PET Imaging of Tau Deposition in the Aging Human Brain
By Michael Schöll, Samuel N. Lockhart, D. Schonhaut, James P. O'Neil, Mustafa Janabi, Rik Ossenkoppele, Suzanne L. Baker, Jacob W. Vogel, J. Faria, H. Schwimmer and 2 more. Neuron, 2016
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SUMMARY Tau pathology is a hallmark of Alzheimer’s disease (AD) but also occurs in normal cognitive aging. Using the tau PET agent 18F-AV-1451, we examined retention patterns in cognitively normal older people in relation to young controls and AD patients. Age and β-amyloid (measured using PiB PET) were differentially associated with tau tracer retention in healthy aging. Older age was related to increased tracer retention in regions of the medial temporal lobe, which predicted worse episodic memory performance. PET detection of tau in other isocortical regions required the presence of cortical β-amyloid, and was associated with decline in global cognition. Furthermore, patterns of tracer retention corresponded well with Braak staging of neurofibrillary tau pathology. The present study defined patterns of tau tracer retention in normal aging in relation to age, cognition, and β-amyloid deposition.
Subfields: Cognitive Neuroscience, Physiology, Radiology, Nuclear Medicine and Imaging
View Paper: https://www.semanticscholar.org/paper/5a5cc76004cf99ec02d28033d4a48e8cfe9482fd
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Citations in the corpus
- Reconsideration of Amyloid Hypothesis and Tau Hypothesis in Alzheimer's Disease (2018, background): “…al., 2017; Okamura and Yanai, 2017) and that subjective cognitive decline is indicative of early tauopathy in the medial temporal lobe, specifically in the entorhinal cortex, and to a lesser extent with elevated global levels of Aβ (Scholl et al., 2016; Schwarz et al., 2016; Buckley et al., 2017).”
- Tau pathology and neurodegeneration contribute to cognitive impairment in Alzheimer’s disease (2017, background): “Alzheimer’s disease individuals (Cho et al., 2016b; Ossenkoppele et al., 2016; Schöll et al., 2016) by including”