期刊
JOURNAL OF PARKINSONS DISEASE
卷 10, 期 1, 页码 193-206出版社
IOS PRESS
DOI: 10.3233/JPD-191724
关键词
Parkinson's disease; telomere length; senescence; p16; p21; inflammation; biomarker; cognitive impairment; dementia
资金
- Newcastle upon Tyne Hospital Trust (Brain Research Unit) [PD0612]
- Parkinson's UK [J-0802, G-1301]
- National Institute for Health Research (NIHR) Newcastle Biomedical Research Centre in Ageing and Chronic Disease
- Biomedical Research Unit in Lewy Body Dementia based at Newcastle upon Tyne Hospitals NHS Foundation Trust
- Newcastle University
- National Institute for Health Research (NIHR) Cambridge Biomedical Research Centre [146281]
- Academy of Medical Sciences, UK
- Rosetrees Trust
- Stevenage Biosciences Catalyst
- RCUK/UKRI Research Innovation Fellowship - Medical Research Council [MR/R007446]
- Cambridge Centre for Parkinson-Plus
- NIHR [NF-SI-0616-10011]
- WT/MRC Stem Cell Institute [203151/Z/16/Z]
- Wellcome Trust [203151/Z/16/Z] Funding Source: Wellcome Trust
- MRC [MR/J50001X/1, G0601333, MR/R007446/1, G0500997] Funding Source: UKRI
- Parkinson's UK [J-0802, G-1301] Funding Source: researchfish
Background: Cognitive decline is a frequent complication of Parkinson's disease (PD) and the identification of predictive biomarkers for it would help in its management. Objective: Our aim was to analyse whether senescence markers (telomere length, p16 and p21) or their change over time could help to better predict cognitive and motor progression of newly diagnosed PD patients. We also compared these senescence markers to previously analysed markers of inflammation for the same purpose. Methods: This study examined the association of blood-derived markers of cell senescence and inflammation with motor and cognitive function over time in an incident PD cohort (the ICICLE-PD study). Participants (154 newly diagnosed PD patients and 99 controls) underwent physical and cognitive assessments over 36 months of follow up. Mean leukocyte telomere length and the expression of senescence markers p21 and p16 were measured at two time points (baseline and 18 months). Additionally, we selected five inflammatory markers from existing baseline data. Results: We found that PD patients had shorter telomeres at baseline and 18 months compared to age-matched healthy controls which also correlated to dementia at 36 months. Baseline p16 levels were associated with faster rates of motor and cognitive decline over 36 months in PD cases, while a simple inflammatory summary score at baseline best predicted cognitive score over this same time period in PD patients. Conclusion: Our study suggests that both inflammatory and senescence markers (p16) are valuable predictors of clinical progression in PD patients.
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