Tara L Spires

Summary

Affiliation: University of Oxford
Country: UK

Publications

  1. ncbi Environmental enrichment rescues protein deficits in a mouse model of Huntington's disease, indicating a possible disease mechanism
    Tara L Spires
    University Laboratory of Physiology, University of Oxford, Oxford OX1 3PT, United Kingdom
    J Neurosci 24:2270-6. 2004
  2. ncbi Activity-dependent regulation of synapse and dendritic spine morphology in developing barrel cortex requires phospholipase C-beta1 signalling
    Tara L Spires
    University Laboratory of Physiology, University of Oxford, Parks Road, Oxford, UK
    Cereb Cortex 15:385-93. 2005
  3. ncbi Dendritic spine pathology and deficits in experience-dependent dendritic plasticity in R6/1 Huntington's disease transgenic mice
    Tara L Spires
    University Laboratory of Physiology, University of Oxford, Parks Road, Oxford, OX1 3PT, UK
    Eur J Neurosci 19:2799-807. 2004
  4. ncbi Wheel running from a juvenile age delays onset of specific motor deficits but does not alter protein aggregate density in a mouse model of Huntington's disease
    Anton van Dellen
    Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, OX1 3PT, UK
    BMC Neurosci 9:34. 2008
  5. ncbi Nature, nurture and neurology: gene-environment interactions in neurodegenerative disease. FEBS Anniversary Prize Lecture delivered on 27 June 2004 at the 29th FEBS Congress in Warsaw
    Tara L Spires
    MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA
    FEBS J 272:2347-61. 2005
  6. ncbi Dendritic spine abnormalities in amyloid precursor protein transgenic mice demonstrated by gene transfer and intravital multiphoton microscopy
    Tara L Spires
    Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neurosci 25:7278-87. 2005
  7. ncbi Region-specific dissociation of neuronal loss and neurofibrillary pathology in a mouse model of tauopathy
    Tara L Spires
    Department of Neurology, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown 02129, USA
    Am J Pathol 168:1598-607. 2006
  8. ncbi Neuronal structure is altered by amyloid plaques
    Tara L Spires
    Department of Neurology, Alzheimer s Disease Research Laboratory, Massachusetts General Hospital, Charlestown, MA 02129, USA
    Rev Neurosci 15:267-78. 2004
  9. ncbi Spine tingling polymorphisms--is apolipoprotein E involved in dendritic shape and plasticity?
    Tara L Spires
    MassGeneral Institute for Neurodegenerative Disease Harvard Medical School, Charlestown, MA, United States
    Neurobiol Aging 28:687-8; discussion 704-6. 2007
  10. ncbi Abnormal bundling and accumulation of F-actin mediates tau-induced neuronal degeneration in vivo
    Tudor A Fulga
    Department of Pathology, Brigham and Women s Hospital and Harvard Medical School, Harvard New Research Building Room 652, 77 Louis Pasteur Avenue, Boston, MA 02115, USA
    Nat Cell Biol 9:139-48. 2007

Collaborators

Detail Information

Publications12

  1. ncbi Environmental enrichment rescues protein deficits in a mouse model of Huntington's disease, indicating a possible disease mechanism
    Tara L Spires
    University Laboratory of Physiology, University of Oxford, Oxford OX1 3PT, United Kingdom
    J Neurosci 24:2270-6. 2004
    ..These results suggest that environmental enrichment benefits animals at early stages of the disease by rescuing protein deficits, possibly through rescuing transcription or protein transport problems...
  2. ncbi Activity-dependent regulation of synapse and dendritic spine morphology in developing barrel cortex requires phospholipase C-beta1 signalling
    Tara L Spires
    University Laboratory of Physiology, University of Oxford, Parks Road, Oxford, UK
    Cereb Cortex 15:385-93. 2005
    ..Interrupting this regulation leads to changes in synapse and dendritic spine morphology, possibly altering post-synaptic integration of signal...
  3. ncbi Dendritic spine pathology and deficits in experience-dependent dendritic plasticity in R6/1 Huntington's disease transgenic mice
    Tara L Spires
    University Laboratory of Physiology, University of Oxford, Parks Road, Oxford, OX1 3PT, UK
    Eur J Neurosci 19:2799-807. 2004
    ..Furthermore, we demonstrate that Huntington's disease pathology interferes with the normal plastic response of dendritic spines to environmental enrichment...
  4. ncbi Wheel running from a juvenile age delays onset of specific motor deficits but does not alter protein aggregate density in a mouse model of Huntington's disease
    Anton van Dellen
    Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, OX1 3PT, UK
    BMC Neurosci 9:34. 2008
    ..Furthermore, wheel running initiated in adulthood ameliorates the rear-paw clasping motor sign, but not an accelerating rotarod deficit...
  5. ncbi Nature, nurture and neurology: gene-environment interactions in neurodegenerative disease. FEBS Anniversary Prize Lecture delivered on 27 June 2004 at the 29th FEBS Congress in Warsaw
    Tara L Spires
    MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA
    FEBS J 272:2347-61. 2005
    ..Here, we review the studies of environmental enrichment relevant to some major neurodegenerative diseases and discuss their research and clinical implications...
  6. ncbi Dendritic spine abnormalities in amyloid precursor protein transgenic mice demonstrated by gene transfer and intravital multiphoton microscopy
    Tara L Spires
    Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neurosci 25:7278-87. 2005
    ..Decreased spine density will likely contribute to altered neural system function and behavioral impairments observed in Tg2576 mice...
  7. ncbi Region-specific dissociation of neuronal loss and neurofibrillary pathology in a mouse model of tauopathy
    Tara L Spires
    Department of Neurology, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown 02129, USA
    Am J Pathol 168:1598-607. 2006
    ..Together, these results imply that neurofibrillary tangles do not necessarily lead to neuronal death...
  8. ncbi Neuronal structure is altered by amyloid plaques
    Tara L Spires
    Department of Neurology, Alzheimer s Disease Research Laboratory, Massachusetts General Hospital, Charlestown, MA 02129, USA
    Rev Neurosci 15:267-78. 2004
    ....
  9. ncbi Spine tingling polymorphisms--is apolipoprotein E involved in dendritic shape and plasticity?
    Tara L Spires
    MassGeneral Institute for Neurodegenerative Disease Harvard Medical School, Charlestown, MA, United States
    Neurobiol Aging 28:687-8; discussion 704-6. 2007
  10. ncbi Abnormal bundling and accumulation of F-actin mediates tau-induced neuronal degeneration in vivo
    Tudor A Fulga
    Department of Pathology, Brigham and Women s Hospital and Harvard Medical School, Harvard New Research Building Room 652, 77 Louis Pasteur Avenue, Boston, MA 02115, USA
    Nat Cell Biol 9:139-48. 2007
    ..These findings raise the possibility that a direct interaction between tau and actin may be a critical mediator of tau-induced neurotoxicity in Alzheimer's disease and related disorders...
  11. ncbi Molecular mechanisms mediating pathological plasticity in Huntington's disease and Alzheimer's disease
    Tara L Spires
    MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown, MA, USA
    J Neurochem 100:874-82. 2007
    ..This review will present evidence for altered plasticity in Huntington's and Alzheimer's diseases, relate these findings to symptomatology, and review possible causes and commonalities...
  12. ncbi Transgenic models of Alzheimer's disease: learning from animals
    Tara L Spires
    Harvard Medical School, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA
    NeuroRx 2:423-37. 2005
    ..This chapter reviews animal models of AD and their contributions to developing therapeutic approaches for AD...