Clifford W Shults

Summary

Affiliation: University of California
Country: USA

Publications

  1. ncbi Potential outcome measures and trial design issues for multiple system atrophy
    Susanne May
    Department of Family and Preventive Medicine, University of California, San Diego, La Jolla, California 92093 0717, USA
    Mov Disord 22:2371-7. 2007
  2. ncbi Antioxidants as therapy for Parkinson's disease
    Clifford W Shults
    Department of Neurosciences, University of California, San Diego, La Jolla, CA 92093, USA
    Antioxid Redox Signal 7:694-700. 2005
  3. ncbi Pilot trial of high dosages of coenzyme Q10 in patients with Parkinson's disease
    Clifford W Shults
    Department of Neurosciences, University of California, San Diego, La Jolla 92093 0662, USA
    Exp Neurol 188:491-4. 2004
  4. ncbi Therapeutic role of coenzyme Q(10) in Parkinson's disease
    Clifford W Shults
    Department of Neurosciences, University of California San Diego, La Jolla, CA 92093, USA
    Pharmacol Ther 107:120-30. 2005
  5. ncbi Lewy bodies
    Clifford W Shults
    Department of Neurosciences, University of California at San Diego, La Jolla, CA 92093, USA
    Proc Natl Acad Sci U S A 103:1661-8. 2006
  6. ncbi Treatments of Parkinson disease: circa 2003
    Clifford W Shults
    Department of Neurosciences, University of California, San Diego, La Jolla, California 92161, USA
    Arch Neurol 60:1680-4. 2003
  7. ncbi Clinical trials of coenzyme Q10 in neurological disorders
    Clifford W Shults
    Department of Neurosciences, University of California, San Diego, La Jolla, 92093, USA
    Biofactors 25:117-26. 2005
  8. ncbi Coenzyme Q10 in neurodegenerative diseases
    Clifford W Shults
    Department of Neurosciences, University of California, San Diego, La Jolla, CA 92093 0662, USA
    Curr Med Chem 10:1917-21. 2003
  9. ncbi Effects of coenzyme Q10 in early Parkinson disease: evidence of slowing of the functional decline
    Clifford W Shults
    Department of Neurosciences, Mail Code 0662, University of California San Diego, 9500 Gilman Dr, La Jolla, CA 92093 0662, USA
    Arch Neurol 59:1541-50. 2002
  10. ncbi alpha-synuclein from platelets is not phosphorylated at serine 129 in Parkinson's disease and multiple system atrophy
    Clifford W Shults
    Department of Neurosciences, University of California, San Diego, La Jolla, CA 92093 0662, USA
    Neurosci Lett 405:223-5. 2006

Detail Information

Publications30

  1. ncbi Potential outcome measures and trial design issues for multiple system atrophy
    Susanne May
    Department of Family and Preventive Medicine, University of California, San Diego, La Jolla, California 92093 0717, USA
    Mov Disord 22:2371-7. 2007
    ..The UMSARS Motor Examination score exhibited the most favorable characteristics as an outcome measure for a therapeutic trial in MSA with 1 year of follow-up...
  2. ncbi Antioxidants as therapy for Parkinson's disease
    Clifford W Shults
    Department of Neurosciences, University of California, San Diego, La Jolla, CA 92093, USA
    Antioxid Redox Signal 7:694-700. 2005
  3. ncbi Pilot trial of high dosages of coenzyme Q10 in patients with Parkinson's disease
    Clifford W Shults
    Department of Neurosciences, University of California, San Diego, La Jolla 92093 0662, USA
    Exp Neurol 188:491-4. 2004
    ..Our data suggest that in future studies of coenzyme Q10 in PD, a dosage of 2400 mg/day (with vitamin E/alpha-tocopherol 1200 IU/day) is an appropriate highest dosage to be studied...
  4. ncbi Therapeutic role of coenzyme Q(10) in Parkinson's disease
    Clifford W Shults
    Department of Neurosciences, University of California San Diego, La Jolla, CA 92093, USA
    Pharmacol Ther 107:120-30. 2005
    ..A phase II trial of coenzyme Q(10) in patients with early, untreated PD demonstrated a positive trend for coenzyme Q(10) to slow progressive disability that occurs in PD...
  5. ncbi Lewy bodies
    Clifford W Shults
    Department of Neurosciences, University of California at San Diego, La Jolla, CA 92093, USA
    Proc Natl Acad Sci U S A 103:1661-8. 2006
    ....
  6. ncbi Treatments of Parkinson disease: circa 2003
    Clifford W Shults
    Department of Neurosciences, University of California, San Diego, La Jolla, California 92161, USA
    Arch Neurol 60:1680-4. 2003
    ....
  7. ncbi Clinical trials of coenzyme Q10 in neurological disorders
    Clifford W Shults
    Department of Neurosciences, University of California, San Diego, La Jolla, 92093, USA
    Biofactors 25:117-26. 2005
  8. ncbi Coenzyme Q10 in neurodegenerative diseases
    Clifford W Shults
    Department of Neurosciences, University of California, San Diego, La Jolla, CA 92093 0662, USA
    Curr Med Chem 10:1917-21. 2003
    ....
  9. ncbi Effects of coenzyme Q10 in early Parkinson disease: evidence of slowing of the functional decline
    Clifford W Shults
    Department of Neurosciences, Mail Code 0662, University of California San Diego, 9500 Gilman Dr, La Jolla, CA 92093 0662, USA
    Arch Neurol 59:1541-50. 2002
    ..Parkinson disease (PD) is a degenerative neurological disorder for which no treatment has been shown to slow the progression...
  10. ncbi alpha-synuclein from platelets is not phosphorylated at serine 129 in Parkinson's disease and multiple system atrophy
    Clifford W Shults
    Department of Neurosciences, University of California, San Diego, La Jolla, CA 92093 0662, USA
    Neurosci Lett 405:223-5. 2006
    ..Immunoblots indicated that platelet alpha-synuclein is not phosphorylated at serine 129 in PD and MSA...
  11. ncbi Dopamine depletion induced up-regulation of HCN3 enhances rebound excitability of basal ganglia output neurons
    Bernhard H Meurers
    Department of Neurology, University of California, Los Angeles, 710 Westwood Plaza, Los Angeles, CA 90095, USA
    Neurobiol Dis 34:178-88. 2009
    ..These data establish HCN3 up-regulation as a novel candidate mechanism that might contribute to the in vivo changes of electrical activity in basal ganglia output neurons of the parkinsonian brain...
  12. ncbi Neurological and neurodegenerative alterations in a transgenic mouse model expressing human alpha-synuclein under oligodendrocyte promoter: implications for multiple system atrophy
    Clifford W Shults
    Department of Neurosciences, University of California, San Diego, La Jolla, California 92093 0624, USA
    J Neurosci 25:10689-99. 2005
    ..Together, these studies support the contention that accumulation of alpha-syn in oligodendrocytes promotes neurodegeneration and recapitulates several of the key functional and neuropathological features of MSA...
  13. ncbi Enhanced substantia nigra mitochondrial pathology in human alpha-synuclein transgenic mice after treatment with MPTP
    David D Song
    Neurology Service, VA San Diego Healthcare System, San Diego, CA 92161 9127, USA
    Exp Neurol 186:158-72. 2004
    ..These findings support the potential involvement of alpha-S expression in the vulnerability of SN neurons to toxicity from mitochondrial complex I inhibitors and the subsequent development of neurodegenerative pathology...
  14. ncbi Dopamine depletion induces distinct compensatory gene expression changes in DARPP-32 signal transduction cascades of striatonigral and striatopallidal neurons
    Bernhard H Meurers
    Department of Neurology, The David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California 90095, USA
    J Neurosci 29:6828-39. 2009
    ..In addition, the data have potential implications for the symptomatic treatment of the disease...
  15. ncbi Alpha-synuclein overexpression in oligodendrocytic cells results in impaired adhesion to fibronectin and cell death
    Kyoko Tsuboi
    Department of Neurosciences, University of California, San Diego, La Jolla, CA 92093, USA
    Mol Cell Neurosci 29:259-68. 2005
    ..It may, therefore, be one of the mechanisms underlying the loss of oligodendrocytes in MSA...
  16. ncbi The adult substantia nigra contains progenitor cells with neurogenic potential
    D Chichung Lie
    Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, California 92037, USA
    J Neurosci 22:6639-49. 2002
    ..This developmental potential of SN progenitor cells might be useful for future endogenous cell replacement strategies in Parkinson's disease...
  17. ncbi Differential neuropathological alterations in transgenic mice expressing alpha-synuclein from the platelet-derived growth factor and Thy-1 promoters
    Edward Rockenstein
    Department of Neurosciences, University of California San Diego, La Jolla, California 92093-0624, USA
    J Neurosci Res 68:568-78. 2002
    ....
  18. ncbi Intrastriatal injection of sonic hedgehog reduces behavioral impairment in a rat model of Parkinson's disease
    Kyoko Tsuboi
    Department of Neurosciences, University of California, San Diego, La Jolla, California 92093, USA
    Exp Neurol 173:95-104. 2002
    ..This is the first demonstration in vivo that Shh reduces behavioral deficits induced by intrastriatal 6-OHDA lesion and suggests that Shh may be useful in the treatment of disorders that affect the nigrostriatal system, such as PD...
  19. ncbi Measuring the effects of therapy in Parkinson disease
    Clifford W Shults
    JAMA 291:2430-1; author reply 2431. 2004
  20. ncbi Effects of Coenzyme Q10 in Huntington's disease and early Parkinson's disease
    M Flint Beal
    Department of Neurology and Neuroscience, New York Presbyterian Hospital, New York, NY 10021, USA
    Biofactors 18:153-61. 2003
  21. ncbi Reexamination of the TEMPO Study
    Clifford W Shults
    Arch Neurol 62:1320; author reply 1321. 2005
  22. ncbi Presence of an APOE4 allele results in significantly earlier onset of Parkinson's disease and a higher risk with dementia
    Nathan Pankratz
    Department of Medical and Molecular Genetics, Indiana University Medical Center, Indianapolis, Indiana, USA
    Mov Disord 21:45-9. 2006
    ..It appears the similarities between PD and AD may be due to an overlap in the diseases' genetic etiology...
  23. ncbi Development and validation of the Unified Multiple System Atrophy Rating Scale (UMSARS)
    Gregor K Wenning
    Department of Neurology, University of Innsbruck, Austria
    Mov Disord 19:1391-402. 2004
    ..Based on our findings, the UMSARS appears to be a multidimensional, reliable, and valid scale for semiquantitative clinical assessments of MSA patients...
  24. ncbi Evaluation of the role of Nurr1 in a large sample of familial Parkinson's disease
    William C Nichols
    Division of Human Genetics, Cincinnati Children s Hospital Medical Center, Cincinnati, Ohio 45229, USA
    Mov Disord 19:649-55. 2004
    ..Taken together, these data suggest that genetic alteration at the Nurr1 locus is not a significant risk factor for the development of Parkinson's disease in our large sample of familial PD patients...
  25. ncbi G2019S mutation in the leucine-rich repeat kinase 2 gene is not associated with multiple system atrophy
    Laurie J Ozelius
    Department of Molecular Genetics, Albert Einstein College of Medicine, Bronx, New York, USA
    Mov Disord 22:546-9. 2007
    ..We conclude that the G2019S mutation in the LRRK2 gene is unlikely to be associated with MSA...
  26. ncbi R1514Q substitution in Lrrk2 is not a pathogenic Parkinson's disease mutation
    William C Nichols
    Division of Human Genetics, Cincinnati Children s Hospital Medical Center, Cincinnati, Ohio 45229, USA
    Mov Disord 22:254-7. 2007
    ..We believe it is imperative that the causative nature of any newly identified genetic variant be determined before it is included in any panel for diagnostic testing...
  27. ncbi Mutations in LRRK2 other than G2019S are rare in a north American-based sample of familial Parkinson's disease
    Nathan Pankratz
    Indiana University Medical Center, Indianapolis, Indiana, USA
    Mov Disord 21:2257-60. 2006
    ..These results indicate that, although the G2019S mutation remains the most common mutation identified in familial PD patients, other mutations in LRRK2 are infrequent...
  28. ncbi Mutations in DJ-1 are rare in familial Parkinson disease
    Nathan Pankratz
    Indiana University Medical Center, Indianapolis, IN, USA
    Neurosci Lett 408:209-13. 2006
    ..No additional missense mutations and no exon deletions or duplications were detected. Our results, in combination with those of previous studies, suggest that alterations in DJ-1 are not a common cause of familial PD...
  29. ncbi Genome-wide linkage analysis and evidence of gene-by-gene interactions in a sample of 362 multiplex Parkinson disease families
    Nathan Pankratz
    Indiana University School of Medicine, Department of Medical and Molecular Genetics IB 130, 975 West Walnut Street, Indianapolis, IN 46202 5251, USA
    Hum Mol Genet 12:2599-608. 2003
    ..4) and X (LOD=3.2). These findings demonstrate consistent evidence of linkage to chromosomes 2 and X and also support the hypothesis that gene-by-gene interactions are important in PD susceptibility...
  30. ncbi Genetic screening for a single common LRRK2 mutation in familial Parkinson's disease
    William C Nichols
    Division of Human Genetics, Cincinnati Children s Hospital Medical Center, Cincinnati, OH 45229, USA
    Lancet 365:410-2. 2005
    ..Thus, our results suggest that a single LRRK2 mutation causes Parkinson's disease in 5% of individuals with familial disease. Screening for this mutation should be a component of genetic testing for Parkinson's disease...