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
- 1 Department of Psychological Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore
- 2 Children’s Hospital Colorado, Center for Gait and Movement Analysis (CGMA), Aurora, CO 80045, USA
- 3 Department of Psychological Medicine, National University Hospital, Singapore, Singapore
- 4 Biomedical Global Institute of Healthcare Research and Technology (BIGHEART), National University of Singapore, Singapore, Singapore
- 5 Center of Excellence in Behavioral Medicine, Nguyen Tat Thanh University, Ho Chi Minh City, Vietnam
- 6 Faculty of Education, Huaibei Normal University, Huaibei, China
- 7 Singapore Immunology Network, Agency for Science, Technology and Research, Singapore, Singapore
- 8 University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA
- 9 Academic Development Department, Duke-NUS Medical School, Singapore, Singapore
Received: July 20, 2020 Accepted: December 18, 2020 Published: January 26, 2021https://doi.org/10.18632/aging.202563
How to Cite
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.
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.
CP: cerebral palsy; MCI: mild cognitive impairment; FHSS: Framingham Heart Study Score; BDNF: brain-derived neurotrophic factor; AD: Alzheimer’s Disease; DS: Down syndrome; CMLA: Commission for Motion Laboratory Accreditation; DSM-V: The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition; ELISA: enzyme-linked immunosorbent assay; CVD: cardiovascular; WAIS: Wechsler Adult Intelligence Scale; BMI: Body-mass index; BP: blood pressure; SE: standard error; SPSS: Statistical Package for the Social Sciences.