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  1. AU="Horne, Patrick"
  2. AU="Mhurchu, Cliona Ni"
  3. AU="Yatoo, Ali Mohd"
  4. AU="Zhang, Zhiru"
  5. AU="Hadie Adams"
  6. AU="Gaskin, Thomas R"
  7. AU="Guo, Chong"
  8. AU="Guocan Wang"
  9. AU="Catherine Crenn-Hebert"
  10. AU="Alistar, Cristina F"
  11. AU="Makhani, Sarah S"
  12. AU="Tayyeb Pourfallah"
  13. AU="Mauad, Thais"

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  1. Artikel: Case Study: Advanced Hepatocellular Carcinoma With Tumor Thrombus.

    Horne, Patrick M

    Clinical liver disease

    2019  Band 13, Heft 6, Seite(n) 162–164

    Sprache Englisch
    Erscheinungsdatum 2019-07-02
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2657644-2
    ISSN 2046-2484
    ISSN 2046-2484
    DOI 10.1002/cld.776
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Portal hypertension and risk of esophageal bleeding.

    Horne, Patrick M

    The Nurse practitioner

    2016  Band 41, Heft 8, Seite(n) 1–3

    Sprache Englisch
    Erscheinungsdatum 2016-08-18
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 604085-8
    ISSN 1538-8662 ; 0361-1817
    ISSN (online) 1538-8662
    ISSN 0361-1817
    DOI 10.1097/01.NPR.0000480594.39784.54
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  3. Artikel: Clinician barriers, perceptions, and practices in treating patients with hepatitis C virus and substance use disorder in the United States.

    Park, Haesuk / Brown, Carolyn / Wilson, Debbie L / Huang, Pei-Lin / Hernández-Con, Pilar / Horne, Patrick / Goodin, Amie / Joseph, Amanda / Segal, Rich / Cabrera, Roniel / Cook, Robert L

    Preventive medicine reports

    2023  Band 32, Seite(n) 102138

    Abstract: The likelihood of clinicians prescribing direct-acting antiviral (DAA) therapy for patients with chronic hepatitis C virus (HCV) and substance use disorder (SUD) was assessed via a survey emailed throughout the United States to clinicians (physicians and ...

    Abstract The likelihood of clinicians prescribing direct-acting antiviral (DAA) therapy for patients with chronic hepatitis C virus (HCV) and substance use disorder (SUD) was assessed via a survey emailed throughout the United States to clinicians (physicians and advanced practice providers) in gastroenterology, hepatology, and infectious disease specialties. Clinicians' perceived barriers and preparedness and actions associated with current and future DAA prescribing practices of HCV-infected patients with SUD were assessed. Of 846 clinicians presumably receiving the survey, 96 completed and returned it. Exploratory factor analyses of perceived barriers indicated a highly reliable (Cronbach alpha = 0.89) model with five factors: HCV stigma and knowledge, prior authorization requirements, and patient- clinician-, and system-related barriers. In multivariable analyses, after controlling for covariates, patient-related barriers (P < 0.01) and prior authorization requirements (P < 0.01) were
    Conclusion: These findings underscore the importance of addressing patient-related barriers and prior authorization requirements-significant problematic barriers-and improving clinicians' beliefs (e.g., medication-assisted therapy should be prescribed before DAAs) and comfort levels for treating patients with HCV and SUD to enhance treatment access for patients with both HCV and SUD.
    Sprache Englisch
    Erscheinungsdatum 2023-02-13
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2785569-7
    ISSN 2211-3355
    ISSN 2211-3355
    DOI 10.1016/j.pmedr.2023.102138
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Evaluating the Efficacy of a Registry linked to a Consent to Re-Contact Program and Communication Strategies for Recruiting and Enrolling Participants into Clinical Trials.

    Flood-Grady, Elizabeth / Clark, Virginia C / Bauer, Angie / Morelli, Lauren / Horne, Patrick / Krieger, Janice L / Nelson, David R

    Contemporary clinical trials communications

    2017  Band 8, Seite(n) 62–66

    Abstract: Introduction: Although registries can rapidly identify clinical study participants, it is unknown which follow up methods for recruiting are most effective. Our goal is to examine the efficacy of three communication strategies for recruiting and ... ...

    Abstract Introduction: Although registries can rapidly identify clinical study participants, it is unknown which follow up methods for recruiting are most effective. Our goal is to examine the efficacy of three communication strategies for recruiting and enrolling patients who were identified via a contact registry (i.e., registry linked to a consent to re-contact program).
    Methods: Patients who met the study criteria were identified via the contact registry and targeted for recruitment. In condition 1, patients established in the university hepatology specialty clinics were contacted one time via phone call by the study coordinator and asked to participate (C1). In condition 2, non-established specialty clinic patients were mailed an IRB-approved letter with study information and instructions for calling the study coordinator to participate (C2). Condition 2A included patients who called within two weeks of receiving the letter (C2A); condition 2B included patients who did not call after receiving the letter but were subsequently contacted via phone call.
    Results: A registry identified 1,060 patients, of which 661were eligible and targeted for recruiting. All 37 patients were reached in C1 and 17 (45.9%) were recruited. Nineteen of the 624 patients in C2A were reached and 10 were recruited whereas 120 of the 605 patients in C2B were reached and 53 (8.7%) were recruited. Seventy patients enrolled with C2B being the most effective (total, cost) recruitment strategy (
    Conclusion: The efficacy of enrolling patients identified via a contact registry into clinical trials varies based on the communication strategies used for recruiting.
    Sprache Englisch
    Erscheinungsdatum 2017-08-24
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article
    ISSN 2451-8654
    ISSN (online) 2451-8654
    DOI 10.1016/j.conctc.2017.08.005
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: A Pragmatic, Randomized Controlled Trial of Oral Antivirals for the Treatment of Chronic Hepatitis C: The PRIORITIZE Study.

    Sulkowski, Mark S / Moon, Juhi S / Sherman, Kenneth E / Morelli, Giuseppe / Darling, Jama M / Muir, Andrew J / Khalili, Mandana / Fishbein, Dawn A / Hinestrosa, Federico / Shiffman, Mitchell L / Di Bisceglie, Adrian / Rajender Reddy, K / Pearlman, Brian / Lok, Anna S / Fried, Michael W / Stewart, Paul W / Peter, Joy / Wadsworth, Summer / Kixmiller, Scott /
    Sloan, Anquenette / Vainorius, Monika / Horne, Patrick M / Michael, Larry / Dong, Meichen / Evon, Donna M / Segal, Jodi B / Nelson, David R

    Hepatology (Baltimore, Md.)

    2021  Band 74, Heft 6, Seite(n) 2952–2964

    Abstract: Background and aims: Multiple direct-acting antiviral (DAA) regimens are available to treat HCV genotype 1 infection. However, comparative effectiveness from randomized controlled trials of DAA regimens is unavailable.: Approach and results: We ... ...

    Abstract Background and aims: Multiple direct-acting antiviral (DAA) regimens are available to treat HCV genotype 1 infection. However, comparative effectiveness from randomized controlled trials of DAA regimens is unavailable.
    Approach and results: We conducted a pragmatic randomized controlled trial (NCT02786537) to compare the effectiveness of DAAs for HCV genotype 1a or 1b on viral response, safety, tolerability, and medication nonadherence. Adults with compensated liver disease, HCV genotype 1, not pregnant or breastfeeding, and with health insurance likely to cover ledipasvir/sofosbuvir (LDV/SOF) were recruited from 34 US viral hepatitis clinics. Participants were randomized (± ribavirin) to LDV/SOF, elbasvir/grazoprevir (EBR/GZR), and paritaprevir/ritonavir/ombitasvir+dasabuvir (PrOD; treatment arm stopped early). Primary outcomes included sustained viral response at 12 weeks (SVR12), clinician-recorded adverse events, patient-reported symptoms, and medication nonadherence. Between June 2016 and March 2018, 1,609 participants were randomized. Among 1,128 participants who received ≥1 dose of EBR/GZR or LDV/SOF (± ribavirin), SVR12 was 95.2% (95% CI, 92.8%-97.6%) and 97.4% (95% CI, 95.5%-99.2%), respectively, with a difference estimate of 2.2% (-0.5% to 4.7%), falling within the "equivalence" interval (-5% to 5%). While most (56%) participants experienced adverse events, few were serious (4.2%) or severe (1.8%). In the absence of ribavirin, discontinuations due to adverse events were rare. Patient-reported symptoms and medication nonadherence were similar. Study limitations were dropout due to insurance denial and loss to follow-up after treatment, limiting the ability to measure SVR12.
    Conclusions: This pragmatic trial demonstrated high SVR12 for participants treated with EBR/GZR and LDV/SOF with few adverse effects. Overall, the two regimens were equivalent in effectiveness. The results support current HCV guidelines that do not distinguish between ribavirin-free EBR/GZR and LDV/SOF.
    Mesh-Begriff(e) 2-Naphthylamine/administration & dosage ; Administration, Oral ; Adolescent ; Adult ; Aged ; Aged, 80 and over ; Anilides/administration & dosage ; Antiviral Agents/administration & dosage ; Benzimidazoles/administration & dosage ; Benzofurans/administration & dosage ; Cyclopropanes/administration & dosage ; Drug Combinations ; Drug Therapy, Combination/methods ; Female ; Fluorenes/administration & dosage ; Follow-Up Studies ; Genotyping Techniques ; Hepacivirus/genetics ; Hepacivirus/isolation & purification ; Hepatitis C, Chronic/blood ; Hepatitis C, Chronic/diagnosis ; Hepatitis C, Chronic/drug therapy ; Hepatitis C, Chronic/virology ; Humans ; Imidazoles/administration & dosage ; Lactams, Macrocyclic/administration & dosage ; Male ; Middle Aged ; Proline/administration & dosage ; Proline/analogs & derivatives ; Quinoxalines/administration & dosage ; RNA, Viral/blood ; Ribavirin/administration & dosage ; Sofosbuvir/administration & dosage ; Sulfonamides/administration & dosage ; Sustained Virologic Response ; Treatment Outcome ; Uracil/administration & dosage ; Uracil/analogs & derivatives ; Valine/administration & dosage ; Young Adult
    Chemische Substanzen Anilides ; Antiviral Agents ; Benzimidazoles ; Benzofurans ; Cyclopropanes ; Drug Combinations ; Fluorenes ; Imidazoles ; Lactams, Macrocyclic ; Quinoxalines ; RNA, Viral ; Sulfonamides ; elbasvir-grazoprevir drug combination ; ledipasvir, sofosbuvir drug combination ; ombitasvir (2302768XJ8) ; Ribavirin (49717AWG6K) ; Uracil (56HH86ZVCT) ; Proline (9DLQ4CIU6V) ; 2-Naphthylamine (CKR7XL41N4) ; dasabuvir (DE54EQW8T1) ; Valine (HG18B9YRS7) ; paritaprevir (OU2YM37K86) ; Sofosbuvir (WJ6CA3ZU8B)
    Sprache Englisch
    Erscheinungsdatum 2021-08-26
    Erscheinungsland United States
    Dokumenttyp Clinical Trial, Phase IV ; Comparative Study ; Journal Article ; Multicenter Study ; Pragmatic Clinical Trial ; Randomized Controlled Trial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.32053
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel: Evidence that TDP-43 is not the major ubiquitinated target within the pathological inclusions of amyotrophic lateral sclerosis.

    Sanelli, Teresa / Xiao, Shangxi / Horne, Patrick / Bilbao, Juan / Zinman, Lorne / Robertson, Janice

    Journal of neuropathology and experimental neurology

    2007  Band 66, Heft 12, Seite(n) 1147–1153

    Abstract: Amyotrophic lateral sclerosis (ALS) is an adult-onset neurodegenerative disease characterized by the presence of various types of ubiquitinated inclusions in the cytoplasm of affected motor neurons. The identification of the ubiquitinated targets within ... ...

    Abstract Amyotrophic lateral sclerosis (ALS) is an adult-onset neurodegenerative disease characterized by the presence of various types of ubiquitinated inclusions in the cytoplasm of affected motor neurons. The identification of the ubiquitinated targets within these inclusions has represented a major challenge, as this may provide new gene candidates and/or clues to understanding the neurodegenerative mechanism(s) underlying the disease. As such, the nuclear factor TAR DNA-binding protein (TDP-43) was recently identified as a component of ubiquitinated skein-like inclusions and round inclusions in ALS. This identification combined with biochemical evidence led to the suggestion that TDP-43 is the key ubiquitinated target and major disease protein in ALS. Here, using 3-dimensional deconvolution imaging, we have obtained remarkable resolution of skein-like inclusions and round inclusions in ALS. Surprisingly we have found that in contrast to current thinking, TDP-43 is not the major ubiquitinated target within these types of inclusions. These findings raise the possibility that TDP-43 may not necessarily be the key disease protein in ALS and indicate that the major target(s) of ubiquitination remain to be identified.
    Mesh-Begriff(e) Aged ; Amyotrophic Lateral Sclerosis/metabolism ; Amyotrophic Lateral Sclerosis/pathology ; DNA-Binding Proteins/metabolism ; Female ; Humans ; Inclusion Bodies/metabolism ; Inclusion Bodies/pathology ; Intermediate Filament Proteins/metabolism ; Male ; Membrane Glycoproteins/metabolism ; Middle Aged ; Nerve Tissue Proteins/metabolism ; Peripherins ; Ubiquitin/metabolism
    Chemische Substanzen DNA-Binding Proteins ; Intermediate Filament Proteins ; Membrane Glycoproteins ; Nerve Tissue Proteins ; Peripherins ; Ubiquitin
    Sprache Englisch
    Erscheinungsdatum 2007-12
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3088-0
    ISSN 1554-6578 ; 0022-3069
    ISSN (online) 1554-6578
    ISSN 0022-3069
    DOI 10.1097/nen.0b013e31815c5edd
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Lack of evidence of monomer/misfolded superoxide dismutase-1 in sporadic amyotrophic lateral sclerosis.

    Liu, Hsueh-Ning / Sanelli, Teresa / Horne, Patrick / Pioro, Erik P / Strong, Michael J / Rogaeva, Ekaterina / Bilbao, Juan / Zinman, Lorne / Robertson, Janice

    Annals of neurology

    2009  Band 66, Heft 1, Seite(n) 75–80

    Abstract: Objective: In familial amyotrophic lateral sclerosis (fALS) harboring superoxide dismutase (SOD1) mutations (fALS1), SOD1 toxicity has been linked to its propensity to misfold and aggregate. It has recently been proposed that misfolded SOD1 may be ... ...

    Abstract Objective: In familial amyotrophic lateral sclerosis (fALS) harboring superoxide dismutase (SOD1) mutations (fALS1), SOD1 toxicity has been linked to its propensity to misfold and aggregate. It has recently been proposed that misfolded SOD1 may be causative of all types of ALS, including sporadic cases (sALS). In the present study, we have used a specific antibody to test for the presence of monomer/misfolded SOD1 in sALS.
    Methods: Sections from lumbar spinal cords of 5 fALS1 cases, 13 sALS cases, and 1 non-SOD1 fALS case were labeled immunocytochemically using SOD1-exposed-dimer-interface (SEDI) antibody, which we have previously validated as being specific for pathological monomer/misfolded forms of SOD1.
    Results: Monomer/misfolded SOD1 was detected with SEDI antibody in all 5 of the fALS1 cases, localizing predominantly to hyaline conglomerate inclusions, a specific pathological feature of fALS1. In contrast, monomer/misfolded SOD1 was not detected in any of the 13 sALS cases or in the non-SOD1 fALS cases. These results were confirmed by immunoprecipitation.
    Interpretation: Although SEDI antibody does not necessarily label all misfolded forms of SOD1, these findings show a distinct difference between fALS1 and sALS, and do not support that monomer/misfolded SOD1 is a common disease entity linking all types of ALS. This is important to our understanding of ALS disease pathogenesis and to considerations of the applicability of using therapeutics that target misfolded SOD1 to non-SOD1-related cases. Ann Neurol 2009;66:75-80.
    Mesh-Begriff(e) Adult ; Aged ; Aged, 80 and over ; Amyotrophic Lateral Sclerosis/genetics ; Amyotrophic Lateral Sclerosis/metabolism ; Amyotrophic Lateral Sclerosis/pathology ; Female ; Humans ; Male ; Middle Aged ; Mutation/genetics ; Protein Folding ; Superoxide Dismutase/genetics ; Superoxide Dismutase/metabolism ; Superoxide Dismutase-1
    Chemische Substanzen SOD1 protein, human ; Superoxide Dismutase (EC 1.15.1.1) ; Superoxide Dismutase-1 (EC 1.15.1.1)
    Sprache Englisch
    Erscheinungsdatum 2009-07
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80362-5
    ISSN 1531-8249 ; 0364-5134
    ISSN (online) 1531-8249
    ISSN 0364-5134
    DOI 10.1002/ana.21704
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  8. Artikel ; Online: An aggregate-inducing peripherin isoform generated through intron retention is upregulated in amyotrophic lateral sclerosis and associated with disease pathology.

    Xiao, Shangxi / Tjostheim, Sonja / Sanelli, Teresa / McLean, Jesse R / Horne, Patrick / Fan, Yuxin / Ravits, John / Strong, Michael J / Robertson, Janice

    The Journal of neuroscience : the official journal of the Society for Neuroscience

    2008  Band 28, Heft 8, Seite(n) 1833–1840

    Abstract: The neuronal intermediate filament protein peripherin is a component of ubiquitinated inclusions and of axonal spheroids in amyotrophic lateral sclerosis (ALS). Overexpression of peripherin causes motor neuron degeneration in transgenic mice and ... ...

    Abstract The neuronal intermediate filament protein peripherin is a component of ubiquitinated inclusions and of axonal spheroids in amyotrophic lateral sclerosis (ALS). Overexpression of peripherin causes motor neuron degeneration in transgenic mice and variations within the peripherin gene have been identified in ALS cases. We have shown previously the abnormal expression of a neurotoxic peripherin splice variant in transgenic mice expressing mutant superoxide dismutase-1. These findings indicated that abnormalities of peripherin splicing may occur in ALS. In the current study, peripherin splice variants were identified by reverse transcription-PCR of human neuronal RNA and comparisons in expression made between control and ALS spinal cord using Western blot analysis and immunocytochemistry. Using this approach we have identified a novel peripherin transcript retaining introns 3 and 4 that results in a 28 kDa splice isoform, designated Per 28. Using an antibody specific to Per 28, we show that this isoform is expressed at low stoichiometric levels from the peripherin gene, however causes peripherin aggregation when its expression is upregulated. Importantly we show an upregulation of Per 28 expression in ALS compared with controls, at both the mRNA and protein levels, and that Per 28 is associated with disease pathology, specifically round inclusions. These findings are the first to establish that peripherin splicing abnormalities occur in ALS, generating aggregation-prone splice isoforms.
    Mesh-Begriff(e) Adolescent ; Adult ; Aged ; Amyotrophic Lateral Sclerosis/genetics ; Amyotrophic Lateral Sclerosis/metabolism ; Amyotrophic Lateral Sclerosis/pathology ; Cell Line, Tumor ; Cells, Cultured ; Female ; Humans ; Intermediate Filament Proteins/biosynthesis ; Intermediate Filament Proteins/genetics ; Intermediate Filament Proteins/physiology ; Introns/physiology ; Male ; Membrane Glycoproteins/biosynthesis ; Membrane Glycoproteins/genetics ; Membrane Glycoproteins/physiology ; Middle Aged ; Nerve Tissue Proteins/biosynthesis ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/physiology ; Peripherins ; Protein Isoforms/biosynthesis ; Protein Isoforms/genetics ; Protein Isoforms/physiology ; Up-Regulation/genetics
    Chemische Substanzen Intermediate Filament Proteins ; Membrane Glycoproteins ; Nerve Tissue Proteins ; PRPH protein, human ; Peripherins ; Protein Isoforms
    Sprache Englisch
    Erscheinungsdatum 2008-02-20
    Erscheinungsland United States
    Dokumenttyp Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 604637-x
    ISSN 1529-2401 ; 0270-6474
    ISSN (online) 1529-2401
    ISSN 0270-6474
    DOI 10.1523/JNEUROSCI.3222-07.2008
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel: Mouse models of Alzheimer's disease: the long and filamentous road.

    Phinney, Amie L / Horne, Patrick / Yang, Jing / Janus, Chris / Bergeron, Catherine / Westaway, David

    Neurological research

    2003  Band 25, Heft 6, Seite(n) 590–600

    Abstract: Alzheimer's disease (AD) is characterized by memory impairment leading to dementia, deposition of amyloid plaques and neurofibrillary tangles (NFTs), and neuronal loss. The major component of plaques is the amyloid beta peptide, A beta, whereas NFTs ... ...

    Abstract Alzheimer's disease (AD) is characterized by memory impairment leading to dementia, deposition of amyloid plaques and neurofibrillary tangles (NFTs), and neuronal loss. The major component of plaques is the amyloid beta peptide, A beta, whereas NFTs contain hyperphosphorylated forms of the microtubule-associated protein tau (tau). Familial AD (FAD) mutations either elevate A beta synthesis by favoring 'secretase' of the Alzheimer beta-amyloid precursor protein (APP) or enhance the fibrillogenic properties of this peptide. Mutations in the tau gene cause a different disease denoted FTPD-17, but suggest that the aberrant forms of tau seen in AD are unlikely to be benign. These findings imply a complex pathogenic cascade in AD and important goals of transgenic modeling are to capture and stratify this pathogenic process. Several laboratories have created APP transgenic (Tg) mice that exhibit AD-like amyloid pathology and A beta burdens. These Tg lines also exhibit deficits in spatial reference and/or working memory, with immunization against A beta attenuating both AD-associated phenotypes. Tangle-like pathologies are observed in mice expressing FTPD-17 mutant forms of tau, but florid tau pathologies based upon the wild type (wt) tau isoforms present in AD have proven more elusive. Creation of animal models with robust amyloid and tau pathologies, yet free of irrelevant confounding pathologies, remains a major objective in this field.
    Mesh-Begriff(e) Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Alzheimer Disease/physiopathology ; Amyloid beta-Peptides/genetics ; Amyloid beta-Peptides/metabolism ; Animals ; Brain/metabolism ; Brain/pathology ; Brain/physiopathology ; Disease Models, Animal ; Humans ; Mice ; Mice, Transgenic ; Neurofibrillary Tangles/genetics ; Neurofibrillary Tangles/metabolism ; tau Proteins/genetics ; tau Proteins/metabolism
    Chemische Substanzen Amyloid beta-Peptides ; tau Proteins
    Sprache Englisch
    Erscheinungsdatum 2003-09
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 424428-x
    ISSN 1743-1328 ; 0161-6412
    ISSN (online) 1743-1328
    ISSN 0161-6412
    DOI 10.1179/016164103101202020
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel: Lack of TDP-43 abnormalities in mutant SOD1 transgenic mice shows disparity with ALS.

    Robertson, Janice / Sanelli, Teresa / Xiao, Shangxi / Yang, Wencheng / Horne, Patrick / Hammond, Robert / Pioro, Erik P / Strong, Michael J

    Neuroscience letters

    2007  Band 420, Heft 2, Seite(n) 128–132

    Abstract: Mislocalization of the TAR-DNA binding protein (TDP-43) from the nucleus to the cytoplasm of diseased motor neurons and association with intraneuronal ubiquitinated inclusions has recently been reported in amyotrophic lateral sclerosis (ALS). Here, we ... ...

    Abstract Mislocalization of the TAR-DNA binding protein (TDP-43) from the nucleus to the cytoplasm of diseased motor neurons and association with intraneuronal ubiquitinated inclusions has recently been reported in amyotrophic lateral sclerosis (ALS). Here, we have investigated TDP-43 immunoreactivity in three lines of mutant SOD1 transgenic mice, G93A, G37R and G85R and compared with labeling in one sporadic ALS case and two familial ALS cases carrying mutations in SOD1, A4T and I113T. Our findings show that there is no mislocalization of TDP-43 to the cytoplasm in motor neurons of mutant SOD1 transgenic mice, nor association of TDP-43 with ubiquitinated inclusions. In contrast, mislocalization of TDP-43 to the cytoplasm and association with ubiquitinated inclusions was found in the ALS cases, including those carrying mutations in SOD1. Interestingly, there was no association of TDP-43 with ubiquitinated hyaline conglomerate inclusions, pathology closely associated with ALS cases carrying mutations in SOD1. Our findings indicate that the process of motor neuron degeneration in mutant SOD1 transgenic mice is unlikely to involve the abnormalities of TDP-43 described in the human disease.
    Mesh-Begriff(e) Active Transport, Cell Nucleus/genetics ; Adult ; Amyotrophic Lateral Sclerosis/genetics ; Amyotrophic Lateral Sclerosis/metabolism ; Amyotrophic Lateral Sclerosis/physiopathology ; Animals ; Cell Nucleus/metabolism ; Cell Nucleus/pathology ; Cytoplasm/metabolism ; Cytoplasm/pathology ; DNA-Binding Proteins/genetics ; Disease Models, Animal ; Disease Progression ; Genetic Predisposition to Disease/genetics ; Humans ; Inclusion Bodies/genetics ; Inclusion Bodies/metabolism ; Male ; Mice ; Mice, Transgenic ; Motor Neurons/metabolism ; Motor Neurons/pathology ; Mutation/genetics ; Nerve Degeneration/genetics ; Nerve Degeneration/metabolism ; Nerve Degeneration/physiopathology ; Protein Transport/genetics ; Superoxide Dismutase/genetics ; Superoxide Dismutase-1
    Chemische Substanzen DNA-Binding Proteins ; SOD1 protein, human ; Sod1 protein, mouse (EC 1.15.1.1) ; Superoxide Dismutase (EC 1.15.1.1) ; Superoxide Dismutase-1 (EC 1.15.1.1)
    Sprache Englisch
    Erscheinungsdatum 2007-06-13
    Erscheinungsland Ireland
    Dokumenttyp Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 194929-9
    ISSN 1872-7972 ; 0304-3940
    ISSN (online) 1872-7972
    ISSN 0304-3940
    DOI 10.1016/j.neulet.2007.03.066
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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