Path integration in normal aging and Alzheimer’s disease

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. Path integration (PI) is an essential component of spatial navigation that is evolutionarily preserved across multiple species and has shared neural mechanisms in rodents and humans.A review of past research highlights that PI impairments are prevalent in the aging population which consists of healthy older adults and older adults with Alzheimer's disease (AD). The observed PI impairments corroborate our current understanding of the neural underpinnings of PI and age- and AD-related pathology.PI performance has the potential to be a sensitive cognitive marker in clinical research and practice for the detection of early AD as well as for the development of effective therapeutics.