Identifying the bioimaging features of Alzheimer’s disease based on pupillary light response-driven brain-wide fMRI in awake mice

Xiaochen Liu, David Hike, Sangcheon Choi, Weitao Man, Chongzhao Ran, Xiaoqing Alice Zhou, Yuanyuan Jiang and Xin Yu ()
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Xiaochen Liu: Massachusetts General Hospital
David Hike: Massachusetts General Hospital
Sangcheon Choi: Massachusetts General Hospital
Weitao Man: Massachusetts General Hospital
Chongzhao Ran: Massachusetts General Hospital
Xiaoqing Alice Zhou: Massachusetts General Hospital
Yuanyuan Jiang: Massachusetts General Hospital
Xin Yu: Massachusetts General Hospital

Nature Communications, 2024, vol. 15, issue 1, 1-13

Abstract: Abstract Pupil dynamics has emerged as a critical non-invasive indicator of brain state changes. In particular, pupillary-light-responses (PLR) in Alzheimer’s disease (AD) patients show potential as biomarkers for brain degeneration. To investigate AD-specific PLR and its underlying neuromodulatory sources, we combine high-resolution awake mouse fMRI with real-time pupillometry to map brain-wide event-related correlation patterns based on illumination-driven pupil constriction ( $${P}_{c}$$ P c ) and post-illumination pupil dilation recovery (amplitude, $${P}_{d}$$ P d , and time, T). The $${P}_{c}$$ P c -driven differential analysis reveals altered visual signal processing and reduced thalamocortical activation in AD mice in comparison with wild-type (WT) control mice. In contrast, the post-illumination pupil dilation recovery-based fMRI highlights multiple brain areas associated with AD brain degeneration, including the cingulate cortex, hippocampus, septal area of the basal forebrain, medial raphe nucleus, and pontine reticular nuclei (PRN). Additionally, the brain-wide functional connectivity analysis highlights the most significant changes in PRN of AD mice, which serves as the major subcortical relay nuclei underlying oculomotor function. This work integrates non-invasive pupil-fMRI measurements in preclinical models to identify pupillary biomarkers based on brain-wide functional changes, including neuromodulatory dysfunction coupled with AD brain degeneration.

Date: 2024
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DOI: 10.1038/s41467-024-53878-y

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