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轻度认知障碍与脑瘫之间的生物标志物和表型的共性:一项初步探索性研究。

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

机构信息

Department of Psychological Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.

University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.

出版信息

Aging (Albany NY). 2021 Jan 26;13(2):1773-1816. doi: 10.18632/aging.202563.

DOI:10.18632/aging.202563
PMID:33497355
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7880365/
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.

摘要

临床上,脑瘫(CP)患者会出现加速的生物学衰老症状。在年轻的 CP 患者中,分子基础和功能的累积缺陷可能导致过早衰老,如心脏病和轻度认知障碍(MCI)。MCI 是健康衰老和痴呆之间的中间阶段,通常在老年时发展。由于它们具有引人注目的平行但“倒置”的疾病轨迹,CP 可能与 MCI 具有相似的病理学和表型,从而增加了在更年轻时发生痴呆的风险。因此,我们通过评估这两个不同的人群(MCI=55,CP=72)来检验这一假设。总共比较了九项措施(例如,血液生物标志物、神经认知、弗雷明汉心脏研究评分(FHSS)。与 MCI 相比,在控制协变量后,CP 中的 FHSS 差值、脑源性神经营养因子(BDNF)水平和收缩压显著降低。有趣的是,高敏 C 反应蛋白、几种代谢结果和神经认知功能在两组之间相似。这项研究支持 CP 和 MCI 之间存在共同的生物学基础和关键表型。因此,我们通过共享的生物标志物提出了一个 CP 中过早衰老结果发展的双重打击模型。未来需要进行纵向随访研究来检查加速的生物学衰老。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25ee/7880365/beb21a110057/aging-13-202563-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25ee/7880365/720239a10c14/aging-13-202563-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25ee/7880365/beb21a110057/aging-13-202563-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25ee/7880365/720239a10c14/aging-13-202563-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25ee/7880365/beb21a110057/aging-13-202563-g002.jpg

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