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PET Imaging of Tau Deposition in the Aging Human Brain

Journal Article · · Neuron
 [1];  [2];  [3];  [4];  [4];  [5];  [4];  [2];  [4];  [2];  [6];  [7]
  1. Univ. of California, Berkeley, CA (United States). Helen Wills Neuroscience Institute; University of Gothenburg (Sweden). MedTech West and the Department of Clinical Neuroscience and Rehabilitation
  2. Univ. of California, Berkeley, CA (United States). Helen Wills Neuroscience Institute
  3. University of California, San Francisco, CA (United States). Department of Neurology, Memory and Aging Center
  4. Lawrence Berkeley National Lab. (LBNL), Berkeley, CA (United States)
  5. Univ. of California, Berkeley, CA (United States). Helen Wills Neuroscience Institut; University of California, San Francisco, CA (United States). Department of Neurology, Memory and Aging Center; VU University Medical Center, Amsterdam (The Netherlands). Department of Neurology & Alzheimer Center, Neuroscience Campus Amsterdam
  6. Univ. of California, Berkeley, CA (United States). Helen Wills Neuroscience Institute; University of California, San Francisco, CA (United States). Department of Neurology, Memory and Aging Center ; Lawrence Berkeley National Lab. (LBNL), Berkeley, CA (United States)
  7. Univ. of California, Berkeley, CA (United States). Helen Wills Neuroscience Institute; Lawrence Berkeley National Lab. (LBNL), Berkeley, CA (United States)
Tau pathology is a hallmark of Alzheimer’s disease (AD) but also occurs in normal cognitive aging. In this study, 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. In conclusion, the present study defined patterns of tau tracer retention in normal aging in relation to age, cognition, and β-amyloid deposition.
Research Organization:
Lawrence Berkeley National Laboratory (LBNL), Berkeley, CA (United States)
Sponsoring Organization:
National Institutes of Health (NIH); USDOE
Grant/Contract Number:
AC02-05CH11231
OSTI ID:
1379129
Journal Information:
Neuron, Journal Name: Neuron Journal Issue: 5 Vol. 89; ISSN 0896-6273
Publisher:
Cell Press / ElsevierCopyright Statement
Country of Publication:
United States
Language:
English

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