scholarly journals Using florbetapir positron emission tomography to explore cerebrospinal fluid cut points and gray zones in small sample sizes

2015 ◽  
Vol 1 (4) ◽  
pp. 440-446 ◽  
Author(s):  
Philip S.J. Weston ◽  
Ross W. Paterson ◽  
Marc Modat ◽  
Ninon Burgos ◽  
Manuel J. Cardoso ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Cerebrospinal Fluid ◽  
Small Sample ◽  
Emission Tomography ◽  
Sample Sizes ◽  
Cut Points ◽  
Positron Emission ◽  
Small Sample Sizes

scholarly journals Association of weight change with cerebrospinal fluid biomarkers and amyloid positron emission tomography in preclinical Alzheimer’s disease

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Oriol Grau-Rivera ◽  
◽  
Irene Navalpotro-Gomez ◽  
Gonzalo Sánchez-Benavides ◽  
Marc Suárez-Calvet ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Weight Loss ◽  
Cerebrospinal Fluid ◽  
Weight Change ◽  
Emission Tomography ◽  
Link Type ◽  
Preclinical Ad ◽  
Positron Emission ◽  
T Tau

Abstract Background Recognizing clinical manifestations heralding the development of Alzheimer’s disease (AD)-related cognitive impairment could improve the identification of individuals at higher risk of AD who may benefit from potential prevention strategies targeting preclinical population. We aim to characterize the association of body weight change with cognitive changes and AD biomarkers in cognitively unimpaired middle-aged adults. Methods This prospective cohort study included data from cognitively unimpaired adults from the ALFA study (n = 2743), a research platform focused on preclinical AD. Cognitive and anthropometric data were collected at baseline between April 2013 and November 2014. Between October 2016 and February 2020, 450 participants were visited in the context of the nested ALFA+ study and underwent cerebrospinal fluid (CSF) extraction and acquisition of positron emission tomography images with [18F]flutemetamol (FTM-PET). From these, 408 (90.1%) were included in the present study. We used data from two visits (average interval 4.1 years) to compute rates of change in weight and cognitive performance. We tested associations between these variables and between weight change and categorical and continuous measures of CSF and neuroimaging AD biomarkers obtained at follow-up. We classified participants with CSF data according to the AT (amyloid, tau) system and assessed between-group differences in weight change. Results Weight loss predicted a higher likelihood of positive FTM-PET visual read (OR 1.27, 95% CI 1.00–1.61, p = 0.049), abnormal CSF p-tau levels (OR 1.50, 95% CI 1.19–1.89, p = 0.001), and an A+T+ profile (OR 1.64, 95% CI 1.25–2.20, p = 0.001) and was greater among participants with an A+T+ profile (p < 0.01) at follow-up. Weight change was positively associated with CSF Aβ42/40 ratio (β = 0.099, p = 0.032) and negatively associated with CSF p-tau (β = − 0.141, p = 0.005), t-tau (β = − 0.147 p = 0.004) and neurogranin levels (β = − 0.158, p = 0.002). In stratified analyses, weight loss was significantly associated with higher t-tau, p-tau, neurofilament light, and neurogranin, as well as faster cognitive decline in A+ participants only. Conclusions Weight loss predicts AD CSF and PET biomarker results and may occur downstream to amyloid-β accumulation in preclinical AD, paralleling cognitive decline. Accordingly, it should be considered as an indicator of increased risk of AD-related cognitive impairment. Trial registration NCT01835717, NCT02485730, NCT02685969.

Arguments against the biomarker-driven diagnosis of AD

2012 ◽  
Vol 25 (2) ◽  
pp. 177-181 ◽  
Author(s):  
Helen F.K. Chiu ◽  
Henry Brodaty
Keyword(s):  
Magnetic Resonance Imaging ◽  
Positron Emission Tomography ◽  
Cerebrospinal Fluid ◽  
Magnetic Resonance ◽  
Early Diagnosis ◽  
Research Agenda ◽  
Emission Tomography ◽  
Resonance Imaging ◽  
Positron Emission ◽  
Magnetic Resonance Imaging Mri

Impressive developments in the biomarker diagnosis of Alzheimer's disease (AD and pre-symptomatic states, using cerebrospinal fluid (CSF), positron emission tomography (PET), magnetic resonance imaging (MRI), and proteomics, have been at the forefront of research in the last decade. With the publication of the criteria of Dubois et al. (2007) and the revised National Institute on Aging and Alzheimer's Association (NIA–AA) criteria for the diagnosis of AD (Jack et al., 2011), this has further ignited the interest and enthusiasm for researchers and clinicians in the field. In some of the major conferences on dementia in recent years, the topic of the biomarker-driven diagnosis of AD has dominated the research agenda. But many questions arise as to how this research will translate into practice. Here, we would like to put forward our arguments against a biomarker-driven diagnosis of AD, and we would caution that very early diagnosis of AD may not result in better care of the subjects.

scholarly journals Actinomyces cavernous sinus infection: a case and systematic literature review

2018 ◽  
Vol 18 (5) ◽  
pp. 373-377 ◽  
Author(s):  
Michal Lubomski ◽  
James Dalgliesh ◽  
Kenneth Lee ◽  
Omprakash Damodaran ◽  
Genevieve McKew ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Cerebrospinal Fluid ◽  
Literature Review ◽  
Cavernous Sinus ◽  
Emission Tomography ◽  
Filamentous Bacteria ◽  
Painful Ophthalmoplegia ◽  
Hunt Syndrome ◽  
Positron Emission ◽  
History Of

A 63-year-old man presented with a 2-month history of progressive right-sided exophthalmos, painful ophthalmoplegia and fevers. As more features developed, he was diagnosed with giant cell arteritis, then Tolosa-Hunt syndrome, and transiently responded to corticosteroids. A bland cerebrospinal fluid and highly metabolically active brain (18F)-fluoro-D-glucose-positron emission tomography suggested lymphoma. Biopsy of the mass showed sulphur granules with Gram-positive filamentous bacteria with Actinomyces-like colonies. Actinomyces cavernous sinus infections are rare and indolent. They often mimic non-infective causes including other inflammatory and infiltrative conditions, vascular and neoplastic causes, particularly lymphoma. Clinicians should consider infective cavernous sinus syndromes in people with a fluctuating painful ophthalmoplegia that responds poorly to corticosteroids. The term Tolosa-Hunt syndrome is problematic and should be retired or used only with reservation.

scholarly journals Characterization of an APP/tau rat model of Alzheimer’s disease by positron emission tomography and immunofluorescent labeling

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Thomas Filip ◽  
Severin Mairinger ◽  
Joerg Neddens ◽  
Michael Sauberer ◽  
Stefanie Flunkert ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Cerebrospinal Fluid ◽  
Rat Model ◽  
Brain Regions ◽  
Emission Tomography ◽  
Transgenic Rats ◽  
Positive Correlation ◽  
Cross Breeding ◽  
Regional Brain ◽  
Positron Emission

Abstract Background To better understand the etiology and pathomechanisms of Alzheimer’s disease, several transgenic animal models that overexpress human tau or human amyloid-beta (Aβ) have been developed. In the present study, we generated a novel transgenic rat model by cross-breeding amyloid precursor protein (APP) rats with tau rats. We characterized this model by performing positron emission tomography scans combined with immunofluorescent labeling and cerebrospinal fluid analyses. Methods APP/Tau rats were generated by cross-breeding male McGill-R-Thy1-APP transgenic rats with female hTau-40/P301L transgenic rats. APP/Tau double transgenic rats and non-transgenic (ntg) littermates aged 7, 13, and 21 months were subjected to dynamic [11C] PiB scan and dynamic [18F]THK-5317 scans. For regional brain analysis, a template was generated from anatomical MR images of selected animals, which was co-registered with the PET images. Regional analysis was performed by application of the simplified reference tissue model ([11C]PiB data), whereas [18F]THK-5317 data were analyzed using a 2-tissue compartment model and Logan graphical analysis. In addition, immunofluorescent labeling (tau, amyloid) and cerebrospinal fluid analyses were performed. Results [11C]PiB binding potential (BPND) and [18F]THK-5317 volume of distribution (VT) showed an increase with age in several brain regions in the APP/Tau group but not in the ntg control group. Immunohistochemical analysis of brain slices of PET-scanned animals revealed a positive correlation between Aβ labeling and [11C]PiB regional BPND. Tau staining yielded a trend towards higher levels in the cortex and hippocampus of APP/Tau rats compared with ntg littermates, but without reaching statistical significance. No correlation was found between tau immunofluorescence labeling results and the respective [18F]THK-5317 VT values. Conclusions We thoroughly characterized a novel APP/Tau rat model using combined PET imaging and immunofluorescence analysis. We observed an age-related increase in [11C]PiB and [18F]THK-5317 binding in several brain regions in the APP/Tau group but not in the ntg group. Although we were able to reveal a positive correlation between amyloid labeling and [11C]PiB regional brain uptake, we observed relatively low human tau and amyloid fibril expression levels and a somewhat unstable brain pathology which questions the utility of this animal model for further studies.

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