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Curr Biol. 2018 Apr 2;28(7):1108-1115.e6. doi: 10.1016/j.cub.2018.02.038. Epub 2018 Mar 15.

Compromised Grid-Cell-like Representations in Old Age as a Key Mechanism to Explain Age-Related Navigational Deficits.

Author information

1
German Center for Neurodegenerative Diseases (DZNE), Aging & Cognition Research Group, Leipziger Str. 44, 39120 Magdeburg, Germany. Electronic address: matthias.stangl@dzne.de.
2
German Center for Neurodegenerative Diseases (DZNE), Aging & Cognition Research Group, Leipziger Str. 44, 39120 Magdeburg, Germany.
3
Otto-von-Guericke-University Magdeburg, Department of Neurology, Leipziger Str. 44, 39120 Magdeburg, Germany.
4
German Center for Neurodegenerative Diseases (DZNE), Aging & Cognition Research Group, Leipziger Str. 44, 39120 Magdeburg, Germany; Center for Behavioral Brain Sciences, Universitätsplatz 2, 39106 Magdeburg, Germany.

Abstract

A progressive loss of navigational abilities in old age has been observed in numerous studies, but we have only limited understanding of the neural mechanisms underlying this decline [1]. A central component of the brain's navigation circuit are grid cells in entorhinal cortex [2], largely thought to support intrinsic self-motion-related computations, such as path integration (i.e., keeping track of one's position by integrating self-motion cues) [3-6]. Given that entorhinal cortex is particularly vulnerable to neurodegenerative processes during aging and Alzheimer's disease [7-14], deficits in grid cell function could be a key mechanism to explain age-related navigational decline. To test this hypothesis, we conducted two experiments in healthy young and older adults. First, in an fMRI experiment, we found significantly reduced grid-cell-like representations in entorhinal cortex of older adults. Second, in a behavioral path integration experiment, older adults showed deficits in computations of self-position during path integration based on body-based or visual self-motion cues. Most strikingly, we found that these path integration deficits in older adults could be explained by their individual magnitudes of grid-cell-like representations, as reduced grid-cell-like representations were associated with larger path integration errors. Together, these results show that grid-cell-like representations in entorhinal cortex are compromised in healthy aging. Furthermore, the association between grid-cell-like representations and path integration performance in old age supports the notion that grid cells underlie path integration processes. We therefore conclude that impaired grid cell function may play a key role in age-related decline of specific higher-order cognitive functions, such as spatial navigation.

KEYWORDS:

aging; entorhinal cortex; fMRI; grid cells; human; path integration; spatial navigation

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