% IMPORTANT: The following is UTF-8 encoded. This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.
@ARTICLE{Segen:163428,
author = {Segen, Vladislava and Ying, Johnson and Morgan, Erik and
Brandon, Mark and Wolbers, Thomas},
title = {{P}ath integration in normal aging and {A}lzheimer's
disease.},
journal = {Trends in cognitive sciences},
volume = {26},
number = {2},
issn = {1364-6613},
address = {Amsterdam [u.a.]},
publisher = {Elsevier Science},
reportid = {DZNE-2022-00188},
pages = {142 - 158},
year = {2022},
abstract = {In this review we discuss converging evidence from human
and rodent research demonstrating how path integration (PI)
is impaired in healthy aging and Alzheimer's disease (AD),
and point to the neural mechanisms that underlie these
deficits. Importantly, we highlight that (i) the grid cell
network in the entorhinal cortex is crucial for PI in both
humans and rodents, (ii) PI deficits are present in healthy
aging and are significantly more pronounced in patients with
early-stage AD, (iii) compromised entorhinal grid cell
computations in healthy older adults and in young adults at
risk of AD are linked to PI deficits, and (iv) PI and grid
cell deficits may serve as sensitive markers for
pathological decline in early AD.},
subtyp = {Review Article},
keywords = {Aged / Aging / Alzheimer Disease / Entorhinal Cortex:
pathology / Humans / Alzheimer’s disease (Other) / aging
(Other) / entorhinal cortex (Other) / grid cells (Other) /
navigation (Other) / path integration (Other)},
cin = {AG Wolbers},
ddc = {150},
cid = {I:(DE-2719)1310002},
pnm = {353 - Clinical and Health Care Research (POF4-353)},
pid = {G:(DE-HGF)POF4-353},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:34872838},
doi = {10.1016/j.tics.2021.11.001},
url = {https://pub.dzne.de/record/163428},
}