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000163428 0247_ $$2doi$$a10.1016/j.tics.2021.11.001
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000163428 037__ $$aDZNE-2022-00188
000163428 041__ $$aEnglish
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000163428 1001_ $$0P:(DE-2719)9001409$$aSegen, Vladislava$$b0$$eFirst author$$udzne
000163428 245__ $$aPath integration in normal aging and Alzheimer's disease.
000163428 260__ $$aAmsterdam [u.a.]$$bElsevier Science$$c2022
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000163428 520__ $$aIn 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.
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000163428 650_7 $$2Other$$aAlzheimer’s disease
000163428 650_7 $$2Other$$aaging
000163428 650_7 $$2Other$$aentorhinal cortex
000163428 650_7 $$2Other$$agrid cells
000163428 650_7 $$2Other$$anavigation
000163428 650_7 $$2Other$$apath integration
000163428 650_2 $$2MeSH$$aAged
000163428 650_2 $$2MeSH$$aAging
000163428 650_2 $$2MeSH$$aAlzheimer Disease
000163428 650_2 $$2MeSH$$aEntorhinal Cortex: pathology
000163428 650_2 $$2MeSH$$aHumans
000163428 7001_ $$aYing, Johnson$$b1
000163428 7001_ $$aMorgan, Erik$$b2
000163428 7001_ $$aBrandon, Mark$$b3
000163428 7001_ $$0P:(DE-2719)2810583$$aWolbers, Thomas$$b4$$eLast author$$udzne
000163428 773__ $$0PERI:(DE-600)2010989-1$$a10.1016/j.tics.2021.11.001$$gVol. 26, no. 2, p. 142 - 158$$n2$$p142 - 158$$tTrends in cognitive sciences$$v26$$x1364-6613$$y2022
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000163428 9141_ $$y2022
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