

Section: Tau Imaging Research Findingsmentioning

confidence: 99%

Section: Tau Imaging Approachesmentioning

confidence: 99%

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Tau Imaging in Alzheimer's Disease Diagnosis and Clinical Trials

et al. 2017

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“…Positron emission tomography (PET) ligands binding to tau aggregates might prove useful for improving the diagnosis of different tauopathies, including PSP. In recent years, the advent of the tau tracers 18 F‐AV‐1451 (T‐807),8 18 F‐THK‐5351,9 and (2‐((1 E ,3 E )‐4‐(6‐(11C‐methylamino)pyridin‐3‐yl)buta‐1,3‐dienyl)benzo[ d ]thiazol‐6‐ol) ( 11 C‐PBB310) has increased the interest in tau PET imaging in neurodegenerative diseases, but their clinical utility is not fully known to date.…”

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confidence: 99%

Increased basal ganglia binding of ¹⁸F‐AV‐1451 in patients with progressive supranuclear palsy

et al. 2016

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BackgroundProgressive supranuclear palsy (PSP) is difficult to diagnose accurately. The recently developed tau PET tracers may improve the diagnostic work‐up of PSP.MethodsRegional tau accumulation was studied using 18F‐AV‐1451 PET in 11 patients with PSP and 11 age‐matched healthy controls in the Swedish BioFinder study.Results 18F‐AV‐1451 standard uptake volume ratios were significantly higher in the basal ganglia in PSP patients when compared with controls (globus pallidus 1.75 vs 1.50; putamen 1.51 vs 1.35). Retention in the basal ganglia was correlated with age in both groups (r = .43–.78, P < .05). In PSP, we observed a significant correlation between clinical deterioration measured with the PSP rating scale and standard uptake volume ratios in the globus pallidus (r = .74, P < .05). However, no 18F‐AV‐1451 retention was observed in the cerebral cortex or white matter of either PSP patients or controls, and autoradiography did not reveal any specific binding of AV‐1451 to PSP tau aggregates.ConclusionWe found higher 18F‐AV‐1451 retention in the basal ganglia of PSP patients when compared with healthy elderly controls, but also increases with age in both controls and patients. As a result of the overlap in retention between diagnostic groups and the age‐dependent increase present also in controls, 18F‐AV‐1451 PET might not reliably distinguish individual patients with PSP from controls. However, further studies are needed to evaluate whether 18F‐AV‐1451 PET might be useful as a progression marker in clinical PSP trials. © The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.

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“…A variety of radiotracers are available, including those capable of identifying pathophysiological processes recently implicated in epileptogenesis, such as metabolism, neuroinflammation, and hyperphosphorylated tau [60][61][62][63][64]. For example, in vivo [18F]PBR111-PET has found significant inflammation after SE in the hippocampus and amygdala during epileptogenesis [60].…”

Section: Positron Emission Tomographymentioning

confidence: 99%

Neuroimaging the Epileptogenic Process

et al. 2014

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Epilepsy is one of the most common chronic neurological conditions worldwide. Anti-epileptic drugs (AEDs) can suppress seizures, but do not affect the underlying epileptic state, and many epilepsy patients are unable to attain seizure control with AEDs. To cure or prevent epilepsy, disease-modifying interventions that inhibit or reverse the disease process of epileptogenesis must be developed. A major limitation in the development and implementation of such an intervention is the current poor understanding, and the lack of reliable biomarkers, of the epileptogenic process. Neuroimaging represents a non-invasive medical and research tool with the ability to identify early pathophysiological changes involved in epileptogenesis, monitor disease progression, and assess the effectiveness of possible therapies. Here we will provide an overview of studies conducted in animal models and in patients with epilepsy that have utilized various neuroimaging modalities to investigate epileptogenesis.

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Early Clinical PET Imaging Results with the Novel PHF-Tau Radioligand [F-18]-T807

Cited by 606 publications

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Tau Imaging in Alzheimer's Disease Diagnosis and Clinical Trials

Tau Imaging in Alzheimer's Disease Diagnosis and Clinical Trials

Increased basal ganglia binding of ¹⁸F‐AV‐1451 in patients with progressive supranuclear palsy

Neuroimaging the Epileptogenic Process

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Early Clinical PET Imaging Results with the Novel PHF-Tau Radioligand [F-18]-T807

Cited by 606 publications

References 0 publications

Tau Imaging in Alzheimer's Disease Diagnosis and Clinical Trials

Tau Imaging in Alzheimer's Disease Diagnosis and Clinical Trials

Increased basal ganglia binding of 18F‐AV‐1451 in patients with progressive supranuclear palsy

Neuroimaging the Epileptogenic Process

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Increased basal ganglia binding of ¹⁸F‐AV‐1451 in patients with progressive supranuclear palsy