Eng‐King Tan

National Neuroscience Institute

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Ling Ling Chan

Singapore General Hospital

Yi Zhao

Singapore General Hospital

Louis C.S. Tan

Tan Tock Seng Hospital

Wing‐Lok Au

National Neuroscience Institute

Jia Nee Foo

Agency for Science, Technology and Research

Bin Xiao

National Neuroscience Institute

Zheyu Xu

Tan Tock Seng Hospital

Adeline Su Lyn Ng

National Neuroscience Institute

Pavanni Ratnagopal

National Neuroscience Institute

Yinxia Chao

National University of Singapore

Cooperative Institutions

Singapore General Hospital

290

National Neuroscience Institute

287

Molecular Biology Consortium

238

National University of Singapore

218

Duke-NUS Medical School

176

University College London

119

Inserm

Instituto de Salud Carlos III

Tan Tock Seng Hospital

Biomedical Research Networking Center on Neurodegenerative Diseases

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Monoamine oxidase B polymorphism, cigarette smoking and risk of Parkinson's disease: A study in an Asian population

American Journal of Medical Genetics Part B Neuropsychiatric Genetics (2003)

Eng‐King Tan A. Chai S.Y. Lum Hui Shen Chee Eng Tan

Abstract Cigarette smoking is associated with reduced monoamine oxidase B (MAO B) activity. Polymorphisms of the MAO B gene may modify the relationship between smoking and Parkinson's Disease (PD). We examined the association of MAO B intron 13 G/A polymorphism and risk of PD, and the modulation of the polymorphism on smoking and PD in an Asian study population in Singapore. Two hundred and thirty PD patients (mean age 66.0 ± 9.4 years, 63% men) and 241 age, gender, and race matched controls (mean age 64 ± 9.2 years, 58.9% males) were studied. The frequency of G and A alleles in PD and controls was; 66/315 (21.0%) vs. 73/340 (21.5%) and 249/315 (79.0%) vs. 267/340 (78.5%). For women, the genotype frequency in PD and controls was; GG: 7/85 (8.2%) vs. 8/99 (8.1%); GA: 25/85 (29.4%) vs. 27/99 (27.3%); AA: 53/85 (62.4%) vs. 64/99 (64.6%). For men, allele frequency in PD and controls was; A: 118/145 (81.4%) vs. 112/142 (78.9%) and G: 27/145 (18.6%) vs. 30/142 (21.1%). The allele and genotype frequencies were not significantly different between young and late onset PD. The frequency of “ever” smokers in PD and controls was 31/230 (13.5%) vs. 52/241 (21.6%), P = 0.02. A stepwise logistic regression analysis did not reveal any interaction of smoking and the G allele and risk of PD. The MAO B G/A genotype frequency in our Asian population was quite different from Caucasians suggesting that ethnicity specific effects need to be considered in evaluating gene‐environmental interaction. © 2003 Wiley‐Liss, Inc.

Monoamine oxidase B

10.1002/ajmg.b.20035

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Citations (35)

Exploring the relationship between caffeine intake and essential tremor

Journal of the Neurological Sciences (2006)

K.M. Prakash S. Fook‐Choong Y. Yuen Eng‐King Tan

Univariate analysis

Univariate

10.1016/j.jns.2006.09.007

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Citations (14)

Exploring the relationship between Parkinson's disease and hemifacial spasm

Acta Neurologica Scandinavica (2006)

Eng‐King Tan Ling Ling Chan

Case reports of co-existent Parkinson's disease (PD) and hemifacial spasm (HFS) suggest that there may be a relationship between these conditions. Three of 300 (1%) PD patients presented with HFS compared with 0/300 (0%) controls. The mean age of the three PD patients with HFS was 68.7 +/- 8.0 (60-76) years, with the majority having left-sided HFS. All three patients developed HFS symptoms at around the onset of PD and they were significantly older than the 100 patients with HFS alone (P < 0.05). Our study demonstrated no significant increased risk of HFS amongst the general PD population and hence HFS symptoms are unlikely to be of clinical importance for most PD patients.

Hemifacial spasm

10.1111/j.1600-0404.2006.00581.x

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Citations (3)

A 5-Year Longitudinal, Multicentre Validation Study Assessing the Prognostic Value of Plasma Fibronectin in a Cohort of Parkinson's Disease Participants

Shuzhen Zhu Hualin Li Zifeng Huang Yi‐Heng Zeng Jianmin Huang

Background: Evidence suggests that peripheral metabolic inflammatory derangements are associated with the progression of Parkinson’s Disease(PD) and can promote the destruction of the blood brain barrier(BBB); however, no peripheral mediators in dynamically monitoring disease progression have been identified. We aimed to screen and validate potential metabolic inflammatory marker(s) in predicting poor prognosis in PD.Methods: In this two-stage multicenter prospective study, peripheral inflammatory markers including plasma fibronectin(pFN) and phosphorylated α-synuclein from the recruited individuals (218 PD participants in discovery and 84 in validation cohort) were analyzed. Baseline peripheral inflammatory markers including pFN were assessed using LASSO-COX regression and multivariate Cox regression analyses. Independent risk factors for poor prognosis were evaluated. Multivariate linear mixed effects models(LMEMs) were used to evaluate the progression of clinical severity in PD. BBB permeability was measured by dynamic contrast-enhancement magnetic resonance imaging(DCE-MRI).Findings: pFN was identified as the independent risk factor for poor prognosis. The median survival time for low-pFN(< 197·6 mg/L) versus high-pFN(≥ 197·6 mg/L) patients was 7·833 versus 10·250 years in the validation cohort. Rate of change per year in pFN in malignant subtype mirrors rate of change in Hoehn-Yahr stage. Significant negative correlations were observed between pFN and plasma phosphorylated α-synuclein and high striatal BBB permeability on DCE-MRI imaging. Interpretation: We demonstrated that in the malignant PD subtype, there was a greater rate of decline in pFN, and a low baseline of pFN was associated with higher aggregation of α-synuclein and BBB disruption. Our findings suggest that pFN can be a prognostic marker of disease progression in PD.Clinical trial registration no. ChiCTR2100045714Funding This work was supported by the National Natural Science Foundation of China (82071414, 82171253) and National Research Foundation Singapore (EKT).Trial Registration: Clinical trial registration no. ChiCTR2100045714.Funding: This work was supported by the National Natural Science Foundation of China (82071414, 82171253) and National Research Foundation Singapore (EKT).Declaration of Interest: These authors declare no conflict of interest.Ethical Approval: The individuals’ consents have been obtained according to the Declaration of Helsinki, and humoral marker detections were approved by the ethics committee at Zhujiang Hospital of Southern Medical in Guangzhou (Project number 2021-KY-023-01, Clinical trial registration no. ChiCTR2100045714). The study was carried out in accordance with the National Institute of Health Human individuals Policies and Guidance released in Jan 26 and Dec 23, 1999.

Value (mathematics)

Longitudinal Study

10.2139/ssrn.4561063

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Factors influencing peripheral immunity and its links to brain disorders

Translational Psychiatry (2024)

Brendan Jen‐Wei Tan Ling Ling Chan Eng‐King Tan Bin Xiao

10.1038/s41398-024-02963-3

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Increased expression of pathological markers in Parkinson’s disease dementia post-mortem brains compared to dementia with Lewy bodies

BMC Neuroscience (2022)

Haitao Tu Zhi Wei Zhang Lifeng Qiu Yu‐Ning Lin Mei Jiang

Parkinson's disease (PD) and dementia with Lewy bodies (DLB) are common age-related neurodegenerative diseases comprising Lewy body spectrum disorders associated with cortical and subcortical Lewy body pathology. Over 30% of PD patients develop PD dementia (PDD), which describes dementia arising in the context of established idiopathic PD. Furthermore, Lewy bodies frequently accompany the amyloid plaque and neurofibrillary tangle pathology of Alzheimer's disease (AD), where they are observed in the amygdala of approximately 60% of sporadic and familial AD. While PDD and DLB share similar pathological substrates, they differ in the temporal onset of motor and cognitive symptoms; however, protein markers to distinguish them are still lacking.Here, we systematically studied a series of AD and PD pathogenesis markers, as well as mitochondria, mitophagy, and neuroinflammation-related indicators, in the substantia nigra (SN), temporal cortex (TC), and caudate and putamen (CP) regions of human post-mortem brain samples from individuals with PDD and DLB and condition-matched controls.We found that p-APPT668 (TC), α-synuclein (CP), and LC3II (CP) are all increased while the tyrosine hydroxylase (TH) (CP) is decreased in both PDD and DLB compared to control. Also, the levels of Aβ42 and DD2R, IBA1, and p-LRRK2S935 are all elevated in PDD compared to control. Interestingly, protein levels of p-TauS199/202 in CP and DD2R, DRP1, and VPS35 in TC are all increased in PDD compared to DLB.Together, our comprehensive and systematic study identified a set of signature proteins that will help to understand the pathology and etiology of PDD and DLB at the molecular level.

Lewy body

Putamen

Neuropathology

10.1186/s12868-021-00687-4

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Citations (10)

Analysis of the UCHL1 genetic variant in Parkinson's disease among Chinese

Neurobiology of Aging (2009)

Eng‐King Tan Chin-Song Lu Rong Peng Yik Ying Teo Yah-Huei Wu-Chou

Han Chinese

Univariate analysis

Univariate

10.1016/j.neurobiolaging.2008.11.008

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Citations (16)

Physical activity and its impact on non-motor aspects of Parkinson’s disease - the Early Parkinson’s Disease Longitudinal Singapore (PALS) study

Parkinsonism & Related Disorders (2018)

Y.E. Samuel Ng Masoom M. Abbas S.E. Hannah Heng F. Setiawan Sanchalika Acharyya

10.1016/j.parkreldis.2017.11.061

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Citations (1)

Persistent hand spasm: Movement disorder or seizure?

Journal of the Neurological Sciences (2006)

Deidre Anne De Silva Shih-Hui Lim Eng‐King Tan

Movement Disorders

muscle spasm

Seizure Disorders

10.1016/j.jns.2006.11.002

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Citations (2)

Transcriptomic imputation of genetic risk variants uncovers novel whole-blood biomarkers of Parkinson’s disease

npj Parkinson s Disease (2024)

Gabriel Chew Aaron Shengting John F. Ouyang Yueyue Qi Yinxia Chao

Abstract Blood-based gene expression signatures could potentially be used as biomarkers for PD. However, it is unclear whether genetically-regulated transcriptomic signatures can provide novel gene candidates for use as PD biomarkers. We leveraged on the Genotype-Tissue Expression (GTEx) database to impute whole-blood transcriptomic expression using summary statistics of three large-scale PD GWAS. A random forest classifier was used with the consensus whole-blood imputed gene signature (IGS) to discriminate between cases and controls. Outcome measures included Area under the Curve (AUC) of Receiver Operating Characteristic (ROC) Curve. We demonstrated that the IGS ( n = 37 genes) is conserved across PD GWAS studies and brain tissues. IGS discriminated between cases and controls in an independent whole-blood RNA-sequencing study (1176 PD, 254 prodromal, and 860 healthy controls) with mean AUC and accuracy of 64.8% and 69.4% for PD cohort, and 78.8% and 74% for prodromal cohort. PATL2 was the top-performing imputed gene in both PD and prodromal PD cohorts, whose classifier performance varied with biological sex (higher performance for males and females in the PD and prodromal PD, respectively). Single-cell RNA-sequencing studies (scRNA-seq) of healthy humans and PD patients found PATL2 to be enriched in terminal effector CD8+ and cytotoxic CD4+ cells, whose proportions are both increased in PD patients. We demonstrated the utility of GWAS transcriptomic imputation in identifying novel whole-blood transcriptomic signatures which could be leveraged upon for PD biomarker derivation. We identified PATL2 as a potential biomarker in both clinical and prodromic PD.

Imputation (statistics)

Genome-wide Association Study

10.1038/s41531-024-00698-y

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Citations (3)