Michael Strong

Summary

Affiliation: University of Western Ontario
Country: Canada

Publications

  1. ncbi request reprint Consensus criteria for the diagnosis of frontotemporal cognitive and behavioural syndromes in amyotrophic lateral sclerosis
    Michael J Strong
    Department of Clinical Neurological Sciences, The University of Western Ontario, London, Ontario, Canada
    Amyotroph Lateral Scler 10:131-46. 2009
  2. pmc Transient middle cerebral artery occlusion induces microglial priming in the lumbar spinal cord: a novel model of neuroinflammation
    Katie Moisse
    Cell Biology Research Group, Robarts Research Institute, London, Ontario, Canada
    J Neuroinflammation 5:29. 2008
  3. ncbi request reprint The basic aspects of therapeutics in amyotrophic lateral sclerosis
    Michael J Strong
    Department of Clinical Neurological Sciences, Robarts Research Institute, Room 7OF 10, University Campus, London Health Sciences Centre, University of Western Ontario, 339 Windermere Road, London, Ontario, Canada N6A 5A5
    Pharmacol Ther 98:379-414. 2003
  4. ncbi request reprint The pathobiology of amyotrophic lateral sclerosis: a proteinopathy?
    Michael J Strong
    Robarts Research Institute, Department of Clinical Neurological Sciences, The University of Western Ontario, London, Canada
    J Neuropathol Exp Neurol 64:649-64. 2005
  5. ncbi request reprint Primary lateral sclerosis, hereditary spastic paraplegia and amyotrophic lateral sclerosis: discrete entities or spectrum?
    Michael J Strong
    Department of Clinical Neurological Sciences, The University of Western Ontario, The Cell Biology Research Group, Roberts Research Institute, London, Ontario, Canada
    Amyotroph Lateral Scler Other Motor Neuron Disord 6:8-16. 2005
  6. ncbi request reprint Amyotrophic lateral sclerosis: contemporary concepts in etiopathogenesis and pharmacotherapy
    Michael J Strong
    Department of Clinical Neurological Sciences, University of Western Ontario, The Robarts Research Institute, London, Canada
    Expert Opin Investig Drugs 13:1593-614. 2004
  7. doi request reprint The evidence for altered RNA metabolism in amyotrophic lateral sclerosis (ALS)
    Michael J Strong
    Molecular Brain Research Group, Robarts Research Institute, London, Ontario, Canada
    J Neurol Sci 288:1-12. 2010
  8. ncbi request reprint TDP43 is a human low molecular weight neurofilament (hNFL) mRNA-binding protein
    Michael J Strong
    Cell Biology Research Group, Robarts Research Institute, London, Ontario, Canada
    Mol Cell Neurosci 35:320-7. 2007
  9. ncbi request reprint Intermediate filament steady-state mRNA levels in amyotrophic lateral sclerosis
    Michael J Strong
    Cell Biology Research Group, Robarts Research Institute, London, Ont, Canada
    Biochem Biophys Res Commun 316:317-22. 2004
  10. ncbi request reprint In vitro reactive nitrating species toxicity in dissociated spinal motor neurons from NFL (-/-) and hNFL (+/+) transgenic mice
    Michael Strong
    Cell Biology Research Group, Robarts Research Institute, London, Ontario, Canada
    Amyotroph Lateral Scler Other Motor Neuron Disord 4:81-9. 2003

Collaborators

Detail Information

Publications43

  1. ncbi request reprint Consensus criteria for the diagnosis of frontotemporal cognitive and behavioural syndromes in amyotrophic lateral sclerosis
    Michael J Strong
    Department of Clinical Neurological Sciences, The University of Western Ontario, London, Ontario, Canada
    Amyotroph Lateral Scler 10:131-46. 2009
    ....
  2. pmc Transient middle cerebral artery occlusion induces microglial priming in the lumbar spinal cord: a novel model of neuroinflammation
    Katie Moisse
    Cell Biology Research Group, Robarts Research Institute, London, Ontario, Canada
    J Neuroinflammation 5:29. 2008
    ..Following permanent occlusion, neuropathological changes - including a robust glial inflammatory response - also occur downstream of the infarct in the spinal cord...
  3. ncbi request reprint The basic aspects of therapeutics in amyotrophic lateral sclerosis
    Michael J Strong
    Department of Clinical Neurological Sciences, Robarts Research Institute, Room 7OF 10, University Campus, London Health Sciences Centre, University of Western Ontario, 339 Windermere Road, London, Ontario, Canada N6A 5A5
    Pharmacol Ther 98:379-414. 2003
    ..Designing pharmacological strategies to mitigate against this process thus becomes an increasingly complex issue, which is reviewed in this article...
  4. ncbi request reprint The pathobiology of amyotrophic lateral sclerosis: a proteinopathy?
    Michael J Strong
    Robarts Research Institute, Department of Clinical Neurological Sciences, The University of Western Ontario, London, Canada
    J Neuropathol Exp Neurol 64:649-64. 2005
    ..The role of nonneuronal cells in mediating motor neuronal injury is discussed in the context of alterations in tyrosine kinase activity and enhanced protein phosphorylation...
  5. ncbi request reprint Primary lateral sclerosis, hereditary spastic paraplegia and amyotrophic lateral sclerosis: discrete entities or spectrum?
    Michael J Strong
    Department of Clinical Neurological Sciences, The University of Western Ontario, The Cell Biology Research Group, Roberts Research Institute, London, Ontario, Canada
    Amyotroph Lateral Scler Other Motor Neuron Disord 6:8-16. 2005
    ..Only through the development and application of exacting clinical diagnostic criteria to epidemiological studies, along with greater numbers of post-mortem examinations, however, will these questions be answered fully...
  6. ncbi request reprint Amyotrophic lateral sclerosis: contemporary concepts in etiopathogenesis and pharmacotherapy
    Michael J Strong
    Department of Clinical Neurological Sciences, University of Western Ontario, The Robarts Research Institute, London, Canada
    Expert Opin Investig Drugs 13:1593-614. 2004
    ..This review will highlight recent epidemiological and neurochemical advances in our understanding of ALS, and place them into the context of understanding the development of novel treatment avenues for this devastating disease...
  7. doi request reprint The evidence for altered RNA metabolism in amyotrophic lateral sclerosis (ALS)
    Michael J Strong
    Molecular Brain Research Group, Robarts Research Institute, London, Ontario, Canada
    J Neurol Sci 288:1-12. 2010
    ..These observations lead directly to the hypothesis that ALS can be viewed as a disorder of RNA metabolism, thus providing a novel pathway for the development of molecular pharmacotherapies...
  8. ncbi request reprint TDP43 is a human low molecular weight neurofilament (hNFL) mRNA-binding protein
    Michael J Strong
    Cell Biology Research Group, Robarts Research Institute, London, Ontario, Canada
    Mol Cell Neurosci 35:320-7. 2007
    ..TDP43 is a unique hNFL mRNA-binding protein that is altered in its somatotopic localization in ALS spinal motor neurons and potentially contributes to the formation of NF aggregates in ALS through alterations in NF stoichiometry...
  9. ncbi request reprint Intermediate filament steady-state mRNA levels in amyotrophic lateral sclerosis
    Michael J Strong
    Cell Biology Research Group, Robarts Research Institute, London, Ont, Canada
    Biochem Biophys Res Commun 316:317-22. 2004
    ..These findings suggest that disturbances in both NFL and peripherin expression, independently known to contribute to the generation of motor neuron dysfunction in transgenic mice, are evident in ALS...
  10. ncbi request reprint In vitro reactive nitrating species toxicity in dissociated spinal motor neurons from NFL (-/-) and hNFL (+/+) transgenic mice
    Michael Strong
    Cell Biology Research Group, Robarts Research Institute, London, Ontario, Canada
    Amyotroph Lateral Scler Other Motor Neuron Disord 4:81-9. 2003
    ..These observations suggest that NFL deficient motor neurons are at an enhanced risk of cell death mediated by RNS...
  11. ncbi request reprint Amyotrophic lateral sclerosis: a review of current concepts
    Michael Strong
    The Department of Clinical Neurological Sciences, The University of Western Ontario, London, Canada
    Amyotroph Lateral Scler Other Motor Neuron Disord 4:136-43. 2003
    ..Significant advances in both symptomatic and adjunctive therapy have resulted in prolonged quality and duration of life...
  12. ncbi request reprint Tau protein hyperphosphorylation in sporadic ALS with cognitive impairment
    M J Strong
    Cell Biology Research Group, Robart s Research Institute, London, Ontario, Canada
    Neurology 66:1770-1. 2006
    ..Soluble tau from both AD and ALSci was also phosphorylated at S237. Tau hyperphosphorylation is associated with ALS...
  13. ncbi request reprint NMDA induces NOS 1 translocation to the cell membrane in NGF-differentiated PC 12 cells
    Mark Arundine
    The Department of Pathology, The University of Western Ontario, Rm 7 OF 10, UC LHSC, 339 Windermere Road, London, N6A 5C1, Ontario, Canada
    Brain Res 976:149-58. 2003
    ..Our data validate that NGF-differentiated PC12 cells may be employed as a useful in vitro model to further study the regulation of NOS1 subsequent to NMDAR activation...
  14. doi request reprint The syndromes of frontotemporal dysfunction in amyotrophic lateral sclerosis
    Michael J Strong
    Department of Clinical Neurological Sciences, The University of Western Ontario, London, Ontario, Canada
    Amyotroph Lateral Scler 9:323-38. 2008
    ....
  15. ncbi request reprint Tau protein aggregation in the frontal and entorhinal cortices as a function of aging
    Wencheng Yang
    Robarts Research Institute, London, Ontario, Canada
    Brain Res Dev Brain Res 156:127-38. 2005
    ..In this paper we examined the age-dependant deposition of tau protein in the frontal and entorhinal neocortices...
  16. pmc Prognosis of amyotrophic lateral sclerosis with respiratory onset
    Christen L Shoesmith
    Department of Clinical Neurological Sciences, University of Western Ontario, London, Ontario, Canada
    J Neurol Neurosurg Psychiatry 78:629-31. 2007
    ..Non-invasive positive pressure ventilation (NIPPV) significantly improved survival compared with those who did not use NIPPV. This study suggests that ALS with respiratory onset does not necessarily follow a rapidly progressive course...
  17. ncbi request reprint 14-3-3 protein binds to the low molecular weight neurofilament (NFL) mRNA 3' UTR
    Wei Wen Ge
    Cell Biology Research Group, Robarts Research Institute, 100 Perth Drive, London, Ontario, Canada N6A 5K8
    Mol Cell Neurosci 34:80-7. 2007
    ..These data show a novel interaction for 14-3-3 with NFL mRNA, and suggests that 14-3-3 may play a role in regulating NFL mRNA stability...
  18. ncbi request reprint Calcium mediated excitotoxicity in neurofilament aggregate-bearing neurons in vitro is NMDA receptor dependant
    Teresa Sanelli
    Department of Pathology, University of Western Ontario, London, ON, Canada
    J Neurol Sci 256:39-51. 2007
    ..These studies demonstrate that calcium mediated excitotoxicity in NF aggregate-bearing neurons is NMDA receptor dependant...
  19. ncbi request reprint Loss of nitric oxide-mediated down-regulation of NMDA receptors in neurofilament aggregate-bearing motor neurons in vitro: implications for motor neuron disease
    Teresa Sanelli
    Department of Pathology, University of Western Ontario and the Cell Biology Group, Robarts Research Institute, London, Ontario, Canada
    Free Radic Biol Med 42:143-51. 2007
    ..No effect was observed in aggregate-bearing neurons. These findings suggest that the presence of NF aggregates renders motor neurons more susceptible to NMDA-mediated excitotoxicity, and that this can be reversed by NO...
  20. ncbi request reprint Differentiation between primary lateral sclerosis and amyotrophic lateral sclerosis: examination of symptoms and signs at disease onset and during follow-up
    Maria Carmela Tartaglia
    Clinical Neurological Sciences, London Health Sciences Centre, University of Western Ontario, 339 Windermere Road, London, Ontario, Canada
    Arch Neurol 64:232-6. 2007
    ..Both amyotrophic lateral sclerosis (ALS) and primary lateral sclerosis (PLS) are motor neuron diseases, and there is much debate as to whether these are 2 separate disorders or simply 2 points on a continuum...
  21. ncbi request reprint Post-transcriptional control of neurofilaments in development and disease
    Amar Thyagarajan
    Department of Biological Sciences and the Neuroscience Research Center, University at Albany, SUNY, 1400 Washington Avenue, Albany, NY 12222, USA
    Exp Cell Res 313:2088-97. 2007
    ....
  22. doi request reprint Upregulation of GSK3beta expression in frontal and temporal cortex in ALS with cognitive impairment (ALSci)
    Wencheng Yang
    Robarts Research Institute, The University of Western Ontario, London, Ontario, Canada
    Brain Res 1196:131-9. 2008
    ..This supports the potential role for GSK3beta as a therapeutic target in ALS...
  23. ncbi request reprint Lack of TDP-43 abnormalities in mutant SOD1 transgenic mice shows disparity with ALS
    Janice Robertson
    Centre for Research in Neurodegenerative Diseases, Department of Laboratory, Medicine and Pathobiology, University of Toronto, Toronto, Canada M5S 3H2
    Neurosci Lett 420:128-32. 2007
    ..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...
  24. pmc Inhibition of Pin1 reduces glutamate-induced perikaryal accumulation of phosphorylated neurofilament-H in neurons
    Sashi Kesavapany
    Cytoskeletal Protein Regulation Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA
    Mol Biol Cell 18:3645-55. 2007
    ....
  25. ncbi request reprint Neuronal tissue-specific ribonucleoprotein complex formation on SOD1 mRNA: alterations by ALS SOD1 mutations
    Wei Wen Ge
    Cell Biology Research Group, Robarts Research Institute, London, Ontario, Canada
    Neurobiol Dis 23:342-50. 2006
    ..This paper reports RNP complex formation on SOD1 mRNA as a neuronal tissue-specific and ALS-associated mutation sensitive feature...
  26. ncbi request reprint Innate immunity in amyotrophic lateral sclerosis
    Katie Moisse
    Cell Biology Research Group, Robarts Research Institute, Department of Clinical Neurological Sciences, The University of Western Ontario, London, Ontario, Canada
    Biochim Biophys Acta 1762:1083-93. 2006
    ....
  27. pmc A neurotoxic peripherin splice variant in a mouse model of ALS
    Janice Robertson
    Centre for Research in Neurosciences, Research Institute of the McGill University Health Centre, McGill University, Montreal, Quebec, H3G 1A4, Canada
    J Cell Biol 160:939-49. 2003
    ..This evidence suggests that expression of neurotoxic splice variants of peripherin may contribute to the neurodegenerative mechanism in ALS...
  28. ncbi request reprint Selective loss of trans-acting instability determinants of neurofilament mRNA in amyotrophic lateral sclerosis spinal cord
    Wei Wen Ge
    Cell Biology Research Group, Robarts Research Institute, London, Ontario N6A 5K8, Canada
    J Biol Chem 278:26558-63. 2003
    ..These findings suggest that the trans-acting NFL-destabilizing elements are selectively suppressed in ALS homogenates, resulting in an increased stability and level of NFL mRNA...
  29. ncbi request reprint Cognitive impairment, frontotemporal dementia, and the motor neuron diseases
    Michael J Strong
    Department of Clinical Neurological Sciences and the Robarts Research Institute, London, Ontario, Canada
    Ann Neurol 54:S20-3. 2003
  30. ncbi request reprint High threshold for induction of the stress response in motor neurons is associated with failure to activate HSF1
    Zarah Batulan
    Montreal Neurological Institute and Department of Neurology and Neurosurgery, McGill University, Montreal, Quebec, Canada H3A 2B4
    J Neurosci 23:5789-98. 2003
    ..These results indicate that the high threshold for induction of the stress response in motor neurons stems from an impaired ability to activate the main heat shock-stress sensor, HSF1...
  31. ncbi request reprint Microtubule-associated tau protein positive neuronal and glial inclusions in ALS
    Wencheng Yang
    Robarts Research Institute, The University of Western Ontario, London, Canada
    Neurology 61:1766-73. 2003
    ....
  32. ncbi request reprint Activated p38MAPK is a novel component of the intracellular inclusions found in human amyotrophic lateral sclerosis and mutant SOD1 transgenic mice
    Caterina Bendotti
    Laboratory of Molecular Neurobiology, Dept Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri, Via Eritrea, 62, 20157 Milano, Italy
    J Neuropathol Exp Neurol 63:113-9. 2004
    ..Our observations indicate that activation of p38MAPK might contribute significantly to the pathology of motor neurons in ALS...
  33. ncbi request reprint Sequestration of nNOS in neurofilamentous aggregate bearing neurons in vitro leads to enhanced NMDA-mediated calcium influx
    Teresa R Sanelli
    Robarts Research Institute and Department of Pathology, The University of Western Ontario, London, Ontario, Canada
    Brain Res 1004:8-17. 2004
    ....
  34. ncbi request reprint Mutant copper-zinc superoxide dismutase binds to and destabilizes human low molecular weight neurofilament mRNA
    Wei Wen Ge
    Cell Biology Research Group, Robarts Research Institute, London, Ontario N6A 5K8, Canada
    J Biol Chem 280:118-24. 2005
    ..These observations provide an explanation for a novel gain of function in which mutant SOD1 expression in motor neurons alters an intermediate filament protein expression...
  35. ncbi request reprint ALS--not what we thought
    Michael J Strong
    Arch Neurol 63:319-20. 2006
  36. ncbi request reprint Activated microglial supernatant induced motor neuron cytotoxicity is associated with upregulation of the TNFR1 receptor
    Weiyan Wen
    Cell Biology Research Group, Robarts Research Institute, London, Ont, Canada
    Neurosci Res 55:87-95. 2006
    ..The TNFR2 receptor was not involved. These observations have important implications in understanding the mechanism by which microglial activation contributes to the motor neuron degeneration...
  37. ncbi request reprint Temporal profiles of neuronal degeneration, glial proliferation, and cell death in hNFL(+/+) and NFL(-/-) mice
    Jesse R McLean
    Department of Pathology, Schulich School of Medicine, University of Western Ontario, London, Ontario, Canada
    Glia 52:59-69. 2005
    ....
  38. ncbi request reprint Activated microglia (BV-2) facilitation of TNF-alpha-mediated motor neuron death in vitro
    Bei Ping He
    Neurodegeneration Research Group, The John P Robarts Research Institute, University of Western Ontario, London, Ontario, Canada N6A 5A5
    J Neuroimmunol 128:31-8. 2002
    ....
  39. ncbi request reprint TAU mutations are not a predominant cause of frontotemporal dementia in Canadian patients
    Anastasia Levchenko
    Center for Research in Neuroscience, McGill University Health Center Research Institute, Montreal, Quebec, Canada
    Can J Neurol Sci 31:363-7. 2004
    ..In this study, we evaluated the involvement of mutations in the TAU gene in development of frontotemporal dementia phenotype in patients of French or English Canadian origins...
  40. doi request reprint An aggregate-inducing peripherin isoform generated through intron retention is upregulated in amyotrophic lateral sclerosis and associated with disease pathology
    Shangxi Xiao
    Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Ontario, Canada M5S 3H2
    J Neurosci 28:1833-40. 2008
    ..These findings are the first to establish that peripherin splicing abnormalities occur in ALS, generating aggregation-prone splice isoforms...
  41. pmc Amyotrophic lateral sclerosis: update for family physicians
    Christen L Shoesmith
    London Health Sciences Centre, Ontario, Canada
    Can Fam Physician 52:1563-9. 2006
    ..To discuss the epidemiology, pathogenesis, diagnosis, expected course, prognosis, and treatment of amyotrophic lateral sclerosis (ALS), a degenerative disorder of the nervous system associated with progressive weakness...
  42. ncbi request reprint Increasing peak expiratory flow time in amyotrophic lateral sclerosis
    Steven R Wilson
    Division of Respirology, London Health Sciences Center, London, ON, Canada
    Chest 127:156-60. 2005
    ..Increasing peak expiratory flow time (PEFT) may represent a further sensitive measure of declining respiratory muscle strength in ALS...
  43. ncbi request reprint Biochemical markers: summary
    Michael J Strong
    University of Western Ontario, Canada
    Amyotroph Lateral Scler Other Motor Neuron Disord 3:S85-90. 2002