A5039348239- Genetic Neurodegenerative Diseases
- Parkinson's Disease Mechanisms and Treatments
- Mitochondrial Function and Pathology
- Alzheimer's disease research and treatments
- Nuclear Receptors and Signaling
- Neurological disorders and treatments
- Neurological diseases and metabolism
- Endoplasmic Reticulum Stress and Disease
- RNA regulation and disease
- Peripheral Neuropathies and Disorders
- Cholinesterase and Neurodegenerative Diseases
- Hereditary Neurological Disorders
- Neuroinflammation and Neurodegeneration Mechanisms
- Ubiquitin and proteasome pathways
- Autophagy in Disease and Therapy
- Lysosomal Storage Disorders Research
- Amyotrophic Lateral Sclerosis Research
- Pharmacological Effects of Natural Compounds
- Intracerebral and Subarachnoid Hemorrhage Research
- Genetics and Neurodevelopmental Disorders
- Muscle Physiology and Disorders
- Acute Ischemic Stroke Management
- Tryptophan and brain disorders
- Botulinum Toxin and Related Neurological Disorders
- Multiple Sclerosis Research Studies
Chang Gung University
2016-2025
Chang Gung Memorial Hospital
2016-2025
Linkou Chang Gung Memorial Hospital
2015-2024
National Taiwan Normal University
2015-2023
National Taipei University of Technology
2023
Mitsubishi Corporation (Japan)
2015-2016
Duke-NUS Medical School
2013
National Neuroscience Institute
2013
State Key Laboratory of Oncology in South China
2013
Sun Yat-sen University Cancer Center
2013
Huntington's disease (HD) is a neurodegenerative disorder that manifests with movement dysfunction. The expression of mutant Huntingtin (mHTT) disrupts the functions brain cells. Galectin-3 (Gal3) lectin has not been extensively explored in diseases. Herein, we showed plasma Gal3 levels HD patients and mice correlated severity. Moreover, were higher than those controls. up-regulation occurred before motor impairment, its level remained high microglia throughout progression. cell-autonomous...
Abstract Maximum elbow flexor and extensor muscle strength was measured in 9 patients with Parkinson's disease on off antiparkinsonian medication. In addition, the rate of force generation, actively returning to resting levels, passive release “relaxation” were submaximal contractions. The measures contraction time correlated changes clinical status as by Unified Disease Rating Scale. When medication, their reduction significantly greater extension than flexion. flexion did not reach...
Abstract Common genetic variants that increase the risk for Parkinson's disease may differentiate patient subgroups and influence future individualized therapeutic strategies. Herein we show evidence leucine‐rich repeat kinase 2 (LRRK2) c.4883G>C (R1628P) as a factor in ethnic Chinese populations. A study of 1,986 individuals from 3 independent centers Taiwan Singapore demonstrates Lrrk2 R1628P increases (odds ratio, 1.84; 95% confidence interval, 1.20–2.83; p = 0.006). Haplotype analysis...
Genome-wide association studies (GWAS) on Parkinson's disease (PD) have mostly been done in Europeans and Japanese. No study has Han Chinese, which make up nearly a fifth of the world population. We conducted first Chinese GWAS analysing total 22,729 subjects (5,125 PD cases 17,604 controls) from Singapore, Hong Kong, Malaysia, Korea, mainland China Taiwan. performed imputation, merging logistic regression analyses 2,402,394 SNPs passing quality control filters 779 cases, 13,227 controls,...
Neuroinflammation is a common feature of many neurodegenerative diseases, including Huntington's disease (HD). HD an autosomal dominant genetic caused by expanded CAG repeat in exon 1 the huntingtin (HTT) gene. Previous studies demonstrated that levels several proinflammatory cytokines, tumor necrosis factor (TNF)-α, were higher plasma and brain tissues mice patients with HD, suggesting inflammation may contribute to progression. To evaluate pathological role TNF-α pathogenesis, we blocked...
Misfolding and accumulation of amyloid-β (Aβ) in the brains patients with Alzheimer's disease (AD) lead to neuronal loss through various mechanisms, including downregulation eukaryotic elongation factor 2 (EEF2) protein synthesis signaling. This study investigated neuroprotective effects indole coumarin derivatives on Aβ folding EEF2 signaling using SH-SY5Y cells expressing Aβ-green fluorescent (GFP) reporter. Among tested compounds, two (NC009-1, -6) (LM-021, -036) effectively reduced...
Huntington's disease (HD) is a neurodegenerative caused by the expansion of CAG trinucleotide repeat in exon 1 huntingtin (HTT) gene. Here, we report that transcript peroxisome proliferator-activated receptor-γ (PPARγ), transcription factor critical for energy homeostasis, was markedly downregulated multiple tissues mouse model (R6/2) HD and lymphocytes patients. Therefore, downregulation PPARγ seems to be pathomechanism HD. Chronic treatment R6/2 mice with an agonist (thiazolidinedione,...
Amyloid β (Aβ) plays a major role in the neurodegeneration of Alzheimerâs disease (AD). The accumulation misfolded Aβ causes oxidative stress and inflammatory damage leading to apoptotic cell death. Traditional Chinese herbal medicine (CHM) has been widely used treating neurodegenerative diseases by reducing neuroinflammation. We examined neuroprotective effect formulated CHM Shaoyao Gancao Tang (SG-Tang, made Paeonia lactiflora Glycyrrhiza uralensis at 1:1 ratio) AD mouse models. In...
The biomarkers of Parkinson’s disease (PD) remain to be investigated. This work aimed identify blood for PD using targeted metabolomics analysis. We quantified the plasma levels 255 metabolites in 92 patients and 60 healthy controls (HC). were sub-grouped into early (Hoehn–Yahr stage ≤ 2, n = 72) advanced > 20) stages. Fifty-nine phospholipids, 3 fatty acids, amino 7 biogenic amines, demonstrated significant alterations patients. Six them, dihydro sphingomyelin (SM) 24:0, 22:0, 20:0,...
Alzheimer's disease (AD) is a neurodegenerative with progressive memory loss and the cognitive decline. AD mainly caused by abnormal accumulation of misfolded amyloid β (Aβ), which leads to neurodegeneration via number possible mechanisms such as down-regulation brain-derived neurotrophic factor-tropomyosin-related kinase B (BDNF-TRKB) signaling pathway. 7 ,8-Dihydroxyflavone (7,8-DHF), TRKB agonist, has demonstrated potential enhance BDNF-TRKB pathway in various diseases. To expand capacity...
To investigate the sensitivity and specificity of various neutral-position magnetic resonance (MR) imaging findings in diagnosis Hirayama flexion myelopathy.The cervical MR images 46 patients 51 control subjects were evaluated for following findings: localized lower cord atrophy, asymmetric flattening, abnormal curvature, loss attachment (LOA) between posterior dural sac subjacent lamina, noncompressed intramedullary high signal intensity on T2-weighted images. The difference frequency these...
Huntington's disease (HD) is an autosomal dominant neurodegenerative caused by a CAG trinucleotide expansion in the Huntingtin (Htt) gene. Using two mouse models of HD, we demonstrate that urea cycle deficiency characterized hyperammonemia, high blood citrulline and suppression enzymes prominent feature HD. The resultant ammonia toxicity might exacerbate neurological deficits Suppression C/EBPα, crucial transcription factor for enzymes, appears to mediate We found presence mutant Htt, C/EBPα...
Huntington's disease (HD) is an autosomal dominant neurodegenerative caused by a CAG trinucleotide expansion in the Huntingtin (Htt) gene. The resultant mutant Htt protein (mHtt) forms aggregates brain and several peripheral tissues (e.g. liver) causes devastating neuronal degeneration. Metabolic defects resulting from also contribute to HD pathogenesis. Simultaneous improvement of both CNS thus most effective therapeutic strategy highly desirable. We earlier showed that agonist A2A...
Abstract The purpose of this study was to review the clinical manifestations 40 patients who fulfilled criteria for Hirayama disease (juvenile muscular atrophy distal upper extremities), identified in our neuromuscular clinic between February 1995 and December 2005. Of these patients, 87.5% were male. mean age at onset 16.8 years, which 4.5 years later than peak normal growth curve. Progressive muscle weakness wasting characteristic occurred predominantly part right limb. Neurogenic symptoms...