Relevant bibliographies by topics / Tau pet

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Tau pet'

Author: Grafiati
Published: 30 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Tau pet"

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Herholz, Karl. "Tau PET and tauopathies." European Journal of Nuclear Medicine and Molecular Imaging 43, no. 9 (May 10, 2016): 1684–85. http://dx.doi.org/10.1007/s00259-016-3406-5.

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Zimmer, Eduardo Rigon, Antoine Leuzy, Serge Gauthier, and Pedro Rosa-Neto. "Developments in Tau PET Imaging." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 41, no. 5 (September 2014): 547–53. http://dx.doi.org/10.1017/cjn.2014.15.

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ABSTRACTThe presence of neurofibrillary tangles in the brain is a hallmark feature of several neurodegenerative diseases termed “tauopathies,” including Alzheimer’s disease (AD) and the tau molecular subgroup of frontotemporal lobar degeneration (FTLD-tau). Recently, several positron emission tomography (PET) radiopharmaceuticals targeting abnormal conformations of the tau protein have been developed. To date, six novel tau imaging agents—[18F]THK523, [18F]THK5105, [18F]THK5117, [18F]T807, [18F]T808, and [11C]PBB3—have been described and are considered promising as potential tau radioligands. Tau imaging agents offer the opportunity of in vivo topographical mapping and quantification of tau aggregates in parallel with clinical and cognitive assessments. As such, tau imaging is considered of key importance for progress toward earlier and more accurate diagnosis of tauopathies as well as for the monitoring of therapeutic interventions and drug development. Here, we shed light on the most important developments in tau radiopharmaceuticals, highlighting challenges, possibilities and future directions.
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Mattsson-Carlgren, Niklas, Emelie Andersson, Shorena Janelidze, Rik Ossenkoppele, Philip Insel, Olof Strandberg, Henrik Zetterberg, et al. "Aβ deposition is associated with increases in soluble and phosphorylated tau that precede a positive Tau PET in Alzheimer’s disease." Science Advances 6, no. 16 (April 2020): eaaz2387. http://dx.doi.org/10.1126/sciadv.aaz2387.

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The links between β-amyloid (Aβ) and tau in Alzheimer’s disease are unclear. Cognitively unimpaired persons with signs of Aβ pathology had increased cerebrospinal fluid (CSF) phosphorylated tau (P-tau181 and P-tau217) and total-tau (T-tau), which increased over time, despite no detection of insoluble tau aggregates [normal Tau positron emission tomography (PET)]. CSF P-tau and T-tau started to increase before the threshold for Amyloid PET positivity, while Tau PET started to increase after Amyloid PET positivity. Effects of Amyloid PET on Tau PET were mediated by CSF P-tau, and high CSF P-tau predicted increased Tau PET rates. Individuals with MAPT mutations and signs of tau deposition (but without Aβ pathology) had normal CSF P-tau levels. In 5xFAD mice, CSF tau increased when Aβ aggregation started. These results show that Aβ pathology may induce changes in soluble tau release and phosphorylation, which is followed by tau aggregation several years later in humans.
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Okamura, Nobuyuki, and Kazuhiko Yanai. "Applications of tau PET imaging." Nature Reviews Neurology 13, no. 4 (March 17, 2017): 197–98. http://dx.doi.org/10.1038/nrneurol.2017.38.

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Higuchi, Makoto. "PET imaging of tau lesions." Folia Pharmacologica Japonica 145, no. 5 (2015): 268. http://dx.doi.org/10.1254/fpj.145.268.

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Lowe, Val J., Tyler J. Bruinsma, Heather J. Wiste, Hoon-Ki Min, Stephen D. Weigand, Ping Fang, Matthew L. Senjem, et al. "Cross-sectional associations of tau-PET signal with cognition in cognitively unimpaired adults." Neurology 93, no. 1 (May 30, 2019): e29-e39. http://dx.doi.org/10.1212/wnl.0000000000007728.

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ObjectiveTo assess cross-sectional associations of neurofibrillary tangles, measured by tau-PET, with cognitive performance in cognitively unimpaired (CU) adults.MethodsTau- and amyloid-PET were performed in 579 CU participants aged 50–98 from the population-based Mayo Clinic Study of Aging. Associations between tau-PET signal in 43 brain regions and cognitive test scores were assessed using penalized linear regression. In additional models, participants were classified by normal/abnormal global amyloid-PET (A+/A−) and normal/abnormal regional tau-PET (T+/T−). Regional tau-PET cutpoints were defined as standardized uptake value ratio (SUVR) greater than the 95th percentile of tau-PET SUVR in that region among 117 CU participants aged 30–49.ResultsHigher tau-PET signal was associated with poorer memory performance in all medial temporal lobe (MTL) regions and also in the middle temporal pole and frontal olfactory regions. The largest association with tau-PET and memory z scores was seen in the entorhinal cortex; this association was independent of tau-PET signal in other brain regions. Tau-PET in the entorhinal cortex was also associated with poorer global and language performance. In the entorhinal cortex, T+ was associated with lower memory performance among both A− and A+.ConclusionsTau deposition in MTL regions, as reflected by tau-PET signal, was associated with poorer performance on memory tests in CU participants. The association with entorhinal cortex tau-PET was independent of tau-PET signal in other brain regions. Longitudinal studies are needed to understand the fate of CU participants with elevated medial temporal tau-PET signal.
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Tan, Meng-Shan, Yu-Xiang Yang, Hui-Fu Wang, Wei Xu, Chen-Chen Tan, Chuan-Tao Zuo, Qiang Dong, Lan Tan, and Jin-Tai Yu. "PET Amyloid and Tau Status Are Differently Affected by Patient Features." Journal of Alzheimer's Disease 78, no. 3 (November 24, 2020): 1129–36. http://dx.doi.org/10.3233/jad-200124.

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Background: Amyloid-β (Aβ) plaques and tau neurofibrillary tangles are two neuropathological hallmarks of Alzheimer’s disease (AD), which both can be visualized in vivo using PET radiotracers, opening new opportunities to study disease mechanisms. Objective: Our study investigated 11 non-PET factors in 5 categories (including demographic, clinical, genetic, MRI, and cerebrospinal fluid (CSF) features) possibly affecting PET amyloid and tau status to explore the relationships between amyloid and tau pathology, and whether these features had a different association with amyloid and tau status. Methods: We included 372 nondemented elderly from the Alzheimer’s Disease Neuroimaging Initiative cohort. All underwent PET amyloid and tau analysis simultaneously, and were grouped into amyloid/tau quadrants based on previously established abnormality cut points. We examined the associations of above selected features with PET amyloid and tau status using a multivariable logistic regression model, then explored whether there was an obvious correlation between the significant features and PET amyloid or tau levels. Results: Our results demonstrated that PET amyloid and tau status were differently affected by patient features, and CSF biomarker features provided most significant values associating PET findings. CSF Aβ42/40 was the most important factor affecting amyloid PET status, and negatively correlated with amyloid PET levels. CSF pTau could significantly influence both amyloid and tau PET status. Besides CSF pTau and Aβ42, APOE ɛ4 allele status and Mini-Mental State Examination scores also could influence tau PET status, and significantly correlated with tau PET levels. Conclusion: Our results support that tau pathology possibly affected by Aβ-independent factors, implicating the importance of tau pathology in AD pathogenesis.
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Ishikawa, A., M. Tokunaga, I. Matsumoto, T. Minamihisamatsu, S. Uchida, J. Maeda, B. Ji, et al. "Utilities of tau-pet and TSPO-pet for diagnosing severity of tau-induced disease progression." Journal of the Neurological Sciences 381 (October 2017): 664. http://dx.doi.org/10.1016/j.jns.2017.08.1869.

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Zhang, Rui-Qi, Shi-Dong Chen, Xue-Ning Shen, Yu-Xiang Yang, Jia-Ying Lu, Mei Cui, Chuan-Tao Zuo, Qiang Dong, Lan Tan, and Jin-Tai Yu. "Elevated Tau PET Signal Depends on Abnormal Amyloid Levels and Correlates with Cognitive Impairment in Elderly Persons without Dementia." Journal of Alzheimer's Disease 78, no. 1 (October 27, 2020): 395–404. http://dx.doi.org/10.3233/jad-200526.

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Background: The recent developed PET ligands for amyloid-β (Aβ) and tau allow these two neuropathological hallmarks of Alzheimer’s disease (AD) to be mapped and quantified in vivo and to be examined in relation to cognition. Objective: To assess the associations among Aβ, tau, and cognition in non-demented subjects. Methods: Three hundred eighty-nine elderly participants without dementia from the Alzheimer’s Disease Neuroimaging Initiative underwent tau and amyloid PET scans. Cross-sectional comparisons and longitudinal analyses were used to evaluate the relationship between Aβ and tau accumulation. The correlations between biomarkers of both pathologies and performance in memory and executive function were measured. Results: Increased amyloid-PET retention was associated with greater tau-PET retention in widespread cortices. We observed a significant tau increase in the temporal composite regions of interest over 24 months in Aβ+ but not Aβ– subjects. Finally, tau-PET retention but not amyloid-PET retention significantly explained the variance in memory and executive function. Higher level of tau was associated with greater longitudinal memory decline. Conclusion: These findings suggested PET-detectable Aβ plaque pathology may be a necessary antecedent for tau-PET signal elevation. Greater tau-PET retention may demonstrate poorer cognition and predict prospective memory decline in non-demented subjects.
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Jack, Clifford R., Heather J. Wiste, Stephen D. Weigand, Terry M. Therneau, Val J. Lowe, David S. Knopman, Hugo Botha, et al. "Predicting future rates of tau accumulation on PET." Brain 143, no. 10 (June 24, 2020): 3136–50. http://dx.doi.org/10.1093/brain/awaa248.

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Abstract Clinical trials with anti-tau drugs will need to target individuals at risk of accumulating tau. Our objective was to identify variables available in a research setting that predict future rates of tau PET accumulation separately among individuals who were either cognitively unimpaired or cognitively impaired. All 337 participants had: a baseline study visit with MRI, amyloid PET, and tau PET exams, at least one follow-up tau PET exam; and met clinical criteria for membership in one of two clinical diagnostic groups: cognitively unimpaired (n = 203); or cognitively impaired (n = 134, a combined group of participants with either mild cognitive impairment or dementia with Alzheimer’s clinical syndrome). Our primary analyses were in these two clinical groups; however, we also evaluated subgroups dividing the unimpaired group by normal/abnormal amyloid PET and the impaired group by clinical phenotype (mild cognitive impairment, amnestic dementia, and non-amnestic dementia). Linear mixed effects models were used to estimate associations between age, sex, education, APOE genotype, amyloid and tau PET standardized uptake value ratio (SUVR), cognitive performance, cortical thickness, and white matter hyperintensity volume at baseline, and the rate of subsequent tau PET accumulation. Log-transformed tau PET SUVR was used as the response and rates were summarized as annual per cent change. A temporal lobe tau PET meta-region of interest was used. In the cognitively unimpaired group, only higher baseline amyloid PET was a significant independent predictor of higher tau accumulation rates (P < 0.001). Higher rates of tau accumulation were associated with faster rates of cognitive decline in the cognitively unimpaired subgroup with abnormal amyloid PET (P = 0.03), but among the subgroup with normal amyloid PET. In the cognitively impaired group, younger age (P = 0.02), higher baseline amyloid PET (P = 0.05), APOE ε4 (P = 0.05), and better cognitive performance (P = 0.05) were significant independent predictors of higher tau accumulation rates. Among impaired individuals, faster cognitive decline was associated with faster rates of tau accumulation (P = 0.01). While we examined many possible predictor variables, our results indicate that screening of unimpaired individuals for potential inclusion in anti-tau trials may be straightforward because the only independent predictor of high tau rates was amyloidosis. In cognitively impaired individuals, imaging and clinical variables consistent with early onset Alzheimer’s disease phenotype were associated with higher rates of tau PET accumulation suggesting this may be a highly advantageous group in which to conduct proof-of-concept clinical trials that target tau-related mechanisms. The nature of the dementia phenotype (amnestic versus non-amnestic) did not affect this conclusion.
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Dissertations / Theses on the topic "Tau pet"

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Ekaputri, Putu Ayuwidia. "FDG PET and MRI as biomarkers of Tau pathology in Alzheimer’s disease." Thesis, Högskolan i Skövde, Institutionen för biovetenskap, 2021. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-20060.

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Fluorodeoxyglucose Positron Emission Tomography (FDG PET) and Magnetic Resonance Imaging (MRI) are commonly used in a clinical setting as an examination in Alzheimer’s Disease (AD) patients. FDG PET is an imaging tool to evaluate hypometabolism; meanwhile, the MRI observes the brain volume. However, it is still unclear which examination better reflects the tau tangles, which have been known as the hallmark’s pathology of AD. Therefore, this study was conducted to compare FDG PET and MRI in assessing tau pathology in AD, by utilizing a database from the Alzheimer’s Disease Neuroimaging Initiative (ADNI). The presence of tau tangles was confirmed by using the Tau-PET images. In total, 275 cognitively impaired subjects were included as well as a subgroup of 147 subjects with positive amyloid status. Based on the analysis, it was observed that higher Tau-PET is significantly associated with FDG PET hypometabolism and MRI atrophy. A similar result was also seen in the amyloid positive subgroups. By comparing the spearman’s correlation coefficients, it was found that that the correlation was stronger between Tau PET and FDG PET (r=-0.414, p<0.001, and r=-0.475, p<0.001 in the positive amyloid subgroup) compared to Tau-PET and MRI (r=-0.331, p<0.001 and r=-0.440, p<0.001 in the positive amyloid subgroup). Inconclusion, FDG PET better reflects the tau pathology compared to MRI in AD.
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Chen, Siu-ping Chlore, and 陳少萍. "Noah's Ark housing for pet-lovers and SPCA." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1997. http://hub.hku.hk/bib/B31983224.

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Kinstedt, Christine Morgan. "The Development of PET Imaging Agents for Neurodegenerative Disorders." Wright State University / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=wright1590834972520388.

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Jensen, Jordan Royce. "Development of Tau-Selective Imaging Agents for Improved Diagnosis of Alzheimer’s Disease and Other Tauopathies." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1306441097.

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Dhaynaut, Maëva. "PET imaging for the characterization of tauopathies : Alzheimer's disease and chronic traumatic encephalopathy." Electronic Thesis or Diss., Sorbonne université, 2019. http://www.theses.fr/2019SORUS197.

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Les tauopathies sont des maladies neurodégénératives caractérisées par une agrégation intracérébrale de protéines Tau anormales. Au cours de ce travail doctoral, nous avons étudié par tomographie par émission de positons (TEP) l'imagerie des agrégats Tau dans la maladie d'Alzheimer (MA) et l'encéphalopathie traumatique chronique (ETC). Notre premier objectif était de déterminer la capacité de l’imagerie Tau-TEP à améliorer le diagnostic de la MA et de déterminer la viabilité d’un nouveau traitement potentiel. Nous avons établi que l'imagerie Tau-TEP était capable de détecter l'effet bénéfique d'une stimulation cérébrale non invasive, appelée stimulation transcrânienne à courant alternatif (tACS) chez les personnes atteintes de MA. Notre deuxième objectif était de déterminer l'utilité de l'imagerie Tau in vivo dans une population de joueurs de football américains pour aider à la détection précoce de l’ETC. Nous avons démontré que l’imagerie Tau était en mesure de mettre en évidence les premières étapes de la maladie. En outre, nous avons étudié par autoradiographie post-mortem chez des patients diagnostiqués MA et ETC, le schéma de liaison de [18F]-AV-1451 avec [18F]-MK-6240 et [18F]-PI-2620 dans les mêmes échantillons. Ces trois traceurs ont montré un modèle similaire de forte liaison à la protéine Tau dans la MA et un manque de liaison dans le cas de l’ETC. Au total, ces expériences ont permis de confirmer l'utilité potentielle de l’imagerie Tau-TEP pour la détection, quantification des agrégats de Tau avec le suivi de la progression de la maladie dans la MA, tout en restant incertain pour l’ETC
Tauopathies are neurodegenerative diseases characterized by intracerebral aggregation of abnormal Tau proteins. During this university thesis, we studied by Positon Emission Tomography (PET) imaging the Tau burden in Alzheimer’s Disease (AD) and Chronic Traumatic Encephalopathy (CTE), two different taupotahies with similar Tau isoforms. In this context, our first objective was to determine the ability of Tau PET imaging to improve the diagnosis of AD and to determine the viability of a new potential treatment. We have established that Tau PET imaging was able to detect the beneficial effect of a non-invasive brain stimulation, called transcranial alternating current stimulation (tACS) in people with AD. Our second objective was to determine the usefulness of Tau PET imaging in vivo in a population of American football players to help the early detection of CTE. We have demonstrated that in our population, Tau PET imaging was able to highlight the Tau pathology in early stages of CTE. In parallel, we have studied by autoradiography post-mortem from patients with neuro-pathological diagnosis of AD and CTE the binding pattern of three radiotracers widely used in research for Tau imaging. We directly compared the binding properties of [18F]-AV-1451 with [18F]-MK-6240 and [18F]-PI-2620 in the same specimens. These three tracers showed similar strong binding pattern to Tau protein in AD and a lack of binding in CTE brain slices. In total, these experiments allow to confirm the potential utility of Tau PET tracers for the reliable detection, quantification of Tau aggregates and disease-progression tracking in AD, while it remains questionable for CTE
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Degerman, Gunnarsson Malin. "Biomarkers as Monitors of Drug Effect, Diagnostic Tools and Predictors of Deterioration Rate in Alzheimer’s Disease." Doctoral thesis, Uppsala universitet, Institutionen för folkhälso- och vårdvetenskap, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-196965.

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Decreased amyloid-ß42 (Aß42), increased total tau (t-tau) and phosphorylated tau (p-tau) in cerebrospinal fluid (CSF) reflect histopathological core changes in the most common dementia disorder, Alzheimer’s disease (AD). They discriminate AD from healthy controls and predict conversion to AD with a relatively high accuracy. Memantine, an uncompetitive NMDA-receptor antagonist, is indicated for symptomatic treatment of AD. The first aim of this thesis was to investigate effects of memantine on CSF concentrations of Aβ42, tau and p-tau. Secondly, the aim was to explore the relation between these CSF biomarkers and retention of the amyloid biomarker Pittsburgh compound B using positron emission tomography (PIB PET), regional glucose metabolism measured with 18Fluoro-2-deoxy-d-glucose (FDG) PET and neuropsychological test performance. The third aim was to investigate their possible utility as predictors of future rate of AD dementia deterioration. All patients in the studies were recruited from the Memory Clinic, Uppsala University Hospital. In study I CSF p-tau concentrations in 11 AD patients were reduced after twelve months treatment with memantine, indicating that this compound may affect a key pathological process in AD. Results from study II showed that the concentrations of CSF Aß42 are lower in PIB+ patients than in PIB- patients, and that the PIB retention was stable during 12 months. In study III 10 patients with the diagnoses AD (6 PIB+/4 PIB-) and 8 subjects (1 PIB+/7 PIB-) with frontotemporal dementia were included. PIB+ patients had lower psychomotor speed measured by performance on the Trail Making Test A and impaired visual episodic memory compared to the PIB- patients. The initial clinical diagnoses were changed in 33% of the patients (6/18) during follow-up. Study IV is the first-ever report of an association between high CSF tau and dying in severe dementia. These 196 AD patients were followed up to nine years after baseline lumbar puncture. Moreover, CSF t-tau concentrations above median was associated with an increased risk of rapid cognitive decline (OR 3.31 (95% CI 1.53-7.16), independently of baseline functional stage. Thus, a clear association between high levels of CSF t-tau and p-tau and a more aggressive course of the disease was shown.
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Cope, Thomas Edmund. "The physiology of dementia : network reorganisation in progressive non-fluent aphasia as a model of neurodegeneration." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/275884.

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The dementias are persistent or progressive disorders affecting more than one cognitive domain that interfere with an individual’s ability to function at work or home, and represent a decline from a previous level of function. In this thesis I consider the neurophysiology of dementia at a number of levels. I investigate the ways in which the connectivity and function of the brain predisposes to the specific focal patterns of neurodegeneration seen in the various dementias. I aim to identify the mesoscopic changes that occur in individuals with neurodegeneration and how these relate to their cognitive difficulties. I show how, by assessing patients in whom there is focal disruption of brain networks and observing the outcomes in comparison to controls, I can gain insight into the mechanisms by which the normal brain makes predictions and processes language. In Chapter 1, I set the scene for the focussed experimental investigations of model diseases by beginning with an introductory, clinically-focussed review that sets out the features, aetiology, management, epidemiology and prognosis of the dementias. This places these model diseases in the context of the broader clinical challenge posed by the dementias. In Chapter 2, I turn to ‘prototypical’ model diseases that represent neurodegenerative tauopathies with predominantly cortical (Alzheimer’s disease, AD) and subcortical (Progressive Supranuclear Palsy, PSP) disease burdens. I investigate the neurophysiological causes and consequences of Tau accumulation by combining graph theoretical analyses of resting state functional MR imaging and in vivo ‘Tau’ PET imaging using the ligand AV-1451. By relating Tau distribution to the functional connectome I provide in vivo evidence consistent with ‘prion-like’ trans-neuronal spread of Tau in AD but not PSP. This provides important validation of disease modification strategies that aim to halt or slow down the progression of AD by sequestration of pathological Tau in the synapse. In contrast, I demonstrate associations consistent with regional vulnerability to Tau accumulation due to metabolic demand and a lack of trophic support in PSP but not AD. With a cross-sectional approach, using Tau burden as a surrogate marker of disease severity, I then go on to show how the changes in functional connectivity that occur as disease progresses account for the contrasting cognitive phenotypes in AD and PSP. In advancing AD, functional connectivity across the whole brain becomes increasingly random and disorganised, accounting for symptomatology across multiple cognitive domains. In advancing PSP, by contrast, disrupted cortico-subcortical and cortico-brainstem interactions meant that information transfer passed through a larger number of cortical nodes, reducing closeness centrality and eigenvector centrality, while increasing weighted degree, clustering, betweenness centrality and local efficiency. Together, this resulted in increasingly modular processing with inter-network communication taking less direct paths, accounting for the bradyphrenia characteristic of the ‘subcortical dementias’. From chapter 3 onwards, I turn to the in-depth study of a model disease called non-fluent variant Primary Progressive Aphasia (nfvPPA). This disease has a clear clinical phenotype of speech apraxia and agrammatism, associated with a focal pattern of mild atrophy in frontal lobes. Importantly, general cognition is usually well preserved until late disease. In chapter 3 itself, I relate an experiment in which patients with nfvPPA and matched controls performed a receptive language task while having their brain activity recorded with magnetoencephalography. I manipulated expectations and sensory detail to explore the role of top-down frontal contributions to predictive processes in speech perception. I demonstrate that frontal neurodegeneration led to inflexible and excessively precise predictions, and that fronto-temporal interactions play a causal role in reconciling prior predictions with degraded sensory signals. The discussion here concentrates on the insights provided by neurodegenerative disease into the normal function of the brain in processing language. Overall, I demonstrate that higher level frontal mechanisms for cognitive and behavioural flexibility make a critical functional contribution to the hierarchical generative models underlying speech perception In chapter 4, I precisely define the sequence processing and statistical learning abilities of patients with nfvPPA in comparison to patients with non-fluent aphasia due to stroke and neurological controls. I do this by exposing participants to a novel, mixed-complexity artificial grammar designed to assess processing of increasingly complex sequencing relationships, and then assessing the degree of implicit rule learning. I demonstrate that agrammatic aphasics of two different aetiologies are not disproportionately impaired on complex sequencing relationships, and that the learning of phonological and non-linguistic sequences occurs independently in health and disease. In chapter 5, I summarise the synergies between the experimental chapters, and explain how I have applied a systems identification framework to a diverse set of experimental methods, with the common goal of defining the physiology of dementia. I then return to the results of chapter 3 with a clinical focus to explain how inflexible predictions can account for subjective speech comprehension difficulties, auditory processing abnormalities and (in synthesis with chapter 4) receptive agrammatism in nfvPPA. Overall, this body of work has contributed to knowledge in several ways. It has achieved its tripartite aims by: 1) Providing in vivo evidence consistent with theoretical models of trans-neuronal Tau spread (chapter 2), and a comprehensive clinical account of the previously poorly-understood receptive symptomatology of nfvPPA (chapter 5), thus demonstrating that systems neuroscience can provide a translational bridge between the molecular biology of dementia and clinical trials of therapies and medications. In this way, I begin to disentangle the network-level causes of neurodegeneration from its consequences. 2) Providing evidence for a causal role for fronto-temporal interactions in language processing (chapter 3), and demonstrating domain separation of statistical learning between linguistic and non-linguistic sequences (chapter 4), thus demonstrating that studies of patients with neurodegenerative disease can further our understanding of normative brain function. 3) Successfully integrating neuropsychology, behavioural psychophysics, functional MRI, structural MRI, magnetoencephalography and computational modelling to provide comprehensive research training, as the platform for a future research programme in the physiology of dementia.
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Cisek, Katryna. "Rational Optimization of Small Molecules for Alzheimer’s Disease Premortem Diagnosis." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1338325484.

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Ramon, Melanie Elaine. "The effects of demographics and pet ownership on attachment towards and opinion about owned and unowned free-roaming cats." [College Station, Tex. : Texas A&M University, 2006. http://hdl.handle.net/1969.1/ETD-TAMU-1021.

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Lundén, Amanda. "Can Sterol Carrie Protein-2 function as a solubility tag in E.coli?" Thesis, Linköpings universitet, Biologi, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-129803.

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Expressing foreign proteins in E.coli is a major challenge because they often tend to develop into unsolvable and inactive proteins. They aggregate into so called  inclusion bodies which prevent expression of the protein. This problem might be avoided by fusing the gene of the foreign protein with a soluble protein called solubility tags, which  function is to enhance the solubility of the foreign protein. This report investigates whether Sterol Carrier Protein-2 (SCP-2) could function as a solubility tag. The experiment was carried out by fusing SCP-2 to two recombinant proteins, Green fluorescent protein (GFP) and a form of chloroamphenicol acetyl transferase (CATΔ9). The gene fusion was then inserted into a pET-15 vector and transformed into  the E.coli strain BL21(DE3) to be expressed. The results obtained from Western blot and PageBlue staining indicates that SCP-2 does not enhance the solubility of GFP or CATΔ9 since neither of them was expressed.  Furthermore, previous studies have shown that GFP can in fact be expressed  usingmaltose binding protein (MBP) as a solubility tag. Unfortunately, no success has been made regarding CATΔ9. In conclusion, regarding the results from this report, SCP-2 does not function as a solubility tag. However, further studies should be carried out on SCP-2 with more experiments before rejecting the possibility to use SCP-2 as a solubility tag.
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Books on the topic "Tau pet"

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Zhancan, Gao, ed. Pei tai qi tan. Taibei Shi: Huang guan wen hua chu ban you xian gong si, 2013.

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Simmons, Jane. Tai-hsi ho pao pei tan =: Daisy and the egg. London, England: Milet, 2000.

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Phengkǣo, Lō̜m. Kœ̄t pen khon Tai. Krung Thēp: openbooks, 2010.

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Eglitis, Alberts. 40 Gadi pec tam... s.l: Selzemnieks, 1989.

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Wang, Jianquan. Ke ji zhuan an jing fei fen pei mo shi zhi tan tao. Taibei Shi: Cai tuan fa ren Zhonghua jing ji yan jiu yuan, 1998.

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Zhongguo si fa pei chang: Shi wu cao zuo yu li lun tan tao. Beijing Shi: Fu lü chu ban she, 2002.

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1945-, Miller Margaret, ed. Rat-a-tat, pitter pat. New York: Crowell, 1987.

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Benjamin, Alan. Rat-a-tat, pitter pat. New York: Crowell, 1987.

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jian, He shao. Zu zhi pei tai xue. Bei jing: Zhong guo xie he huo yi ke ta xue chu ban she, 2011.

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Liu, Xi. Tao shu zai pei fa. Taibei Shi: Wu zhou chu ban she, 1985.

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Book chapters on the topic "Tau pet"

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Higuchi, Makoto. "Tau PET Imaging." In Advances in Experimental Medicine and Biology, 217–30. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-32-9358-8_18.

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Leuzy, Antoine, Kerstin Heurling, and Michael Schöll. "PET Biomarkers for Tau Pathology." In Radiopharmaceuticals, 227–34. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-27779-6_13.

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Okamura, Nobuyuki, Ryuichi Harada, Shozo Furumoto, and Yukitsuka Kudo. "Tau PET in Neurodegenerative Diseases Manifesting Dementia." In Neuroimaging Diagnosis for Alzheimer's Disease and Other Dementias, 199–210. Tokyo: Springer Japan, 2017. http://dx.doi.org/10.1007/978-4-431-55133-1_10.

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Alvén, Jennifer, Kerstin Heurling, Ruben Smith, Olof Strandberg, Michael Schöll, Oskar Hansson, and Fredrik Kahl. "A Deep Learning Approach to MR-less Spatial Normalization for Tau PET Images." In Lecture Notes in Computer Science, 355–63. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-32245-8_40.

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Ruan, Xiaoan, and Yijun Ruan. "Chromatin Interaction Analysis Using Paired-End Tag Sequencing (ChIA-PET)." In Tag-Based Next Generation Sequencing, 185–210. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2012. http://dx.doi.org/10.1002/9783527644582.ch12.

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Ruan, Xiaoan, and Yijun Ruan. "RNA-PET: Full-Length Transcript Analysis Using 5′- and 3′-Paired-End Tag Next-Generation Sequencing." In Tag-Based Next Generation Sequencing, 73–90. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2012. http://dx.doi.org/10.1002/9783527644582.ch5.

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Abbott, Jason P. "Mahathir, Malaysia and the Labuan International Offshore Financial Centre: Treasure Island, Pet Project or Ghost Town?" In Offshore Finance Centres and Tax Havens, 192–211. London: Palgrave Macmillan UK, 1999. http://dx.doi.org/10.1007/978-1-349-14752-6_8.

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Tang, Chen, Ke Zhong, and Liqun Zhang. "Research on Image Emotional Tag Generation Mechanism Based on the “Cloud Pet Keeping” Phenomenon." In Design, User Experience, and Usability: Users, Contexts and Case Studies, 80–93. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-91806-8_7.

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Choy, Jocelyn, and Melissa J. Fullwood. "Deciphering Noncoding RNA and Chromatin Interactions: Multiplex Chromatin Interaction Analysis by Paired-End Tag Sequencing (mChIA-PET)." In Methods in Molecular Biology, 63–89. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-4035-6_7.

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Ruan, Xiaoan, and Yijun Ruan. "Genome Wide Full-Length Transcript Analysis Using 5′ and 3′ Paired-End-Tag Next Generation Sequencing (RNA-PET)." In Methods in Molecular Biology, 535–62. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-61779-376-9_35.

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Conference papers on the topic "Tau pet"

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Bourgeat, P., V. L. Villemagne, V. Dore, C. L. Masters, D. Ames, C. C. Rowe, O. Salvado, and J. Fripp. "PET-only 18F-AV1451 tau quantification." In 2017 IEEE 14th International Symposium on Biomedical Imaging (ISBI 2017). IEEE, 2017. http://dx.doi.org/10.1109/isbi.2017.7950725.

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Alberts, I., J. Lu, Y. Guan, P. Cumming, K. Shi, C. Zuo, and A. Rominger. "[ 18 F]-PM-PBB3-PET Tau Imaging in Alzheimer’s Dementia and PSP." In NuklearMedizin 2020. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1708175.

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Wind, K., L. Beyer, J. Sauerbeck, G. Biechele, G. Höglinger, B. von Ungern-Sternberg, S. Lindner, et al. "Preclinical head-to-head comparison of SV2A-PET with FDG-PET and structural MRI in a tau mouse model." In NuklearMedizin 2020. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1708384.

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Brendel, M., H. Barthel, T. van Eimeren, K. Marek, L. Beyer, M. Song, J. Sauerbeck, et al. "18 F-PI2620 Tau-PET in Progressive Supranuclear Palsy – A Multi-Center Evaluation." In NuklearMedizin 2020. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1708120.

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Sauerbeck, J., C. Palleis, M. Brendel, C. Prix, M. Gehmeyr, K. Bötzel, A. Danek, et al. "18 F-PI2620 Tau-PET for Assessment of Heterogeneous Neuropathology in Corticobasal Syndrome." In NuklearMedizin 2020. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1708173.

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Barthel, H., M. Patt, JJ Rumpf, D. Saur, ML Schroeter, C. Weise, M. Rullmann, et al. "Erste Erfahrungen mit der Etablierung von [18F]PI-2620, einem Tau-PET-Tracer der neuen Generation." In NuklearMedizin 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1683500.

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Beyer, L., A. Nitschmann, H. Barthel, T. van Eimeren, M. Unterrainer, J. Sauerbeck, M. Song, et al. "Perfusion-Phase 18 F-PI-2620 Tau-PET Imaging as a Surrogate Marker of Neuronal Injury." In NuklearMedizin 2020. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1708352.

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Hong, J., K. Shi, A. Rominger, and H. Choi. "Spatial distribution pattern of tau depositions in Alzheimer’s disease using data-driven approach of flortaucipir PET." In NuklearMedizin 2021 – digital. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1726790.

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Deussing, M., F. Eckenweber, T. Blume, J. Luque, C. Sacher, S. Lindner, B. Ungern-Sternberg, et al. "Longitudinal PET Monitoring of Microglial Activation in Tau Transgenic P301S Mice Predicts Cognitive Deterioration and Metabolic Decline." In NuklearMedizin 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1683638.

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Schröter, N., G. Blazhenets, L. Frings, C. Barkhausen, WH Jost, C. Weiller, M. Rijntjes, and PT Meyer. "Bildgebung von tau Ablagerungen bei den 4R-Tauopathien PSP und CBD: Eine C-11-PPB3-PET Pilotstudie." In NuklearMedizin 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1683662.

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Reports on the topic "Tau pet"

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Barreix, Alberto, Jerónimo Roca, and Fernando Velayos. Quo Vadis Income Tax?: Towards the PIT-CA. Inter-American Development Bank, November 2017. http://dx.doi.org/10.18235/0000903.

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Warf, Don, and Scott Livingston. Little Goose Dam Full Flow PIT-Tag Detection System Project Summary. Office of Scientific and Technical Information (OSTI), April 2009. http://dx.doi.org/10.2172/962410.

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Ama Pokuaa, Fenny, Aba Obrumah Crentsil, Christian Kwaku Osei, and Felix Ankomah Asante. Fiscal and Public Health Impact of a Change in Tobacco Excise Taxes in Ghana. Institute of Development Studies (IDS), November 2020. http://dx.doi.org/10.19088/ictd.2020.003.

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Abstract:
This working paper predicts the fiscal and public health outcomes from a change in the excise tax structure for cigarettes in Ghana. More than 5,000 people are killed by diseases caused by tobacco every year in Ghana (Tobacco Atlas 2018). Currently the country has a unitary tax administration approach, with a uniform ad valorem tax structure on all excisable products, including tobacco. However, the ECOWAS directive on tobacco control, in line with the WHO Framework Convention on Tobacco Control (WHO 2003), recommends a simple tax structure – using a mixed excise system with a minimum specific tax floor to overcome the limitations of an ad valorem system on tobacco products, especially cigarettes. The study therefore simulates mixed tax policy interventions, and assesses their effect on government revenue and public health relative to the current ad valorem tax system. Primary data collection of tobacco prices in three geographical zones of the country was conducted in February 2020, across both rural and urban localities. This was supported with secondary data from national and international databases. Based on the assumption that Ghana adopts a mixed tax structure, the simulation shows that, if the government imposes a specific excise tax of GH₵4.00 (US$0.80) per pack in addition to the current ad valorem rate of 175 per cent of the CIF value, the average retail price of a cigarette pack would increase by 128 per cent, cigarette consumption decrease by 27 per cent, tobacco excise tax revenue increase by 627 per cent, and overall tobacco-related government tax revenue increase by 201 per cent.1 Additionally, there would be significant declines in smoking prevalence (3.3%), smoking intensity (1,448 cigarettes per year), and 3,526 premature smoking-related deaths would be avoided. The paper advocates for a strong tax administration and technical capacity, with continuous commitment by the government to adjust the tax rate in line with the rate of inflation and per capita income growth.
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Skalski, J. R., G. Tartakovsky, S. G. Smith, and P. Westhagen. Pre-1994 Season Projection of Run-Timing Capabilities Using PIT-TAG Databases. Office of Scientific and Technical Information (OSTI), April 1994. http://dx.doi.org/10.2172/224250.

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Newman, Ken. Adult Salmonid PIT-TAG Returns to Columbia River`s Lower Granite Dam. Office of Scientific and Technical Information (OSTI), April 1995. http://dx.doi.org/10.2172/95540.

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Westhagen, Peter, and John Skalski. PitPro 1.1 User's Manual; Pit-tag to SURPH Data Translation Utility, Technical Manual 2003. Office of Scientific and Technical Information (OSTI), July 2003. http://dx.doi.org/10.2172/962976.

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Keefer, M. L., C. C. Caudill, E. L. Johnson, T. S. Clabough, M. A. Jepson, C. T. Boggs, and M. L. Moser. Adult Pacific Lamprey Migration in the Lower Columbia River: 2011 Half-Duplex Pit Tag Studies. Fort Belvoir, VA: Defense Technical Information Center, January 2012. http://dx.doi.org/10.21236/ada581329.

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McCutcheon, Clinton Scott. An Assessment of Freeze Brand and PIT Tag Recovery Data at McNary Dam, 1987 Annual Report. Office of Scientific and Technical Information (OSTI), January 1989. http://dx.doi.org/10.2172/6129816.

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YU, DANTONG, and Shudong Jin. Arra: Tas::89 0227::Tas Recovery Act 100g Ftp: An Ultra-High Speed Data Transfer Service Over Next Generation 100 Gigabit Per Second Network. Office of Scientific and Technical Information (OSTI), March 2014. http://dx.doi.org/10.2172/1121761.

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Keefer, M. L., C. T. Boogs, C. A. Peery, and M. L. Moser. Adult Pacific Lamprey Migration in the Lower Columbia River: 2007 Radiotelemetry and Half-duplex Pit Tag Studies. Fort Belvoir, VA: Defense Technical Information Center, January 2009. http://dx.doi.org/10.21236/ada627343.

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