Research Paper|Volume 13, Issue 2|pp 1773—1816

Commonalities in biomarkers and phenotypes between mild cognitive impairment and cerebral palsy: a pilot exploratory study

Ted Kheng Siang Ng^1,⁸, Alex Tagawa^2,⁸, Roger Chun-Man Ho^1,^3,^4,^5,⁶, Anis Larbi⁷, Ee Heok Kua^1,³, Rathi Mahendran^1,^3,⁹, James J. Carollo^2,⁸, Patricia C. Heyn^2,⁸

¹Department of Psychological Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore
²Children’s Hospital Colorado, Center for Gait and Movement Analysis (CGMA), Aurora, CO 80045, USA
³Department of Psychological Medicine, National University Hospital, Singapore, Singapore
⁴Biomedical Global Institute of Healthcare Research and Technology (BIGHEART), National University of Singapore, Singapore, Singapore
⁵Center of Excellence in Behavioral Medicine, Nguyen Tat Thanh University, Ho Chi Minh City, Vietnam
⁶Faculty of Education, Huaibei Normal University, Huaibei, China
⁷Singapore Immunology Network, Agency for Science, Technology and Research, Singapore, Singapore
⁸University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA
⁹Academic Development Department, Duke-NUS Medical School, Singapore, Singapore

Received: July 20, 2020Accepted: December 18, 2020Published: January 26, 2021

https://doi.org/10.18632/aging.202563

Copyright: © 2021 Ng 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

Clinically, individuals with cerebral palsy (CP) experience symptoms of accelerated biological aging. Accumulative deficits in both molecular underpinnings and functions in young adults with CP can lead to premature aging, such as heart disease and mild cognitive impairment (MCI). MCI is an intermediate stage between healthy aging and dementia that normally develops at old age. Owing to their intriguingly parallel yet “inverted” disease trajectories, CP might share similar pathology and phenotypes with MCI, conferring increased risk for developing dementia at a much younger age. Thus, we examined this hypothesis by evaluating these two distinct populations (MCI= 55, CP = 72). A total of nine measures (e.g., blood biomarkers, neurocognition, Framingham Heart Study Score (FHSS) were compared between the groups. Compared to MCI, upon controlling for covariates, delta FHSS, brain-derived neurotrophic factor (BDNF) levels, and systolic blood pressure were significantly lower in CP. Intriguingly, high-sensitivity CRP, several metabolic outcomes, and neurocognitive function were similar between the two groups. This study supports a shared biological underpinning and key phenotypes between CP and MCI. Thus, we proposed a double-hit model for the development of premature aging outcomes in CP through shared biomarkers. Future longitudinal follow-up studies are warranted to examine accelerated biological aging.