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Research Paper|Volume 12, Issue 24|pp 25319—25336

Cerebellar-limbic neurocircuit is the novel biosignature of physio-cognitive decline syndrome

Li-Kuo Liu1,2, Kun-Hsien Chou3,4, Chih-Chin Heather Hsu5, Li-Ning Peng1,2,6, Wei-Ju Lee1,7, Wei-Ta Chen8,9, Ching-Po Lin3,4,5, Chih-Ping Chung8,9, Pei-Ning Wang8,9, Liang-Kung Chen1,2
  • 1Aging and Health Research Center, National Yang Ming University, Taipei, Taiwan
  • 2Center for Geriatrics and Gerontology, National Yang Ming University, Taipei, Taiwan
  • 3Brain Research Center, National Yang Ming University, Taipei, Taiwan
  • 4Institute of Neuroscience, National Yang Ming University, Taipei, Taiwan
  • 5Department of Biomedical Imaging and Radiological Sciences, National Yang Ming University, Taipei, Taiwan
  • 6Institute of Public Health, National Yang Ming University, Taipei, Taiwan
  • 7Department of Family Medicine, Taipei Veterans General Hospital, Yuanshan Branch, Yilan, Taiwan
  • 8Department of Neurology, School of Medicine, National Yang Ming University, Taipei, Taiwan
  • 9Department of Neurology, Taipei Veterans General Hospital, Taipei, Taiwan
Received: June 3, 2020Accepted: September 20, 2020Published: November 25, 2020
https://doi.org/10.18632/aging.104135

Copyright: © 2020 Liu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Both physical and cognitive deficits occur in the aging process. We operationally defined the phenomenon as physio-cognitive decline syndrome (PCDS) and aimed to decipher its corresponding neuroanatomy patterns and neurocircuit. High resolution 3T brain magnetic resonance imaging (MRI) images from a community-dwelling longitudinal aging cohort were analysed. PCDS was defined as weakness (handgrip strength) and/or slowness (gait speed) concomitant with impairment in any cognitive domain (defined by 1.5 standard deviation below age, sex-matched norms), but without dementia or disability. Among 1196 eligible ≥ 50-year-old (62±9 years, 47.6%men) subjects, 15.9% had PCDS. Compared to the other participants, individuals with PCDS had significantly lower gray-matter volume (GMV) in the bilateral amygdala and thalamus, right hippocampus, right temporo-occipital cortex, and left cerebellum VI and V regions. The regions of reduced GMV in people with PCDS were similar between the middle-aged and older adults; whereas larger clusters with more extensive GMV-depleted regions were observed in ≥65-year-olds with PCDS. Diffusion-weighted tractography showed disrupted hippocampus-amygdala-cerebellum connections in subjects with PCDS. The neuroanatomic characteristics revealed by this study provide evidence for pathophysiological processes associated with concomitant physio-cognitive decline in the elderly. This neurocircuit might constitute a target for future preventive interventions.