A case of tauopathy with auditory agnosia and dysprosody diagnosed by [18F]PM-PBB3 tau PET scan

Author(s):  
Kyoko Mashima ◽  
Mika Konishi ◽  
Toshiki Tezuka ◽  
Daisuke Ito ◽  
Masaru Mimura
Keyword(s):  
Pet Scan ◽  
Neurology ◽  
2018 ◽  
Vol 91 (9) ◽  
pp. e859-e866 ◽  
Author(s):  
Andrew J. Aschenbrenner ◽  
Brian A. Gordon ◽  
Tammie L.S. Benzinger ◽  
John C. Morris ◽  
Jason J. Hassenstab

ObjectiveTo examine the independent and interactive influences of neuroimaging biomarkers on retrospective cognitive decline.MethodsA total of 152 middle-aged and older adult participants with at least 2 clinical and cognitive assessments, a Clinical Dementia Rating score of 0 or 0.5, and a flortaucipir (18F-AV-1451) tau PET scan, a florbetapir (18F-AV-45) amyloid PET scan, and a structural MRI scan were recruited from the Knight Alzheimer Disease Research Center at Washington University in St. Louis. Cognition was assessed with standard measures reflecting episodic memory, executive functioning, semantic fluency, and processing speed.ResultsResults from retrospective longitudinal analyses showed that each biomarker had a univariate association with the global cognitive composite; however, when each marker was analyzed in a single statistical model, only tau was a significant predictor of global cognitive decline. There was an interaction between tau and amyloid such that tau-related cognitive decline was worse in individuals with high amyloid. There was also an interaction with hippocampal volume indicating that individuals with high levels of all 3 pathologies exhibited the greatest declines in cognition. Additional analyses within each cognitive domain indicated that tau had the largest negative influence on tests of episodic memory and executive functioning.ConclusionsTogether, these results suggest that increasing levels of tau most consistently relate to declines in cognition preceding biomarker collection. These findings support models of Alzheimer disease (AD) staging that suggest that elevated β-amyloid alone may be insufficient to produce cognitive change in individuals at risk for AD and support the use of multiple biomarkers to stage AD progression.


2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S609-S609 ◽  
Author(s):  
Takuya Hayashi ◽  
Nobuyuki Kudomi ◽  
Hiroshi Watabe ◽  
Hisashi Oka ◽  
Kohei Hayashida ◽  
...  

2020 ◽  
Author(s):  
L Beyer ◽  
A Nitschmann ◽  
H Barthel ◽  
T van Eimeren ◽  
M Unterrainer ◽  
...  

2005 ◽  
Vol 152 (4) ◽  
pp. 521-525 ◽  
Author(s):  
Athina Markou ◽  
Patrick Manning ◽  
Banu Kaya ◽  
Sam N Datta ◽  
Jamshed B Bomanji ◽  
...  

We report a case of a young woman with Cushing’s syndrome (CS), in whom although endocrine investigations and negative pituitary imaging were suggestive of ectopic ACTH secretion, the results of inferior petrosal sinus (IPS) sampling after coricotropin-releasing hormone (CRH) stimulation were suggestive of pituitary ACTH hypersecretion. 111In-labelled octreotide and high-resolution computer tomography (CT) revealed a lesion possibly responsible for the ACTH source in the thymus. Thymectomy confirmed concomitant ectopic CRH and probable ACTH production by a thymic neuroendocrine carcinoma. After an 8-year remission period the patient developed a clinical and biochemical relapse. A high-resolution computed tomography (CT) scan of the thorax showed a 2-cm nodule in the thymic bed, which was positive on a [18F]fluoro-2-deoxy-d-glucose ([18F]FDG) positron emission tomography (PET) scan. However, a repeated thymectomy did not result in remission. A repeat [18F]FDG PET study showed persistent disease in the thymic bed and also uptake in the adrenals. The patient underwent bilateral adrenalectomy, which resulted in clinical remission. A further [18F]FDG PET scan 8 months later showed no progression of the thymic tumor and confirmed complete excision of the adrenals. This is a rare case of concomitant CRH and ACTH secretion from a thymic carcinoid tumor; the case illustrates the usefulness of functional imaging with [18F]FDG PET in the diagnosis, management and follow-up of neuroendocrine tumors.


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