Journal Article (Review Article)

DZNE-2022-00188

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Path integration in normal aging and Alzheimer's disease.

Segen, V. (First author)DZNE* ; Ying, J. ; Morgan, E. ; Brandon, M. ; Wolbers, T. (Last author)DZNE*

2022
Elsevier Science Amsterdam [u.a.]

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Please use a persistent id in citations: doi:10.1016/j.tics.2021.11.001

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.

Keyword(s): Aged (MeSH) ; Aging (MeSH) ; Alzheimer Disease (MeSH) ; Entorhinal Cortex: pathology (MeSH) ; Humans (MeSH) ; Alzheimer’s disease ; aging ; entorhinal cortex ; grid cells ; navigation ; path integration

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Contributing Institute(s):

1. Aging, Cognition and Technology (AG Wolbers)

Research Program(s):

1. 353 - Clinical and Health Care Research (POF4-353) (POF4-353)

Appears in the scientific report 2022

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Database coverage:
; Clarivate Analytics Master Journal List ; Current Contents - Life Sciences ; Current Contents - Social and Behavioral Sciences ; Ebsco Academic Search ; Essential Science Indicators ; IF >= 20 ; JCR ; SCOPUS ; Science Citation Index Expanded ; Social Sciences Citation Index ; Web of Science Core Collection

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