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High Levels of Mutant Huntingtin Protein in Tear Fluid From Huntington’s Disease Gene Expansion Carriers
Marlies Gijs, Nynke Jorna, Nicole Datson, Chantal Beekman, Cira Dansokho, Alexander Weiss, David E. J. Linden, Mayke Oosterloo
J Mov Disord. 2024;17(2):181-188.   Published online February 21, 2024
DOI: https://doi.org/10.14802/jmd.24014
  • 2,983 View
  • 237 Download
  • 2 Web of Science
  • 2 Crossref
AbstractAbstract PDFSupplementary Material
Objective
Huntington’s disease (HD) is an autosomal dominant, fully penetrant, neurodegenerative disease that most commonly affects middle-aged adults. HD is caused by a CAG repeat expansion in the HTT gene, resulting in the expression of mutant huntingtin (mHTT). Our aim was to detect and quantify mHTT in tear fluid, which, to our knowledge, has never been measured before.
Methods
We recruited 20 manifest and 13 premanifest HD gene expansion carriers, and 20 age-matched controls. All patients underwent detailed assessments, including the Unified Huntington’s Disease Rating Scale (UHDRS) total motor score (TMS) and total functional capacity (TFC) score. Tear fluid was collected using paper Schirmer’s strips. The level of tear mHTT was determined using single-molecule counting SMCxPRO technology.
Results
The average tear mHTT levels in manifest (67,223 ± 80,360 fM) and premanifest patients (55,561 ± 45,931 fM) were significantly higher than those in controls (1,622 ± 2,179 fM). We noted significant correlations between tear mHTT levels and CAG repeat length, “estimated years to diagnosis,” disease burden score and UHDRS TMS and TFC. The receiver operating curve demonstrated an almost perfect score (area under the curve [AUC] = 0.9975) when comparing controls to manifest patients. Similarly, the AUC between controls and premanifest patients was 0.9846. The optimal cutoff value for distinguishing between controls and manifest patients was 4,544 fM, whereas it was 6,596 fM for distinguishing between controls and premanifest patients.
Conclusion
Tear mHTT has potential for early and noninvasive detection of alterations in HD patients and could be integrated into both clinical trials and clinical diagnostics.

Citations

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  • Unveiling brain disorders using liquid biopsy and Raman spectroscopy
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    Nanoscale.2024; 16(25): 11879.     CrossRef
  • Ocular tear fluid biomarkers collected by contact lenses
    Nikolay Boychev, Vincent Yeung, Menglu Yang, Levi N. Kanu, Amy E. Ross, Liangju Kuang, Lin Chen, Joseph B. Ciolino
    Biochemical and Biophysical Research Communications.2024; 734: 150744.     CrossRef
Review Articles
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Clinical and Imaging Features of Multiple System Atrophy: Challenges for an Early and Clinically Definitive Diagnosis
Hirohisa Watanabe, Yuichi Riku, Kazuhiro Hara, Kazuya Kawabata, Tomohiko Nakamura, Mizuki Ito, Masaaki Hirayama, Mari Yoshida, Masahisa Katsuno, Gen Sobue
J Mov Disord. 2018;11(3):107-120.   Published online August 9, 2018
DOI: https://doi.org/10.14802/jmd.18020
  • 20,623 View
  • 1,262 Download
  • 26 Web of Science
  • 27 Crossref
AbstractAbstract PDF
Multiple system atrophy (MSA) is an adult-onset, progressive neurodegenerative disorder. Patients with MSA show various phenotypes during the course of their illness, including parkinsonism, cerebellar ataxia, autonomic failure, and pyramidal signs. Patients with MSA sometimes present with isolated autonomic failure or motor symptoms/ signs. The median duration from onset to the concomitant appearance of motor and autonomic symptoms is approximately 2 years but can range up to 14 years. As the presence of both motor and autonomic symptoms is essential for the current diagnostic criteria, early diagnosis is difficult when patients present with isolated autonomic failure or motor symptoms/signs. In contrast, patients with MSA may show severe autonomic failure and die before the presentation of motor symptoms/signs, which are currently required for the diagnosis of MSA. Recent studies have also revealed that patients with MSA may show nonsupporting features of MSA such as dementia, hallucinations, and vertical gaze palsy. To establish early diagnostic criteria and clinically definitive categorization for the successful development of disease-modifying therapy or symptomatic interventions for MSA, research should focus on the isolated phase and atypical symptoms to develop specific clinical, imaging, and fluid biomarkers that satisfy the requirements for objectivity, for semi- or quantitative measurements, and for uncomplicated, worldwide availability. Several novel techniques, such as automated compartmentalization of the brain into multiple parcels for the quantification of gray and white matter volumes on an individual basis and the visualization of α-synuclein and other candidate serum and cerebrospinal fluid biomarkers, may be promising for the early and clinically definitive diagnosis of MSA.

Citations

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    Hirohisa Watanabe, Sayuri Shima, Yasuaki Mizutani, Akihiro Ueda, Mizuki Ito
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  • α-Synuclein Strains and Their Relevance to Parkinson’s Disease, Multiple System Atrophy, and Dementia with Lewy Bodies
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    Movement Disorders.2022; 37(1): 119.     CrossRef
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    Chi‐Ying R. Lin, Anisha Viswanathan, Tiffany X. Chen, Hiroshi Mitsumoto, Jean P. Vonsattel, Phyllis L. Faust, Sheng‐Han Kuo
    Annals of Clinical and Translational Neurology.2022; 9(7): 988.     CrossRef
  • The “Black Straight-Line Sign” in the Putamen in Diffusion-Weighted Imaging: A Potential Diagnostic MRI Marker for Multiple System Atrophy
    Yiming Zheng, Xiwen Wang, Huajian Zhao, Yanyan Jiang, Ying Zhu, Jing Chen, Wei Sun, Zhaoxia Wang, Yunchuang Sun
    Frontiers in Neurology.2022;[Epub]     CrossRef
  • Clinical Aspects of the Differential Diagnosis of Parkinson’s Disease and Parkinsonism
    Hae-Won Shin, Sang-Wook Hong, Young Chul Youn
    Journal of Clinical Neurology.2022; 18(3): 259.     CrossRef
  • Clinical Features and Neuroimaging Findings of Neuropil Antibody–Positive Idiopathic Sporadic Ataxia of Unknown Etiology
    Akira Takekoshi, Akio Kimura, Nobuaki Yoshikura, Isamu Yamakawa, Makoto Urushitani, Katsuya Nakamura, Kunihiro Yoshida, Takayoshi Shimohata
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  • Changes of Amide Proton Transfer Imaging in Multiple System Atrophy Parkinsonism Type
    Shuhua Li, Piu Chan, Chunmei Li, Haibo Chen, Min Chen, Wen Su, Kai Li, Na Lu, Lu Yu, Defa Chu, Pu-Yeh Wu
    Frontiers in Aging Neuroscience.2020;[Epub]     CrossRef
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    Nobuaki Yoshikura, Akio Kimura, Takayoshi Shimohata
    Nihon Naika Gakkai Zasshi.2020; 109(6): 1138.     CrossRef
  • Purva Rupeeyam of bhela indriya sthana-an explorative study
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Structure, Distribution, and Genetic Profile of α-Synuclein and Their Potential Clinical Application in Parkinson’s Disease
Xiaoli Si, Jiali Pu, Baorong Zhang
J Mov Disord. 2017;10(2):69-79.   Published online May 8, 2017
DOI: https://doi.org/10.14802/jmd.16061
  • 11,263 View
  • 354 Download
  • 15 Web of Science
  • 11 Crossref
AbstractAbstract PDF
Parkinson’s disease (PD), the second most common neurodegenerative disorder after Alzheimer’s disease, is characterized by the loss of nigral dopaminergic neurons. PD leads to a series of clinical symptoms, including motor and non-motor disturbances. α-synuclein, the major component of Lewy bodies, is a hallmark lesion in PD. In this review, we concentrate on presenting the latest research on the structure, distribution, and function of α-synuclein, and its interactions with PD. We also summarize the clinic applications of α-synuclein, which suggest its use as a biomarker, and the latest progress in α-synuclein therapy.

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    Younghee Yim, Won-Jin Moon
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Article image
Cerebrospinal Fluid Amyloid β1-42, Tau, and Alpha-Synuclein Predict the Heterogeneous Progression of Cognitive Dysfunction in Parkinson’s Disease
Ju-Hee Kang
J Mov Disord. 2016;9(2):89-96.   Published online May 25, 2016
DOI: https://doi.org/10.14802/jmd.16017
  • 21,033 View
  • 250 Download
  • 18 Web of Science
  • 18 Crossref
AbstractAbstract PDF
Parkinson’s disease (PD) is a neurodegenerative disease with heterogeneous pathological and clinical features. Cognitive dysfunction, a frequent non-motor complication, is a risk factor for poor prognosis and shows inter-individual variation in its progression. Of the clinical studies performed to identify biomarkers of PD progression, the Parkinson’s Progression Markers Initiative (PPMI) study is the largest study that enrolled drug-naïve and very early stage PD patients. The baseline characteristics of the PPMI cohort were recently published. The diagnostic utility of cerebrospinal fluid (CSF) biomarkers, including alpha-synuclein (α-syn), total tau, phosphorylated tau at Thr181, and amyloid β1-42, was not satisfactory. However, the baseline data on CSF biomarkers in the PPMI study suggested that the measurement of the CSF biomarkers enables the prediction of future cognitive decline in PD patients, which was consistent with previous studies. To prove the hypothesis that the interaction between Alzheimer’s pathology and α-syn pathology is important to the progression of cognitive dysfunction in PD, longitudinal observational studies must be followed. In this review, the neuropathological nature of heterogeneous cognitive decline in PD is briefly discussed, followed by a summarized interpretation of baseline CSF biomarkers derived from the data in the PPMI study. The combination of clinical, biochemical, genetic and imaging biomarkers of PD constitutes a feasible strategy to predict the heterogeneous progression of PD.

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