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@ARTICLE{Hoenig:834205,
author = {Hoenig, Merle Christine and Bischof, Gerard Nisal and
Hammes, Jochen and Faber, Jennifer and Fliessbach, Klaus and
van Eimeren, Thilo and Drzezga, Alexander},
title = {{T}au pathology and cognitive reserve in {A}lzheimer's
disease},
journal = {Neurobiology of aging},
volume = {57},
issn = {0197-4580},
address = {Amsterdam [u.a.]},
publisher = {Elsevier Science},
reportid = {FZJ-2017-04188},
pages = {1 - 7},
year = {2017},
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.},
cin = {INM-3},
ddc = {610},
cid = {I:(DE-Juel1)INM-3-20090406},
pnm = {572 - (Dys-)function and Plasticity (POF3-572)},
pid = {G:(DE-HGF)POF3-572},
typ = {PUB:(DE-HGF)16},
UT = {WOS:000406296500002},
pubmed = {pmid:28577411},
doi = {10.1016/j.neurobiolaging.2017.05.004},
url = {https://juser.fz-juelich.de/record/834205},
}