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Tau and PET

Hugo Botha, William G Mantyh, Melissa E Murray, David S Knopman, Scott A Przybelski, Heather J Wiste, Jonathan Graff-Radford, Keith A Josephs, Christopher G Schwarz, Walter K Kremers, Bradley F Boeve, Ronald C Petersen, Mary M Machulda, Joseph E Parisi, Dennis W Dickson, Val Lowe, Clifford R Jack, David T Jones
Predicting underlying pathology based on clinical presentation has historically proven difficult, especially in older cohorts. Age-related hippocampal sclerosis may account for a significant proportion of elderly participants with amnestic dementia. Advances in molecular neuroimaging have allowed for detailed biomarker-based phenotyping, but in the absence of antemortem markers of hippocampal sclerosis, cases of mixed pathology remain problematic. We evaluated the utility of 18F-FDG-PET to differentiate flortaucipir tau PET negative from flortaucipir positive amnestic mild cognitive impairment and dementia and used an autopsy confirmed cohort to test the hypothesis that hippocampal sclerosis might account for the observed pattern...
March 12, 2018: Brain: a Journal of Neurology
Clifford R Jack, Heather J Wiste, Christopher G Schwarz, Val J Lowe, Matthew L Senjem, Prashanthi Vemuri, Stephen D Weigand, Terry M Therneau, Dave S Knopman, Jeffrey L Gunter, David T Jones, Jonathan Graff-Radford, Kejal Kantarci, Rosebud O Roberts, Michelle M Mielke, Mary M Machulda, Ronald C Petersen
Our objective was to compare different whole-brain and region-specific measurements of within-person change on serial tau PET and evaluate its utility for clinical trials. We studied 126 individuals: 59 cognitively unimpaired with normal amyloid, 37 cognitively unimpaired with abnormal amyloid, and 30 cognitively impaired with an amnestic phenotype and abnormal amyloid. All had baseline amyloid PET and two tau PET, MRI, and clinical assessments. We compared the topography across all cortical regions of interest of tau PET accumulation rates and the rates of four different whole-brain or region-specific meta-regions of interest among the three clinical groups...
March 12, 2018: Brain: a Journal of Neurology
Claudio Liguori, Mariangela Pierantozzi, Agostino Chiaravalloti, Giulia M Sancesario, Nicola B Mercuri, Flaminia Franchini, Orazio Schillaci, Giuseppe Sancesario
Late-life depression (LLD) and Alzheimer's Disease (AD) are the two most frequent neuropsychiatric disorders affecting elderly. LLD and AD may clinically present with depressive and cognitive symptoms. Therefore, when cognitive decline is coupled with depression in the elderly, the differential diagnosis between LLD and AD could be challenging. The aim of the present study was to evaluate in a population of elderly patients affected by depression and dementia the usefulness of CSF AD biomarkers (tau proteins and β-amyloid42 -Aβ42 ) and 2-[18F]fluoro-2-deoxy-d-glucose positron emission tomography (18FFDG-PET) in early differentiating LLD from AD...
2018: Frontiers in Aging Neuroscience
Elena Rodriguez-Vieitez, Agneta Nordberg
The recent progress in the development of in vivo biomarkers is rapidly changing how neurodegenerative diseases are conceptualized and diagnosed, and how clinical trials are designed today. Alzheimer's disease (AD)-the most common neurodegenerative disorder-is characterized by a complex neuropathology involving the deposition of extracellular amyloid-β (Aβ) plaques and intracellular neurofibrillary tangles (NFT) of hyperphosphorylated tau proteins, accompanied by the activation of glial cells-astrocytes and microglia-and neuroinflammatory responses, leading to neurodegeneration and cognitive dysfunction...
2018: Methods in Molecular Biology
Tessa Timmers, Bart N M van Berckel, Adriaan A Lammertsma, Rik Ossenkoppele
Alzheimer's disease is a neurodegenerative condition that is neuropathologically characterized by the presence of amyloid-β plaques and neurofibrillary tangles consisting of tau. Recently, several positron emission tomography (PET) tracers have been developed that yielded promising initial results. In this chapter, we discuss how tau PET can be used in the context in clinical trials. We argue that simplified reference tissue models based on dynamic data acquisition are most suitable for accurately measuring changes in tau pathology in trials tailored to reduce cerebral tau load...
2018: Methods in Molecular Biology
Ismini C Mainta, Maria I Vargas, Sara Trombella, Giovanni B Frisoni, Paul G Unschuld, Valentina Garibotto
Multiple factors, namely amyloid, tau, inflammation, metabolic, and perfusion changes, contribute to the cascade of neurodegeneration and functional decline occurring in Alzheimer's disease (AD). These molecular and cellular processes and related functional and morphological changes can be visualized in vivo by two imaging modalities, namely positron emission tomography (PET) and magnetic resonance imaging (MRI). These imaging biomarkers are now part of the diagnostic algorithm and of particular interest for patient stratification and targeted drug development...
2018: Methods in Molecular Biology
Kurt A Jellinger, Amos D Korczyn
BACKGROUND: Dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD), which share many clinical, neurochemical, and morphological features, have been incorporated into DSM-5 as two separate entities of major neurocognitive disorders with Lewy bodies. Despite clinical overlap, their diagnosis is based on an arbitrary distinction concerning the time of onset of motor and cognitive symptoms, namely as early cognitive impairment in DLB and later onset following that of motor symptoms in PDD...
March 6, 2018: BMC Medicine
Azadeh Firouzian, Alex Whittington, Graham E Searle, Ivan Koychev, Giovanna Zamboni, Simon Lovestone, Roger N Gunn
BACKGROUND: AD is a progressive neurodegenerative disorder that is associated with the accumulation of two different insoluble protein aggregates, Aβ plaques and hyperphosphorylated tau. This study aimed to investigate the optimal acquisition and quantification of [18 F]AV45 and [18 F]AV1451 to image Aβ and tau, respectively, in subjects with AD. Fifteen subjects with early stage AD underwent a T1-weighted structural MRI and two dynamic PET scans to image Aβ (60 min, [18 F]AV45) and tau (120 min, [18 F]AV1451)...
March 2, 2018: EJNMMI Research
Oskar Hansson, John Seibyl, Erik Stomrud, Henrik Zetterberg, John Q Trojanowski, Tobias Bittner, Valeria Lifke, Veronika Corradini, Udo Eichenlaub, Richard Batrla, Katharina Buck, Katharina Zink, Christina Rabe, Kaj Blennow, Leslie M Shaw
INTRODUCTION: We studied whether fully automated Elecsys cerebrospinal fluid (CSF) immunoassay results were concordant with PET and predicted clinical progression, even with cutoffs established in an independent cohort. METHODS: Cutoffs for Elecsys amyloid-β1-42 (Aβ), total tau/Aβ(1-42), and phosphorylated tau/Aβ(1-42) were defined against [18 F]flutemetamol PET in Swedish BioFINDER (n = 277) and validated against [18 F]florbetapir PET in Alzheimer's Disease Neuroimaging Initiative (n = 646)...
February 27, 2018: Alzheimer's & Dementia: the Journal of the Alzheimer's Association
Elliott H St A, Metser U, de Perrot M, Cho J, Bradbury P, Veit Haibach P, Hussey D, Tau N
OBJECTIVE: To compare the N and M staging accuracy of positron emission tomography (PET) versus CT, as per the American Joint Committee on Cancer (AJCC) 8th edition in patients with malignant pleural mesothelioma (MPM) being considered for multimodality therapy in a tertiary referral center. A secondary aim was to assess survival outcome of patients chosen for surgical management after PET. METHODS: A retrospective, single institution comparison of PET and CT was performed in patients with histologically proven MPM being considered for multimodality therapy...
March 2, 2018: British Journal of Radiology
Cristina Lois, Ivan Gonzalez, Keith A Johnson, Julie C Price
The two neuropathological hallmarks of Alzheimer's disease (AD) are amyloid-[Formula: see text] plaques and neurofibrillary tangles of tau protein. Fifteen years ago, Positron Emission Tomography (PET) with Pittsburgh Compound B (11 C-PiB) enabled selective in-vivo visualization of amyloid-[Formula: see text] plaque deposits and has since provided valuable information about the role of amyloid-[Formula: see text] deposition in AD. The progression of tau deposition has been shown to be highly associated with neuronal loss, neurodegeneration, and cognitive decline...
March 1, 2018: Brain Imaging and Behavior
Jonathan Vogelgsang, Hedieh Shahpasand-Kroner, Rebekka Vogelgsang, Frank Streit, Ruth Vukovich, Jens Wiltfang
The cerebrospinal fluid (CSF) biomarkers amyloid-β42 (Aβ42 ), total Tau, and phospho-181-Tau represent important diagnostic tools to support the clinical diagnosis of Alzheimer's disease (AD). Acquiring CSF by lumbar puncture is considered a moderately invasive procedure, while blood sampling is minimally invasive with calculable risks and can be performed by trained non-medical staff. Thus, the identification of reliable and robust blood biomarkers of AD-related neuropathology would be significantly advantageous in daily practice and would allow more patients to be screened...
February 26, 2018: Experimental Brain Research. Experimentelle Hirnforschung. Expérimentation Cérébrale
Andréa L Benedet, Lei Yu, Aurélie Labbe, Sulantha Mathotaarachchi, Tharick A Pascoal, Monica Shin, Min-Su Kang, Serge Gauthier, Guy A Rouleau, Judes Poirier, David A Bennett, Pedro Rosa-Neto
Objective: To verify whether CYP polymorphisms are associated with amyloid-β (Aβ) pathology across the spectrum of clinical Alzheimer disease using in vivo and postmortem data from 2 independent cohorts. Methods: A candidate-gene approach tested the association between 5 genes (28 single nucleotide polymorphisms) and Aβ load measured in vivo by the global [18 F]florbetapir PET standardized uptake value ratio (SUVR) in 338 Alzheimer's Disease Neuroimaging Initiative participants...
February 2018: Neurology. Genetics
Keith A Josephs, Peter R Martin, Hugo Botha, Christopher G Schwarz, Joseph R Duffy, Heather M Clark, Mary M Machulda, Jonathan Graff-Radford, Stephen D Weigand, Matthew L Senjem, Rene L Utianski, Daniel A Drubach, Bradley F Boeve, David T Jones, David S Knopman, Ronald C Petersen, Clifford R Jack, Val J Lowe, Jennifer L Whitwell
OBJECTIVES: To assess [ 18 F]AV-1451 tau-PET uptake patterns across the primary progressive aphasia (PPA) variants (logopenic, semantic and agrammatic), examine regional uptake patterns of [ 18 F]AV-1451 independent of clinical diagnosis, and compare the diagnostic utility of [ 18 F]AV-1451, [ 18 F]-fluorodeoxygluclose (FDG)-PET and MRI to differentiate the PPA variants. METHODS: We performed statistical parametric mapping of [ 18 F]AV-1451 across 40 PPA patients (logopenic-PPA=14, semantic-PPA=13 and agrammatic-PPA=13) compared to 80 cognitively normal, PiB-negative controls, age and gender matched 2:1...
February 16, 2018: Annals of Neurology
Victor L Villemagne, Vincent Doré, Samantha C Burnham, Colin L Masters, Christopher C Rowe
Most neurodegenerative disorders are associated with aggregated protein deposits. In the case of Alzheimer disease (AD), extracellular amyloid-β (Aβ) aggregates and intracellular tau neurofibrillary tangles are the two neuropathological hallmarks of the disease. Aβ-PET imaging has already been approved for clinical use and is being used in clinical trials of anti-Aβ therapies both for patient recruitment and as an outcome measure. These studies have shown that Aβ accumulation is a protracted process that can extend for more than 2 decades before the onset of clinical AD...
February 16, 2018: Nature Reviews. Neurology
Long Xie, Sandhitsu R Das, Laura E M Wisse, Ranjit Ittyerah, Paul A Yushkevich, David A Wolk
Neurofibrillary tangle (NFT) pathology is linked to neurodegeneration in the medial temporal lobe (MTL). Using a tailored pipeline, we correlated atrophy rate, as measured from retrospective longitudinal MRI, with NFT burden, measured from 18F-AV-1451 PET, within MTL regions of earliest NFT pathology. In amyloid-β positive but not amyloid-β negative individuals, we found significant correlation between 18F-AV-1451 uptake and atrophy rate that was strongest in the transentorhinal cortex, the first region with NFT pathology...
2018: Journal of Alzheimer's Disease: JAD
Charles B Malpas, Michael M Saling, Dennis Velakoulis, Patricia Desmond, Rodney J Hicks, Henrik Zetterberg, Kaj Blennow, Terence J O'Brien
The two cardinal pathologies of Alzheimer's disease (AD) develop according to distinct anatomical trajectories. Cerebral tau-related pathology first accumulates in the mesial temporal region, while amyloid-related pathology first appears in neocortex. The eventual distributions of these pathologies reflect their anatomical origins. An implication is that the cardinal pathologies might exert preferential effects on the structurofunctional brain changes observed in AD. We investigated this hypothesis in 39 patients with dementia of the Alzheimer's type...
2018: Journal of Alzheimer's Disease: JAD
Hugo Botha, William G Mantyh, Jonathan Graff-Radford, Mary M Machulda, Scott A Przybelski, Heather J Wiste, Matthew L Senjem, Joseph E Parisi, Ronald C Petersen, Melissa E Murray, Bradley F Boeve, Val J Lowe, David S Knopman, Clifford R Jack, David T Jones
OBJECTIVE: To describe the phenomenon of tau-negative amnestic dementia mimicking Alzheimer disease (AD) clinically and radiologically and to highlight the importance of biomarkers in AD research. METHODS: Eight participants with amnestic mild cognitive impairment or AD dementia were evaluated by a behavioral neurologist and had a standardized neuropsychological battery performed. All participants completed structural (MRI) and molecular (amyloid and tau PET) imaging...
February 7, 2018: Neurology
Yakeel T Quiroz, Reisa A Sperling, Daniel J Norton, Ana Baena, Joseph F Arboleda-Velasquez, Danielle Cosio, Aaron Schultz, Molly Lapoint, Edmarie Guzman-Velez, John B Miller, Leo A Kim, Kewei Chen, Pierre N Tariot, Francisco Lopera, Eric M Reiman, Keith A Johnson
Importance: It is critically important to improve our ability to diagnose and track Alzheimer disease (AD) as early as possible. Individuals with autosomal dominant forms of AD can provide clues as to which and when biological changes are reliably present prior to the onset of clinical symptoms. Objective: To characterize the associations between amyloid and tau deposits in the brains of cognitively unimpaired and impaired carriers of presenilin 1 (PSEN1) E280A mutation...
February 12, 2018: JAMA Neurology
Julia Neitzel, Rachel Nuttall, Christian Sorg
Previous animal research suggests that the spread of pathological agents in Alzheimer's disease (AD) follows the direction of signaling pathways. Specifically, tau pathology has been suggested to propagate in an infection-like mode along axons, from transentorhinal cortices to medial temporal lobe cortices and consequently to other cortical regions, while amyloid-beta (Aβ) pathology seems to spread in an activity-dependent manner among and from isocortical regions into limbic and then subcortical regions. These directed connectivity-based spread models, however, have not been tested directly in AD patients due to the lack of an in vivo method to identify directed connectivity in humans...
2018: Frontiers in Neurology
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