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  1. AU=Chen Chiung-Mei
  2. AU="Bayram, Zübeyde"
  3. AU="Stone, Nimalie D"
  4. AU="Sizemore, Lindsey"
  5. AU="Zimmermann, Christopher"
  6. AU="Sanchez, Vanessa" AU="Sanchez, Vanessa"
  7. AU="Bello, Muideen"
  8. AU="Wezel, Anouk"
  9. AU="Clouston, Sean"
  10. AU="Olumade, Testimony J"
  11. AU=Wang Xinling AU=Wang Xinling
  12. AU="Donghua Chen"
  13. AU="Ioannis Seimenis"
  14. AU="Benjamin B Lindsey"
  15. AU="Mythili, S"
  16. AU="Mayer, Paul M"
  17. AU="Matthews, Anberitha T"
  18. AU="Zhou, Haikun"
  19. AU=Gentric Graldine
  20. AU=Lynn Joanne
  21. AU="Evangelou, Iliana"
  22. AU="Stryjewski, Martin E"
  23. AU="Stahnisch, Frank W."
  24. AU="Murakami, Tomoaki"
  25. AU="Mangal, Chris"
  26. AU="Hashem Koohy"
  27. AU="Taylor, Eric B"
  28. AU="Giroux, Nicholas S"
  29. AU="Carmen Avila-Casado"
  30. AU=Coke Christopher J.
  31. AU="Nascimento, José Hamilton do"
  32. AU="Parel, Philip M"
  33. AU="Sandrine Barbaux"
  34. AU="Sarkar, S."
  35. AU="Maymi, Valerie"
  36. AU="Ager, Casey"

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  1. Artikel ; Online: Increased

    Chiang, Ping-I / Chen, Chiung-Mei

    BMC neurology

    2023  Band 23, Heft 1, Seite(n) 280

    Abstract: Background: Parsonage-Turner Syndrome (PTS) is a rare brachial plexopathy characterized by the sudden onset of pain in the shoulder girdle followed by upper limb weakness. PTS is frequently under-recognized or misdiagnosed as other more common ... ...

    Abstract Background: Parsonage-Turner Syndrome (PTS) is a rare brachial plexopathy characterized by the sudden onset of pain in the shoulder girdle followed by upper limb weakness. PTS is frequently under-recognized or misdiagnosed as other more common neurological disorders presenting in a similar fashion, such as cervical radiculopathy which may require surgical intervention. Accurate diagnosis and prompt management implicate a good prognosis. Although electrophysiological studies are considered the most important for evaluating peripheral nerve injuries, it usually takes time, up to 3 weeks after the initial insult of the nerve for electromyogram (EMG) and nerve conduction studies (NCS) to display abnormalities. In the cases of PTS, especially when initial EMG/NCS and magnetic resonance neurography (MRN) results are inconclusive,
    Case presentation: A 60-year-old right-handed Taiwanese woman presented with sudden onset of intense and sharp left shoulder girdle pain without radiating to the arm, followed by muscle weakness of her left arm in abduction and elevation 3 days after the onset of pain. A detailed neurological examination and EMG and NCS suggested the clinical diagnosis of left brachial plexopathy. MRN imaging revealed no significant abnormality.
    Conclusions: We present increased
    Mesh-Begriff(e) Humans ; Female ; Middle Aged ; Brachial Plexus Neuritis/diagnostic imaging ; Fluorodeoxyglucose F18 ; Positron Emission Tomography Computed Tomography ; Brachial Plexus Neuropathies ; Muscle, Skeletal/diagnostic imaging ; Pain ; Muscle Weakness
    Chemische Substanzen Fluorodeoxyglucose F18 (0Z5B2CJX4D)
    Sprache Englisch
    Erscheinungsdatum 2023-07-26
    Erscheinungsland England
    Dokumenttyp Case Reports ; Journal Article
    ZDB-ID 2041347-6
    ISSN 1471-2377 ; 1471-2377
    ISSN (online) 1471-2377
    ISSN 1471-2377
    DOI 10.1186/s12883-023-03328-x
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Biomarker of Neuroinflammation in Parkinson's Disease.

    Liu, Tsai-Wei / Chen, Chiung-Mei / Chang, Kuo-Hsuan

    International journal of molecular sciences

    2022  Band 23, Heft 8

    Abstract: Parkinson's disease (PD) is caused by abnormal accumulation of α-synuclein in dopaminergic neurons of the substantia nigra, which subsequently causes motor symptoms. Neuroinflammation plays a vital role in the pathogenesis of neurodegeneration in PD. ... ...

    Abstract Parkinson's disease (PD) is caused by abnormal accumulation of α-synuclein in dopaminergic neurons of the substantia nigra, which subsequently causes motor symptoms. Neuroinflammation plays a vital role in the pathogenesis of neurodegeneration in PD. This neuroinflammatory neurodegeneration involves the activation of microglia, upregulation of proinflammatory factors, and gut microbiota. In this review, we summarized the recent findings on detection of PD by using inflammatory biomarkers, such as interleukin (IL)-1β, IL-2, IL-6, IL-10, tumor necrosis factor (TNF)-α; regulated upon activation, normal T cell expressed and presumably secreted (RANTES) and high-sensitivity c-reactive protein (hsCRP); and radiotracers such as [11C]PK11195 and [18F]-FEPPA, as well as by monitoring disease progression and the treatment response. Many PD-causing mutations in
    Mesh-Begriff(e) Animals ; Anti-Inflammatory Agents/pharmacology ; Biomarkers/metabolism ; Disease Models, Animal ; Dopaminergic Neurons/metabolism ; Humans ; Mice ; Mice, Inbred C57BL ; Microglia/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Neuroinflammatory Diseases ; Parkinson Disease/metabolism
    Chemische Substanzen Anti-Inflammatory Agents ; Biomarkers ; NLR Family, Pyrin Domain-Containing 3 Protein
    Sprache Englisch
    Erscheinungsdatum 2022-04-08
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms23084148
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel: The Role of Oxidative Stress in Parkinson's Disease.

    Chang, Kuo-Hsuan / Chen, Chiung-Mei

    Antioxidants (Basel, Switzerland)

    2020  Band 9, Heft 7

    Abstract: Parkinson's disease (PD) is caused by progressive neurodegeneration of dopaminergic (DAergic) neurons with abnormal accumulation of α-synuclein in substantia nigra (SN). Studies have suggested the potential involvement of dopamine, iron, calcium, ... ...

    Abstract Parkinson's disease (PD) is caused by progressive neurodegeneration of dopaminergic (DAergic) neurons with abnormal accumulation of α-synuclein in substantia nigra (SN). Studies have suggested the potential involvement of dopamine, iron, calcium, mitochondria and neuroinflammation in contributing to overwhelmed oxidative stress and neurodegeneration in PD. Function studies on PD-causative mutations of
    Sprache Englisch
    Erscheinungsdatum 2020-07-08
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2704216-9
    ISSN 2076-3921
    ISSN 2076-3921
    DOI 10.3390/antiox9070597
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel: A Novel SETX Mutation in a Taiwanese Patient with Autosomal Recessive Cerebellar Ataxia Detected by Targeted Next-Generation Sequencing, and a Literature Review.

    Chiang, Ping-I / Liao, Ting-Wei / Chen, Chiung-Mei

    Brain sciences

    2022  Band 12, Heft 2

    Abstract: Ataxia with oculomotor apraxia type 2 (AOA2), also known as autosomal recessive spinocerebellar ataxia with axonal neuropathy-2 (SCAN2) (OMIM #606002), is a neurodegenerative disorder characterized by early-onset progressive cerebellar ataxia, ... ...

    Abstract Ataxia with oculomotor apraxia type 2 (AOA2), also known as autosomal recessive spinocerebellar ataxia with axonal neuropathy-2 (SCAN2) (OMIM #606002), is a neurodegenerative disorder characterized by early-onset progressive cerebellar ataxia, polyneuropathy, and elevated levels of alpha-fetoprotein. It is caused by mutations in the SETX (OMIM #608465) gene. The prevalence of this disease is widely varied, from non-existent up to 1/150,000, depending on the region. Until now, no cases of AOA2/SCAN2 have been reported in Taiwan.
    Methods: Next-generation sequencing was used to detect disease-causing mutations of SETX in a Taiwanese patient presenting with autosomal recessive cerebellar ataxia, polyneuropathy, and elevated alpha-fetoprotein. The candidate mutations were further confirmed by polymerase chain reaction (PCR) and Sanger sequencing.
    Results: A compound heterozygous mutation of SETX c.6859C > T (p.R2287X) and c.7034-7036del was identified. The c.6859C > T (p.R2287X) has been previously found in a Saudi Arabia family, whereas c.7034-7036del is a novel mutation. Both mutations were predicted by bioinformatics programs to be likely pathogenic (having a damaging effect). We also reviewed the literature to address the reported clinical features of AOA2 from different populations.
    Conclusions: To our knowledge, we are the first to report a Taiwanese patient with AOA2/SCAN2, a result obtained by utilizing next-generation sequencing. The literature review shows that ataxia, polyneuropathy, and elevated AFP are common features and ocular motor apraxia (OMA) is a variable sign of AOA2 from different populations. OMA is rare and saccadic ocular pursuit and nystagmus are common in East Asian AOA2.
    Sprache Englisch
    Erscheinungsdatum 2022-01-28
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2651993-8
    ISSN 2076-3425
    ISSN 2076-3425
    DOI 10.3390/brainsci12020173
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  5. Artikel ; Online: Biomarker of Neuroinflammation in Parkinson’s Disease

    Tsai-Wei Liu / Chiung-Mei Chen / Kuo-Hsuan Chang

    International Journal of Molecular Sciences, Vol 23, Iss 4148, p

    2022  Band 4148

    Abstract: Parkinson’s disease (PD) is caused by abnormal accumulation of α-synuclein in dopaminergic neurons of the substantia nigra, which subsequently causes motor symptoms. Neuroinflammation plays a vital role in the pathogenesis of neurodegeneration in PD. ... ...

    Abstract Parkinson’s disease (PD) is caused by abnormal accumulation of α-synuclein in dopaminergic neurons of the substantia nigra, which subsequently causes motor symptoms. Neuroinflammation plays a vital role in the pathogenesis of neurodegeneration in PD. This neuroinflammatory neurodegeneration involves the activation of microglia, upregulation of proinflammatory factors, and gut microbiota. In this review, we summarized the recent findings on detection of PD by using inflammatory biomarkers, such as interleukin (IL)-1β, IL-2, IL-6, IL-10, tumor necrosis factor (TNF)-α; regulated upon activation, normal T cell expressed and presumably secreted (RANTES) and high-sensitivity c-reactive protein (hsCRP); and radiotracers such as [11C]PK11195 and [18F]-FEPPA, as well as by monitoring disease progression and the treatment response. Many PD-causing mutations in SNCA , LRRK2 , PRKN , PINK1 , and DJ-1 are also associated with neuroinflammation. Several anti-inflammatory medications, including nonsteroidal anti-inflammatory drugs (NSAID), inhibitors of TNF-α and NLR family pyrin domain containing 3 (NLRP3), agonists of nuclear factor erythroid 2-related factor 2 (NRF2), peroxisome proliferator-activated receptor gamma (PPAR-γ), and steroids, have demonstrated neuroprotective effects in in vivo or in vitro PD models. Clinical trials applying objective biomarkers are required to investigate the therapeutic potential of anti-inflammatory medications for PD.
    Schlagwörter Parkinson’s disease ; inflammation ; microglia ; biomarker ; interleukin (IL)-1β ; IL-2 ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2022-04-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  6. Artikel ; Online: Alternations of Lipoprotein Profiles in the Plasma as Biomarkers of Huntington’s Disease

    Kuo-Hsuan Chang / Mei-Ling Cheng / Chi-Jen Lo / Chun-Ming Fan / Yih-Ru Wu / Chiung-Mei Chen

    Cells, Vol 12, Iss 385, p

    2023  Band 385

    Abstract: Alterations in lipid composition and disturbed lipoprotein metabolism are involved in the pathomechanism of Huntington’s disease (HD). Here, we measured 112 lipoprotein subfractions and components in the plasma of 20 normal controls, 24 symptomatic ( ... ...

    Abstract Alterations in lipid composition and disturbed lipoprotein metabolism are involved in the pathomechanism of Huntington’s disease (HD). Here, we measured 112 lipoprotein subfractions and components in the plasma of 20 normal controls, 24 symptomatic (sympHD) and 9 presymptomatic (preHD) HD patients. Significant changes were found in 30 lipoprotein subfractions and components in all HD patients. Plasma levels of total cholesterol (CH), apolipoprotein (Apo)B, ApoB-particle number (PN), and components of low-density lipoprotein (LDL) were lower in preHD and sympHD patients. Components of LDL4, LDL5, LDL6 and high-density lipoprotein (HDL)4 demonstrated lower levels in preHD and sympHD patients compared with controls. Components in LDL3 displayed lower levels in sympHD compared with the controls, whereas components in very low-density lipoprotein (VLDL)5 were higher in sympHD patients compared to the controls. The levels of components in HDL4 and VLDL5 demonstrated correlation with the scores of motor assessment, independence scale or functional capacity of Unified Huntington’s Disease Rating Scale. These findings indicate the potential of components of VLDL5, LDL3, LDL4, LDL5 and HDL4 to serve as the biomarkers for HD diagnosis and disease progression, and demonstrate substantial evidence of the involvement of lipids and apolipoproteins in HD pathogenesis.
    Schlagwörter Huntington’s disease ; biomarker ; lipoprotein ; high-density lipoprotein ; low-density lipoprotein ; very low-density lipoprotein ; Biology (General) ; QH301-705.5
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2023-01-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  7. Artikel: Focused Ultrasound-Induced Blood-Brain Barrier Opening Enhanced α-Synuclein Expression in Mice for Modeling Parkinson's Disease.

    Lin, Chung-Yin / Huang, Ching-Yun / Chen, Chiung-Mei / Liu, Hao-Li

    Pharmaceutics

    2022  Band 14, Heft 2

    Abstract: Parkinson's disease (PD) is characterized by α-synuclein (αSNCA) aggregation in dopaminergic neurons. Gradual accumulation of αSNCA aggregates in substantia nigra (SN) diminishes the normal functioning of soluble αSNCA, leading to a loss of dopamine (DA) ...

    Abstract Parkinson's disease (PD) is characterized by α-synuclein (αSNCA) aggregation in dopaminergic neurons. Gradual accumulation of αSNCA aggregates in substantia nigra (SN) diminishes the normal functioning of soluble αSNCA, leading to a loss of dopamine (DA) neurons. In this study, we developed focused ultrasound-targeted microbubble destruction (UTMD)-mediated PD model that could generate the disease phenotype via αSNCA CNS gene delivery. The formation of neuronal aggregates was analyzed with immunostaining. To evaluate the DA cell loss, we used tyrosine hydroxylase immunostaining and HPLC analysis on DA and its two metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA). This loss of DA was associated with a dose-dependent impairment in motor function, as assessed by the rotarod motor assessment. We demonstrate that UTMD-induced SNCA expression initiates αSNCA aggregation and results in a 50% loss of DA in SN. UTMD-related dose-dependent neuronal loss was identified, and it correlates with the degree of impairment of motor function. In comparison to chemical neurotoxin 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated and conventional intracerebral (IC)-injected animal models of PD, the UTMD-mediated αSNCA-based mouse model offers the advantage of mimicking the rapid development of the PD phenotype. The PD models that we created using UTMD also prove valuable in assessing specific aspects of PD pathogenesis and can serve as a useful PD model for the development of new therapeutic strategies.
    Sprache Englisch
    Erscheinungsdatum 2022-02-18
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2527217-2
    ISSN 1999-4923
    ISSN 1999-4923
    DOI 10.3390/pharmaceutics14020444
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel ; Online: X-linked adrenoleukodystrophy caused by a novel mutation presenting with various phenotypes in a Taiwanese family.

    Chien, Chia-Yin / Chang, Kuo-Hsuan / Chen, Chiung-Mei

    Clinica chimica acta; international journal of clinical chemistry

    2021  Band 514, Seite(n) 100–106

    Abstract: X-linked adrenoleukodystrophy (X-ALD) is a peroxisomal disorder that primarily affects the white matter of central nervous system and the adrenal cortex. It is caused by mutations in the adenosine triphosphate-binding cassette, subfamily D, member 1 ( ... ...

    Abstract X-linked adrenoleukodystrophy (X-ALD) is a peroxisomal disorder that primarily affects the white matter of central nervous system and the adrenal cortex. It is caused by mutations in the adenosine triphosphate-binding cassette, subfamily D, member 1 (ABCD1) gene that results in elevated plasma levels of very long chain fatty acids (VLCFAs). The disease is characterized by an unpredictable variation in phenotypic expressions, including childhood cerebral form (CCALD) and adrenomyeloneuropathy (AMN). Genetic analysis is a reliable method for the diagnosis of X-ALD. We reported a 46-year-old male admitted to Department of Neurology, Chang Gung Memorial Hospital with progressive paraparesis and Addison's disease, which was diagnosed when he was around 20-year-old. Plasma levels of VLCFA showed that his C26:0, C24:0/C22:0 and C26:0/C22:0 ratios were significantly elevated. A novel missense mutation (p.Arg163Cys) caused by the nucleotide change c.487C > T in exon 1 was identified in the ABCD1 gene of the proband and his subclinical family members. In this article, we reviewed the mutations that had been reported at the same position with different phenotypes. Given that the nerve conduction study (NCS) of the proband demonstrated a rare finding of demyelinating polyneuropathy with conduction blocks, we also reviewed the findings of NCS in patients with AMN in literature.
    Mesh-Begriff(e) Adrenoleukodystrophy/diagnosis ; Adrenoleukodystrophy/genetics ; Humans ; Male ; Middle Aged ; Mutation ; Mutation, Missense ; Phenotype ; Young Adult
    Sprache Englisch
    Erscheinungsdatum 2021-01-08
    Erscheinungsland Netherlands
    Dokumenttyp Case Reports ; Journal Article
    ZDB-ID 80228-1
    ISSN 1873-3492 ; 0009-8981
    ISSN (online) 1873-3492
    ISSN 0009-8981
    DOI 10.1016/j.cca.2020.12.017
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel: A Neuroprotective Action of Quercetin and Apigenin through Inhibiting Aggregation of Aβ and Activation of TRKB Signaling in a Cellular Experiment.

    Chiu, Ya-Jen / Teng, Yu-Shan / Chen, Chiung-Mei / Sun, Ying-Chieh / Hsieh-Li, Hsiu Mei / Chang, Kuo-Hsuan / Lee-Chen, Guey-Jen

    Biomolecules & therapeutics

    2023  Band 31, Heft 3, Seite(n) 285–297

    Abstract: Alzheimer's disease (AD) is a neurodegenerative disease with progressive memory loss and the cognitive decline. AD is mainly caused by abnormal accumulation of misfolded amyloid β (Aβ), which leads to neurodegeneration via a number of possible mechanisms ...

    Abstract Alzheimer's disease (AD) is a neurodegenerative disease with progressive memory loss and the cognitive decline. AD is mainly caused by abnormal accumulation of misfolded amyloid β (Aβ), which leads to neurodegeneration via a number of possible mechanisms such as down-regulation of brain-derived neurotrophic factor-tropomyosin-related kinase B (BDNF-TRKB) signaling pathway. 7 ,8-Dihydroxyflavone (7,8-DHF), a TRKB agonist, has demonstrated potential to enhance BDNF-TRKB pathway in various neurodegenerative diseases. To expand the capacity of flavones as TRKB agonists, two natural flavones quercetin and apigenin, were evaluated. With tryptophan fluorescence quenching assay, we illustrated the direct interaction between quercetin/apigenin and TRKB extracellular domain. Employing Aβ folding reporter SH-SY5Y cells, we showed that quercetin and apigenin reduced Aβ-aggregation, oxidative stress, caspase-1 and acetylcholinesterase activities, as well as improved the neurite outgrowth. Treatments with quercetin and apigenin increased TRKB Tyr516 and Tyr817 and downstream cAMP-response-element binding protein (CREB) Ser133 to activate transcription of BDNF and BCL2 apoptosis regulator (BCL2), as well as reduced the expression of pro-apoptotic BCL2 associated X protein (BAX). Knockdown of TRKB counteracted the improvement of neurite outgrowth by quercetin and apigenin. Our results demonstrate that quercetin and apigenin are to work likely as a direct agonist on TRKB for their neuroprotective action, strengthening the therapeutic potential of quercetin and apigenin in treating AD.
    Sprache Englisch
    Erscheinungsdatum 2023-01-17
    Erscheinungsland Korea (South)
    Dokumenttyp Journal Article
    ZDB-ID 2734146-X
    ISSN 2005-4483 ; 1976-9148
    ISSN (online) 2005-4483
    ISSN 1976-9148
    DOI 10.4062/biomolther.2022.136
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel ; Online: Alternations of Lipoprotein Profiles in the Plasma as Biomarkers of Huntington's Disease.

    Chang, Kuo-Hsuan / Cheng, Mei-Ling / Lo, Chi-Jen / Fan, Chun-Ming / Wu, Yih-Ru / Chen, Chiung-Mei

    Cells

    2023  Band 12, Heft 3

    Abstract: Alterations in lipid composition and disturbed lipoprotein metabolism are involved in the pathomechanism of Huntington's disease (HD). Here, we measured 112 lipoprotein subfractions and components in the plasma of 20 normal controls, 24 symptomatic ( ... ...

    Abstract Alterations in lipid composition and disturbed lipoprotein metabolism are involved in the pathomechanism of Huntington's disease (HD). Here, we measured 112 lipoprotein subfractions and components in the plasma of 20 normal controls, 24 symptomatic (sympHD) and 9 presymptomatic (preHD) HD patients. Significant changes were found in 30 lipoprotein subfractions and components in all HD patients. Plasma levels of total cholesterol (CH), apolipoprotein (Apo)B, ApoB-particle number (PN), and components of low-density lipoprotein (LDL) were lower in preHD and sympHD patients. Components of LDL4, LDL5, LDL6 and high-density lipoprotein (HDL)4 demonstrated lower levels in preHD and sympHD patients compared with controls. Components in LDL3 displayed lower levels in sympHD compared with the controls, whereas components in very low-density lipoprotein (VLDL)5 were higher in sympHD patients compared to the controls. The levels of components in HDL4 and VLDL5 demonstrated correlation with the scores of motor assessment, independence scale or functional capacity of Unified Huntington's Disease Rating Scale. These findings indicate the potential of components of VLDL5, LDL3, LDL4, LDL5 and HDL4 to serve as the biomarkers for HD diagnosis and disease progression, and demonstrate substantial evidence of the involvement of lipids and apolipoproteins in HD pathogenesis.
    Mesh-Begriff(e) Humans ; Triglycerides ; Huntington Disease/diagnosis ; Lipoproteins ; Lipoproteins, LDL/metabolism ; Apolipoproteins B ; Biomarkers
    Chemische Substanzen Triglycerides ; Lipoproteins ; Lipoproteins, LDL ; Apolipoproteins B ; Biomarkers
    Sprache Englisch
    Erscheinungsdatum 2023-01-20
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells12030385
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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