John K Fink

Summary

Affiliation: University of Michigan
Country: USA

Publications

  1. doi request reprint Hereditary spastic paraplegia: clinico-pathologic features and emerging molecular mechanisms
    John K Fink
    Department of Neurology, University of Michigan and Geriatric Research Education and Clinical Center, Ann Arbor Veterans Affairs Medical Center, 5014 BSRB, 109 Zina Pitcher Place, Ann Arbor, MI 48109 2200, USA
    Acta Neuropathol 126:307-28. 2013
  2. ncbi request reprint Hereditary spastic paraplegia
    John K Fink
    Department of Neurology, University of Michigan and the Geriatric Research Education and Clinical Care Center of the Ann Arbor Veterans Affairs Medical Center, Ann Arbor, MI 48109 0940, USA
    Curr Neurol Neurosci Rep 6:65-76. 2006
  3. ncbi request reprint Advances in the hereditary spastic paraplegias
    John K Fink
    Department of Neurology, University of Michigan and Geriatric Research Education and Clinical Center, Ann Arbor Veterans Affairs Medical Center, Ann Arbor, MI, USA
    Exp Neurol 184:S106-10. 2003
  4. ncbi request reprint The hereditary spastic paraplegias: nine genes and counting
    John K Fink
    Department of Neurology, University of Michigan, 5214 Cancer Geriatrics Center Bldg, Box 0940, 1500 E Medical Center Drive, Ann Arbor, MI 48109, USA
    Arch Neurol 60:1045-9. 2003
  5. ncbi request reprint Hereditary spastic paraplegia
    John K Fink
    Department of Neurology, University of Michigan, Geriatric Research Education and Care Center, Ann Arbor Veterans Affairs Medical Center, Ann Arbor, MI, USA
    Neurol Clin 20:711-26. 2002
  6. doi request reprint Treatment of Wilson's disease with tetrathiomolybdate: V. Control of free copper by tetrathiomolybdate and a comparison with trientine
    George J Brewer
    Department of Human Genetics, University of Michigan, Ann Arbor, MI, USA
    Transl Res 154:70-7. 2009
  7. doi request reprint Motor neuron disease due to neuropathy target esterase gene mutation: clinical features of the index families
    Shirley Rainier
    Department of Neurology, University of Michigan, 5013 BSRB, 109 Zina Pitcher Place, Ann Arbor, Michigan 48109, USA
    Muscle Nerve 43:19-25. 2011
  8. pmc Neuropathy target esterase gene mutations cause motor neuron disease
    Shirley Rainier
    Department of Neurology, University of Michigan, Ann Arbor, MI 48109, USA
    Am J Hum Genet 82:780-5. 2008
  9. doi request reprint Motor neuron disease due to neuropathy target esterase mutation: enzyme analysis of fibroblasts from human subjects yields insights into pathogenesis
    Nichole D Hein
    Department of Neurology, University of Michigan, Ann Arbor, MI 48109, USA
    Toxicol Lett 199:1-5. 2010
  10. doi request reprint Neuropathy target esterase (NTE): overview and future
    Rudy J Richardson
    Toxicology Program, University of Michigan, Ann Arbor, MI 48109 2029, USA
    Chem Biol Interact 203:238-44. 2013

Collaborators

Detail Information

Publications26

  1. doi request reprint Hereditary spastic paraplegia: clinico-pathologic features and emerging molecular mechanisms
    John K Fink
    Department of Neurology, University of Michigan and Geriatric Research Education and Clinical Center, Ann Arbor Veterans Affairs Medical Center, 5014 BSRB, 109 Zina Pitcher Place, Ann Arbor, MI 48109 2200, USA
    Acta Neuropathol 126:307-28. 2013
    ..elegans) for many types of HSP permits exploration of disease mechanisms and potential treatments. This review highlights emerging concepts of this large group of clinically similar disorders...
  2. ncbi request reprint Hereditary spastic paraplegia
    John K Fink
    Department of Neurology, University of Michigan and the Geriatric Research Education and Clinical Care Center of the Ann Arbor Veterans Affairs Medical Center, Ann Arbor, MI 48109 0940, USA
    Curr Neurol Neurosci Rep 6:65-76. 2006
    ..Prenatal genetic testing in HSP is possible for some individuals with the increasing availability of HSP gene analysis...
  3. ncbi request reprint Advances in the hereditary spastic paraplegias
    John K Fink
    Department of Neurology, University of Michigan and Geriatric Research Education and Clinical Center, Ann Arbor Veterans Affairs Medical Center, Ann Arbor, MI, USA
    Exp Neurol 184:S106-10. 2003
    ..Twenty HSP loci and nine HSP genes have been discovered. This progress has yielded new insights into the diverse molecular pathogenesis that underlies these clinically similar disorders...
  4. ncbi request reprint The hereditary spastic paraplegias: nine genes and counting
    John K Fink
    Department of Neurology, University of Michigan, 5214 Cancer Geriatrics Center Bldg, Box 0940, 1500 E Medical Center Drive, Ann Arbor, MI 48109, USA
    Arch Neurol 60:1045-9. 2003
    ..Insights into the molecular causes of HSPs are beginning to emerge. This review summarizes these advances in HSPs' genetics...
  5. ncbi request reprint Hereditary spastic paraplegia
    John K Fink
    Department of Neurology, University of Michigan, Geriatric Research Education and Care Center, Ann Arbor Veterans Affairs Medical Center, Ann Arbor, MI, USA
    Neurol Clin 20:711-26. 2002
    ..Nonetheless, the identification of these genes and the ability to generate animal models of these forms of HSP will permit direct exploration of the molecular basis of HSP...
  6. doi request reprint Treatment of Wilson's disease with tetrathiomolybdate: V. Control of free copper by tetrathiomolybdate and a comparison with trientine
    George J Brewer
    Department of Human Genetics, University of Michigan, Ann Arbor, MI, USA
    Transl Res 154:70-7. 2009
    ..Tetrathiomolybdate controlled copper less well in the dose regimen study (study 3) than in the previous 2 studies of tetrathiomolybdate treatment, probably because of a change in the way "away from food" tetrathiomolybdate was given...
  7. doi request reprint Motor neuron disease due to neuropathy target esterase gene mutation: clinical features of the index families
    Shirley Rainier
    Department of Neurology, University of Michigan, 5013 BSRB, 109 Zina Pitcher Place, Ann Arbor, Michigan 48109, USA
    Muscle Nerve 43:19-25. 2011
    ..Motor neuron degeneration in subjects with NTE mutations supports the role of NTE and its biochemical cascade in the molecular pathogenesis of OPIDN and possibly other degenerative neurologic disorders...
  8. pmc Neuropathy target esterase gene mutations cause motor neuron disease
    Shirley Rainier
    Department of Neurology, University of Michigan, Ann Arbor, MI 48109, USA
    Am J Hum Genet 82:780-5. 2008
    ....
  9. doi request reprint Motor neuron disease due to neuropathy target esterase mutation: enzyme analysis of fibroblasts from human subjects yields insights into pathogenesis
    Nichole D Hein
    Department of Neurology, University of Michigan, Ann Arbor, MI 48109, USA
    Toxicol Lett 199:1-5. 2010
    ....
  10. doi request reprint Neuropathy target esterase (NTE): overview and future
    Rudy J Richardson
    Toxicology Program, University of Michigan, Ann Arbor, MI 48109 2029, USA
    Chem Biol Interact 203:238-44. 2013
    ....
  11. ncbi request reprint De novo occurrence of novel SPG3A/atlastin mutation presenting as cerebral palsy
    Shirley Rainier
    Department of Neurology, University of Michigan, Ann Arbor, USA
    Arch Neurol 63:445-7. 2006
    ..Such subjects resemble those with spastic diplegic cerebral palsy. To date, only 9 SPG3A mutations have been reported...
  12. doi request reprint Constructs of human neuropathy target esterase catalytic domain containing mutations related to motor neuron disease have altered enzymatic properties
    Nichole D Hein
    Department of Neurology, University of Michigan, Ann Arbor, MI 48109 2029, USA
    Toxicol Lett 196:67-73. 2010
    ..Taken together, the results from specific activity, inhibition, and aging experiments suggest that the mutations found in association with NTE-MND have functional correlates in altered enzymological properties of NTE...
  13. pmc Normal dopaminergic nigrostriatal innervation in SPG3A hereditary spastic paraplegia
    Roger L Albin
    Geriatrics Research, Education, and Clinical Center, Ann Arbor VAHS, Ann Arbor, Michigan 48109 2200, USA
    J Neurogenet 22:289-94. 2008
    ..This major difference between human SPG3A/atlastin-1 mutations and the Drosophila atl(l) phenotype has several possible explanations...
  14. doi request reprint Myelopolyneuropathy and pancytopenia due to copper deficiency and high zinc levels of unknown origin II. The denture cream is a primary source of excessive zinc
    Peter Hedera
    Department of Neurology, Vanderbilt University, Nashville, TN 37232 8552, USA
    Neurotoxicology 30:996-9. 2009
    ..Their copper and zinc normalized after stopping denture cream, further confirming that this is the source of high zinc. Inappropriate use of denture cream appears to be the sole source of excessive zinc in these patients...
  15. ncbi request reprint Porphyric neuropathy
    James W Albers
    Department of Neurology, 1C325 0032 University Hospital, University of Michigan Health System, 1500 East Medical Center Drive, Ann Arbor 48109 0032, USA
    Muscle Nerve 30:410-22. 2004
    ..The severity of the neuropathy and the availability of potential treatments, including avoidance of provocative factors, make identification important...
  16. ncbi request reprint Treatment of Wilson disease with ammonium tetrathiomolybdate: III. Initial therapy in a total of 55 neurologically affected patients and follow-up with zinc therapy
    George J Brewer
    Department of Human Genetics, University of Michigan Medical School, 4909 Buhl, Ann Arbor, MI 48109 0618, USA
    Arch Neurol 60:379-85. 2003
    ..It is unclear what anticopper drug to use for patients with Wilson disease who present with neurologic manifestations because penicillamine often makes them neurologically worse and zinc is slow acting...
  17. ncbi request reprint Cerebrotendinous xanthomatosis: possible higher prevalence than previously recognized
    Matthew T Lorincz
    Department of Neurology, University of Michigan, Ann Arbor, 48109, USA
    Arch Neurol 62:1459-63. 2005
    ..Cerebrotendinous xanthomatosis (CTX) is a rare but treatable neurodegenerative disorder caused by 27-sterol hydroxylase (CYP27) deficiency...
  18. ncbi request reprint Motor neuron disease due to neuropathy target esterase gene mutation: Clinical features of the index families
    Shirley Rainier
    Department of Neurology, University of Michigan, 5013 BSRB, 109 Zina Pitcher Place, Ann Arbor, Michigan 48109, USA
    Muscle Nerve 43:19-25. 2011
    ..Motor neuron degeneration in subjects with NTE mutations supports the role of NTE and its biochemical cascade in the molecular pathogenesis of OPIDN and possibly other degenerative neurologic disorders. Muscle Nerve, 2011...
  19. ncbi request reprint Myofibrillogenesis regulator 1 gene mutations cause paroxysmal dystonic choreoathetosis
    Shirley Rainier
    Department of Neurology, University of Michigan, Ann Arbor, MI 48109, USA
    Arch Neurol 61:1025-9. 2004
    ..Previously, we and others identified a locus for autosomal dominant PDC on chromosome 2q33-2q35...
  20. ncbi request reprint Treatment of Wilson disease with ammonium tetrathiomolybdate: IV. Comparison of tetrathiomolybdate and trientine in a double-blind study of treatment of the neurologic presentation of Wilson disease
    George J Brewer
    Department of Human Genetics, University of Michigan Medical School, 5024 Kresge Bldg II, Ann Arbor, MI 48109 0534, USA
    Arch Neurol 63:521-7. 2006
    ..To compare tetrathiomolybdate and trientine in treating patients with the neurologic presentation of Wilson disease for the frequency of neurologic worsening, adverse effects, and degree of neurologic recovery...
  21. pmc NIPA1 gene mutations cause autosomal dominant hereditary spastic paraplegia (SPG6)
    Shirley Rainier
    Department of Neurology, University of Michigan, Ann Arbor, MI 48109, USA
    Am J Hum Genet 73:967-71. 2003
    ..Identification of the NIPA1 function and ligand will aid an understanding of axonal neurodegeneration in HSP and may have important therapeutic implications...
  22. ncbi request reprint Myelopolyneuropathy and pancytopenia due to copper deficiency and high zinc levels of unknown origin: further support for existence of a new zinc overload syndrome
    Peter Hedera
    Department of Neurology, University of Michigan, Ann Arbor, USA
    Arch Neurol 60:1303-6. 2003
    ..To describe a patient with idiopathic zinc overload without an identifiable source and secondary copper deficiency causing myelopolyneuropathy and pancytopenia...
  23. ncbi request reprint The second kindred with autosomal dominant distal myopathy linked to chromosome 14q: genetic and clinical analysis
    Peter Hedera
    Department of Neurology, University of Michigan Medical Center, Ann Arbor, USA
    Arch Neurol 60:1321-5. 2003
    ..Genetic causes within this subgroup of muscle disorders remain largely unknown. An MPD linked to chromosome 14q11-q13 (MPD1) is rare, and to our knowledge, only one family with definitive linkage has been described...
  24. ncbi request reprint White matter changes in Wilson disease
    Peter Hedera
    Department of Neurology, University of Michigan Medical Center, Ann Arbor, Mich 48109 0940, USA
    Arch Neurol 59:866-7. 2002
  25. ncbi request reprint Hereditary spastic paraplegia: the pace quickens
    John K Fink
    Ann Neurol 51:669-72. 2002
  26. ncbi request reprint Hereditary spastic paraplegia: spastin phenotype and function
    John K Fink
    Arch Neurol 61:830-3. 2004

Research Grants21

  1. Paroxysmal dystonic choreoathetosis
    John Fink; Fiscal Year: 2003
    ..abstract_text> ..
  2. Hereditary Spastic Paraplegia due to SPG3A/atlastin mutation
    John Fink; Fiscal Year: 2007
    ....
  3. International Symposium for Hereditary Spastic Paraplegia
    John Fink; Fiscal Year: 2007
    ....
  4. HEREDITARY SPASTIC PARAPLEGIA--CLINICAL, HISTOCHEMICAL,
    John Fink; Fiscal Year: 2001
    ..abstract_text> ..
  5. Hereditary Spastic Paraplegia due to SPG3A/atlastin mutation
    John Fink; Fiscal Year: 2009
    ....