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IMPAIRED PATH INTEGRATION IS ASSOCIATED WITH EARLY TAU PATHOLOGY IN THE ENTORHINAL-HIPPOCAMPAL NEURAL NETWORKS
Sui Hin Hoand 7 co-authors
University of Cambridge
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS05-09AM-091
Presentation
Date TBA
Board: PS05-09AM-091
Event Information
Poster Board
PS05-09AM-091
Poster
View posterAbstract
Path integration (PI) may be one of the earliest cognitive functions impaired in Alzheimer’s disease, preceding general memory loss. The entorhinal-hippocampal neural networks are critical for path integration function and are the first regions with increased Tau hyperphosphorylation in AD. However, the neural mechanisms that underlie PI impairment during early tauopathy are unknown. To address this, we tested an early entorhinal-hippocampal tauopathy mouse model and hTauKI control in a battery of cognitive and behavioural tests to 1) establish if PI is indeed amongst the first cognitive abilities affected, and 2) identify what neural changes in entorhinal-hippocampal regions may lead to such impairments.
We used a homecage monitoring system to simultaneously assess working memory (T-maze), object memory (novel object recognition), locomotion and quiescence patterns. To test PI ability, we tested the mice in a virtual reality (VR) navigation task combined with two-photon imaging to study hippocampal CA1 neural activity. We found that 1) PI, but not cue-based navigation, was impaired in early Tau pathology, 2) PI impairment follows an age-dependent disease progression, and 3) it was accompanied by disrupted CA1 place field formation, reduced spatial information and decreased field stability.
We used a homecage monitoring system to simultaneously assess working memory (T-maze), object memory (novel object recognition), locomotion and quiescence patterns. To test PI ability, we tested the mice in a virtual reality (VR) navigation task combined with two-photon imaging to study hippocampal CA1 neural activity. We found that 1) PI, but not cue-based navigation, was impaired in early Tau pathology, 2) PI impairment follows an age-dependent disease progression, and 3) it was accompanied by disrupted CA1 place field formation, reduced spatial information and decreased field stability.
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