Format

Send to

Choose Destination
Neurobiol Aging. 2017 Sep;57:1-7. doi: 10.1016/j.neurobiolaging.2017.05.004. Epub 2017 May 10.

Tau pathology and cognitive reserve in Alzheimer's disease.

Author information

1
Department of Nuclear Medicine, University Hospital Cologne, Cologne, Germany; Research Training Group - Neural Circuit Analysis, Department of Mathematics and Natural Sciences, University of Cologne, Cologne, Germany. Electronic address: merle.hoenig@uk-koeln.de.
2
Department of Nuclear Medicine, University Hospital Cologne, Cologne, Germany; Institute of Neuroscience and Medicine (INM-3), Cognitive Neuroscience, Research Center Jülich, Jülich, Germany.
3
Department of Nuclear Medicine, University Hospital Cologne, Cologne, Germany.
4
German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany; Department of Neurology, University Hospital Bonn, Bonn, Germany.
5
German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany; Department of Psychiatry and Psychotherapy, University Hospital Bonn, Bonn, Germany.
6
Department of Nuclear Medicine, University Hospital Cologne, Cologne, Germany; Institute of Neuroscience and Medicine (INM-3), Cognitive Neuroscience, Research Center Jülich, Jülich, Germany; German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.
7
Department of Nuclear Medicine, University Hospital Cologne, Cologne, Germany; German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.

Abstract

Cognitive reserve (CR) is defined as the ability to maintain functionality despite accumulating pathology. Education has been used as a proxy for CR. For example, by using positron emission tomography imaging, higher educated Alzheimer's disease (AD) patients presented increased amyloid β pathology than lower educated patients despite equal symptomatology. Whether similar associations exist for in vivo tau pathology remains elusive. We utilized [18F]AV-1451 positron emission tomography imaging to examine whether high-educated AD patients (n = 12) present more severe tau pathology compared with low-educated patients (n = 12) despite equal clinical severity in regions of interest corresponding to the pathologic disease stages defined by Braak & Braak. We report tau pathology in advanced Braak stages associated with parietal and frontal regions in high-educated AD patients, whereas in low-educated AD patients tau accumulation is still confined to lower Braak stages associated with temporal and cingulate regions. Highly educated AD patients seem to be able to tolerate more tau tangle pathology than lower educated patients with comparable cognitive impairment supporting the cognitive reserve hypothesis.

KEYWORDS:

Alzheimer's disease; Cognitive reserve; Education; Positron emission tomography; Tau pathology; [(18)F]AV-1451

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center