T B Shea

Summary

Affiliation: University of Massachusetts
Country: USA

Publications

  1. ncbi request reprint Dynein mediates retrograde neurofilament transport within axons and anterograde delivery of NFs from perikarya into axons: regulation by multiple phosphorylation events
    Jennifer Motil
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, Lowell, Massachusetts 01854, USA
    Cell Motil Cytoskeleton 63:266-86. 2006
  2. ncbi request reprint Apple juice concentrate maintains acetylcholine levels following dietary compromise
    Amy Chan
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts, Lowell, MA 01854, USA
    J Alzheimers Dis 9:287-91. 2006
  3. pmc Lack of Correlation of WAIS Digit Span with Clox 1 and the Dementia Rating Scale in MCI
    Jevin Jay Lortie
    Department of Psychology, Knox College Galesburg, IL 61401, USA
    Int J Alzheimers Dis 2012:829743. 2012
  4. pmc Caspase-mediated truncation of tau potentiates aggregation
    Sangmook Lee
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts, One University Avenue, Lowell, MA 01854, USA
    Int J Alzheimers Dis 2012:731063. 2012
  5. ncbi request reprint The discontinuous nature of neurofilament transport accommodates both establishment and repair of the axonal neurofilament array
    Thomas B Shea
    Department of Biological Sciences, Center for Cellular Neurobiology and Neurodegeneration Research, University of Massachusetts, Lowell, One University Avenue, Lowell, MA 01854, USA
    Cytoskeleton (Hoboken) 70:67-73. 2013
  6. doi request reprint Positive argument for debate in J Neural Transmission: Alzheimer's disease: are we intervening too late? Yes, by years if not decades
    Thomas B Shea
    Departments of Biological Sciences and Nursing, Center for Cellular Neurobiology and Neurodegeneration Research, UMASS Lowell, Lowell, MA 01854, USA
    J Neural Transm 119:1529-32. 2012
  7. doi request reprint Nutrition and dementia: are we asking the right questions?
    Thomas B Shea
    Center for Cellular Neurobiology and Neurodegeneration Research, Departments of Biological Sciences, Clinical Laboratory and Nutritional Sciences and Nursing, UMASS Lowell, MA 01854, USA
    J Alzheimers Dis 30:27-33. 2012
  8. ncbi request reprint Folate, the methionine cycle, and Alzheimer's disease
    Thomas B Shea
    Center for Cellular Neurobiology and Neurodegeneration Research, University of Massachusetts Lowell, One University Avenue, Lowell, MA 01854, USA
    J Alzheimers Dis 9:359-60. 2006
  9. ncbi request reprint Folate quenches oxidative damage in brains of apolipoprotein E-deficient mice: augmentation by vitamin E
    Thomas B Shea
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, 1 University Avenue, Lowell 01854, USA
    Brain Res Mol Brain Res 108:1-6. 2002
  10. ncbi request reprint Vitamin E deficiency does not induce compensatory antioxidant increases in central nervous system tissue of apolipoprotein E-deficient mice
    Thomas B Shea
    Center for Cellular Neurobiology and Neurodegeneration Research, University of Massachusetts, Lowell, MA 01854, USA
    J Alzheimers Dis 5:9-14. 2003

Research Grants

Collaborators

  • W K Chan
  • Flaubert Tchantchou
  • Harish C Pant
  • Jean Pierre Julien
  • Rajesh Kumar
  • L I Benowitz
  • E J Rogers
  • L A Flanagan
  • R A Nixon
  • R J Nicolosi
  • Robert D Goldman
  • R Rozen
  • S C Collins
  • Garth Hall
  • M P Mattson
  • Amy Chan
  • Daniela Ortiz
  • Sangmook Lee
  • Maya Dubey
  • A Chan
  • Cheolwha Jung
  • Ruth Remington
  • Jacob Kushkuley
  • James Suchy
  • Jason DeFuria
  • Jennifer Motil
  • Aurea Pimenta
  • Pei I Ho
  • Jevin Jay Lortie
  • J T Yabe
  • Sirikarnt Dhitavat
  • Fatma J Ekinci
  • Lydia Kifle
  • James Paskavitz
  • Sheryl Perry
  • Amy Y Chan
  • Ram K Sihag
  • Pulkit Chaudhury
  • D Ortiz
  • Catherine M Moran
  • Teresa M Chylinski
  • Maria Dawn-Linsley
  • Lindsay Tjiattas
  • Daniela D Ortiz
  • Shelia M Mihalick
  • Jason T Yabe
  • Sirakarnt Dhitavat
  • Heather Hoffmann
  • F S Wang
  • T Chylinski
  • P I Ho
  • Ambar Ahmed
  • J Zemianek
  • Shailesh Metkar
  • R Remington
  • A Lepore
  • E Kotyla
  • Franck Letournel
  • Joel Eyer
  • Jean Francois Leterrier
  • James Levasseur
  • Jun Yao
  • Shelly Rasmussen
  • Hilda Kabiru
  • Ayat Alsaraby
  • Boyang Chu
  • V Graves
  • Masaki Inagaki
  • Tomoya Yamaguchi
  • Daniela T Ortiz
  • Po Chen
  • Valerie Graves
  • Eva Maria Mandelkow
  • Ezequiel Rivera
  • Qinzhang Zhu
  • Michelle Donnelly
  • Daniela O Ortiz
  • Kerrie Mitton
  • Sadaf Hoda
  • Sirikarnt Dhivant
  • David Ashline
  • FENG SONG WANG
  • Ezequiel R Rivera
  • D Ashline
  • T Katchmar
  • M D Linsley
  • A Pimenta
  • S D Kattar
  • S Dhitavat

Detail Information

Publications96

  1. ncbi request reprint Dynein mediates retrograde neurofilament transport within axons and anterograde delivery of NFs from perikarya into axons: regulation by multiple phosphorylation events
    Jennifer Motil
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, Lowell, Massachusetts 01854, USA
    Cell Motil Cytoskeleton 63:266-86. 2006
    ....
  2. ncbi request reprint Apple juice concentrate maintains acetylcholine levels following dietary compromise
    Amy Chan
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts, Lowell, MA 01854, USA
    J Alzheimers Dis 9:287-91. 2006
    ..These findings provide a likely mechanism by which consumption of antioxidant-rich foods such as apples can prevent the decline in cognitive performance that accompanies dietary and genetic deficiencies and aging...
  3. pmc Lack of Correlation of WAIS Digit Span with Clox 1 and the Dementia Rating Scale in MCI
    Jevin Jay Lortie
    Department of Psychology, Knox College Galesburg, IL 61401, USA
    Int J Alzheimers Dis 2012:829743. 2012
    ..Performance in Clox 1 was, therefore, not a predictor of performance in the Digit Span Test. These findings support the use of a test battery containing the Digit Span test to detect and track cognitive decline in MCI...
  4. pmc Caspase-mediated truncation of tau potentiates aggregation
    Sangmook Lee
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts, One University Avenue, Lowell, MA 01854, USA
    Int J Alzheimers Dis 2012:731063. 2012
    ..These findings suggest that caspase activation is one potential route, rather than an obligatory initiation step, in aggregation, and that N- and C-terminal truncation contribute differentially to aggregation...
  5. ncbi request reprint The discontinuous nature of neurofilament transport accommodates both establishment and repair of the axonal neurofilament array
    Thomas B Shea
    Department of Biological Sciences, Center for Cellular Neurobiology and Neurodegeneration Research, University of Massachusetts, Lowell, One University Avenue, Lowell, MA 01854, USA
    Cytoskeleton (Hoboken) 70:67-73. 2013
    ..We further demonstrate how this transport method provides for NF maintenance following maturation and encompasses the potential for regeneration...
  6. doi request reprint Positive argument for debate in J Neural Transmission: Alzheimer's disease: are we intervening too late? Yes, by years if not decades
    Thomas B Shea
    Departments of Biological Sciences and Nursing, Center for Cellular Neurobiology and Neurodegeneration Research, UMASS Lowell, Lowell, MA 01854, USA
    J Neural Transm 119:1529-32. 2012
    ..The introduction of novel detection methods at the earliest indications of cognitive impairment may provide a window of opportunity for initiation of preventative approaches...
  7. doi request reprint Nutrition and dementia: are we asking the right questions?
    Thomas B Shea
    Center for Cellular Neurobiology and Neurodegeneration Research, Departments of Biological Sciences, Clinical Laboratory and Nutritional Sciences and Nursing, UMASS Lowell, MA 01854, USA
    J Alzheimers Dis 30:27-33. 2012
    ....
  8. ncbi request reprint Folate, the methionine cycle, and Alzheimer's disease
    Thomas B Shea
    Center for Cellular Neurobiology and Neurodegeneration Research, University of Massachusetts Lowell, One University Avenue, Lowell, MA 01854, USA
    J Alzheimers Dis 9:359-60. 2006
  9. ncbi request reprint Folate quenches oxidative damage in brains of apolipoprotein E-deficient mice: augmentation by vitamin E
    Thomas B Shea
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, 1 University Avenue, Lowell 01854, USA
    Brain Res Mol Brain Res 108:1-6. 2002
    ....
  10. ncbi request reprint Vitamin E deficiency does not induce compensatory antioxidant increases in central nervous system tissue of apolipoprotein E-deficient mice
    Thomas B Shea
    Center for Cellular Neurobiology and Neurodegeneration Research, University of Massachusetts, Lowell, MA 01854, USA
    J Alzheimers Dis 5:9-14. 2003
    ..The lack of a compensatory response to vitamin E deprivation highlights the importance of dietary vitamin E in prevention of chronic neurodegeneration...
  11. doi request reprint Organizational dynamics, functions, and pathobiological dysfunctions of neurofilaments
    Thomas B Shea
    Departments of Biological Sciences and Biochemistry, Center for Cellular Neurobiology and Neurodegeneration Research, University of Massachusetts Lowell, One University Avenue, Lowell, MA 01854, England
    Results Probl Cell Differ 48:29-45. 2009
    ..Finally, we address how C-terminal phosphorylation is regionally and temporally regulated by a balance of kinase and phosphatase activities, and how misregulation of this balance might contribute to motor neuron disease...
  12. ncbi request reprint Differential susceptibity of transgenic mice lacking one or both apolipoprotein alleles to folate and vitamin E deprivation
    Thomas B Shea
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, Lowell, MA 01854, USA
    J Alzheimers Dis 6:269-73. 2004
    ..They further suggest that the impact of partial deficiency in ApoE function may present a latent risk that may manifest only when compounded by other factors such as dietary deficiency...
  13. ncbi request reprint Does neurofilament phosphorylation regulate axonal transport?
    Thomas B Shea
    Center for Cellular Neurobiology and Neurodegeneration Research, Departments of Biological Sciences and Biochemistry, University of Massachusetts Lowell, One University Avenue, Lowell, MA 01854, USA
    Trends Neurosci 26:397-400. 2003
    ..We present evidence that these deletion studies remain consistent with, rather than refute, a role for C-terminal phosphorylation in regulation of neurofilament axonal transport...
  14. ncbi request reprint Efficacy of vitamin E, phosphatidyl choline and pyruvate on Abeta neurotoxicity in culture
    T B Shea
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, Lowell, MA 01854, USA
    J Nutr Health Aging 7:252-5. 2003
    ..These data underscore the potential efficacy of a combinatorial neuroprotective formulation against Abeta neurotoxicity...
  15. doi request reprint Regulation of neurofilament dynamics by phosphorylation
    Thomas B Shea
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, One University Avenue, Lowell, MA 01854, USA
    Eur J Neurosci 27:1893-901. 2008
    ..Finally, we address how C-terminal phosphorylation is regionally and temporally regulated by a balance of kinase and phosphatase activities, and how misregulation of this balance can contribute to motor neuron disease...
  16. ncbi request reprint Cyclin-dependent kinase 5 increases perikaryal neurofilament phosphorylation and inhibits neurofilament axonal transport in response to oxidative stress
    Thomas B Shea
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, One University Avenue, 01854, USA
    J Neurosci Res 76:795-800. 2004
    ..These findings indicate that oxidative stress can compromise NF dynamics via hyperactivation of cdk5 and suggest that antioxidants may alleviate multiple aspects of neuropathology in motor neuron disease...
  17. ncbi request reprint The S-adenosyl homocysteine hydrolase inhibitor 3-deaza-adenosine prevents oxidative damage and cognitive impairment following folate and vitamin E deprivation in a murine model of age-related, oxidative stress-induced neurodegeneration
    Thomas B Shea
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, Lowell, MA, USA
    Neuromolecular Med 5:171-80. 2004
    ....
  18. ncbi request reprint Effects of dietary supplementation with N-acetyl cysteine, acetyl-L-carnitine and S-adenosyl methionine on cognitive performance and aggression in normal mice and mice expressing human ApoE4
    Amy Chan
    Center for Cellular Neurobiology and Neurodegeneration Research, University of Massachusetts Lowell, Lowell, MA 01854, USA
    Neuromolecular Med 9:264-9. 2007
    ..Maintenance of neurotransmitter levels and prevention of oxidative damage underscore the efficacy of a therapeutic approach that utilizes a combination of neuroprotective agents...
  19. ncbi request reprint Traffic jams: dynamic models for neurofilament accumulation in motor neuron disease
    Thomas B Shea
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, Lowell, MA 01854, USA
    Traffic 8:445-7. 2007
    ....
  20. ncbi request reprint Cdk5 regulates axonal transport and phosphorylation of neurofilaments in cultured neurons
    Thomas B Shea
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts, Lowell, One University Avenue, Lowell, MA 01854, USA
    J Cell Sci 117:933-41. 2004
    ..These findings suggest that Cdk5-p35 activity regulates normal NF distribution and that overexpression of Cdk5-p35 induces perikaryal accumulation of phosphorylated-NFs similar to those observed under pathological conditions...
  21. ncbi request reprint Nanosphere-mediated delivery of vitamin E increases its efficacy against oxidative stress resulting from exposure to amyloid beta
    Thomas B Shea
    Center for Cellular Neurobiology and Neurodegeneration Research, University of Massachusetts, Lowell, Lowell, MA 01854, USA
    J Alzheimers Dis 7:297-301. 2005
    ..By contrast, encapsulated vitamin E was equally effective if administered 1 hr after Abeta exposure. These findings suggest suggests that nanosphere-mediated delivery methods may be a useful adjunct for antioxidant therapy in AD...
  22. doi request reprint Neurofilament phosphorylation regulates axonal transport by an indirect mechanism: a merging of opposing hypotheses
    Thomas B Shea
    Department of Biological Sciences, Center for Cellular Neurobiology and Neurodegeneration Research, University of Massachusetts Lowell, Lowell, Massachusetts 01854, USA
    Cytoskeleton (Hoboken) 68:589-95. 2011
    ..Herein, we demonstrate how comparison of transport and distribution of differentially phosphorylated NFs along axons identify common ground between these hypotheses and may resolve this controversy...
  23. ncbi request reprint Apolipoprotein E deficiency promotes increased oxidative stress and compensatory increases in antioxidants in brain tissue
    Thomas B Shea
    Center for Cellular Neurobiology and Neurodegeneration Research, University of Massachusetts at Lowell, Lowell, MA 01854, USA
    Free Radic Biol Med 33:1115-20. 2002
    ..These data support the hypothesis that ApoE deficiency is associated with oxidative damage, and demonstrate a combinatorial influence of genetic predisposition, dietary deficiency, and oxidative stress on oxidative damage relevant to AD...
  24. ncbi request reprint Quantification of antioxidant activity in brain tissue homogenates using the 'total equivalent antioxidant capacity'
    Thomas B Shea
    Center for Cellular Neurobiology, University of Massachusetts Lowell, 01854, Lowell, MA, USA
    J Neurosci Methods 125:55-8. 2003
    ..The rapid nature of this assay compared to HPLC, coupled with its lack of requirement for sophisticated equipment, makes it well suited for analyses of multiple tissue samples...
  25. ncbi request reprint Aluminum inhibits neurofilament assembly, cytoskeletal incorporation, and axonal transport. Dynamic nature of aluminum-induced perikaryal neurofilament accumulations as revealed by subunit turnover
    T B Shea
    Department of Biological Sciences, University of Massachusetts at Lowell, MA 01854, USA
    Mol Chem Neuropathol 32:17-39. 1997
    ....
  26. ncbi request reprint The order of exposure of tau to signal transduction kinases alters the generation of "AD-like" phosphoepitopes
    T B Shea
    Department of Biological Sciences, University of Massachusetts at Lowell 01854, USA
    Cell Mol Neurobiol 19:223-33. 1999
    ....
  27. ncbi request reprint Selective stabilization of microtubules within the proximal region of developing axonal neurites
    T B Shea
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell 01854, USA
    Brain Res Bull 48:255-61. 1999
    ....
  28. ncbi request reprint Neuronal intermediate filament protein alpha-internexin facilitates axonal neurite elongation in neuroblastoma cells
    T B Shea
    Department of Biological Sciences, Center for Cellular Neurobiology and Neurodegeneration Research, University of Massachusetts at Lowell, Lowell 01854, USA
    Cell Motil Cytoskeleton 43:322-33. 1999
    ..These data extend earlier cell-free demonstrations that NF-H preferentially associates with NF-L rather than alpha-IN...
  29. ncbi request reprint S-adenosyl methionine: a natural therapeutic agent effective against multiple hallmarks and risk factors associated with Alzheimer's disease
    Thomas B Shea
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, UMASS Lowell, One University Avenue, Lowell, MA 01854, USA
    J Alzheimers Dis 13:67-70. 2008
    ..These findings support and extend prior studies, some of which are decades old, and support the notion that nutritional supplementation may represent an important augmentation for therapy in Alzheimer's disease...
  30. ncbi request reprint Acetyl-L-carnitine protects against amyloid-beta neurotoxicity: roles of oxidative buffering and ATP levels
    Sirakarnt Dhitavat
    Center for Neurobiology and Neurodegeneration Research, University of Massachusetts Lowell, Lowell, Massachusetts 01854, USA
    Neurochem Res 27:501-5. 2002
    ..ALCAR prevented ATP depletion; therefore, ALCAR may mediate its protective effect by buffering oxidative stress and maintaining ATP levels...
  31. ncbi request reprint Efficacy of vitamin E, phosphatidyl choline, and pyruvate on buffering neuronal degeneration and oxidative stress in cultured cortical neurons and in central nervous tissue of apolipoprotein E-deficient mice
    Thomas B Shea
    Center for Cellular Neurobiology and Neurodegeneration Research, University of Massachusetts, Lowell, MA 01854, USA
    Free Radic Biol Med 33:276-82. 2002
    ..These data underscore the possibility that critical nutritional deficiencies may modulate the impact of genetic compromise on neurodegeneration...
  32. ncbi request reprint Dietary supplementation with apple juice concentrate alleviates the compensatory increase in glutathione synthase transcription and activity that accompanies dietary- and genetically-induced oxidative stress
    F Tchantchou
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biochemistry, University of Massachusetts Lowell, Lowell, MA 01854, USA
    J Nutr Health Aging 8:492-6. 2004
    ..These findings provide further evidence that the antioxidant potential of AJC can compensate for dietary and genetic deficiencies that otherwise promote neurodegeneration...
  33. ncbi request reprint Dietary and genetic compromise in folate availability reduces acetylcholine, cognitive performance and increases aggression: critical role of S-adenosyl methionine
    A Chan
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts, Lowell, MA 01854, USA
    J Nutr Health Aging 12:252-61. 2008
    ....
  34. ncbi request reprint Homocysteine potentiates beta-amyloid neurotoxicity: role of oxidative stress
    P I Ho
    Center for Cellular Neurobiology and Neurodegeneration Research and Department of Biochemistry, University of Massachusetts-Lowell, Lowell, Massachusetts 01854, USA
    J Neurochem 78:249-53. 2001
    ..These findings underscore that moderate accumulation of excitotoxins at concentrations that alone do not appear to initiate adverse events may enhance the effects of other factors known to cause neurodegeneration such as Abeta...
  35. ncbi request reprint Beta-amyloid and ionophore A23187 evoke tau hyperphosphorylation by distinct intracellular pathways: differential involvement of the calpain/protein kinase C system
    T B Shea
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts at Lowell, 01854, USA
    J Neurosci Res 49:759-68. 1997
    ..Moreover, although betaA invoked calcium influx in these cells, our findings further suggest that the induction of tau hyperphosphorylation by betaA may not be due to calcium influx...
  36. ncbi request reprint Folate deprivation increases presenilin expression, gamma-secretase activity, and Abeta levels in murine brain: potentiation by ApoE deficiency and alleviation by dietary S-adenosyl methionine
    Amy Chan
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, Lowell, Massachusetts 01854, USA
    J Neurochem 102:753-60. 2007
    ..These findings link nutritional and genetic risk factors for age-related neurodegeneration and underscore that dietary supplementation with SAM may be useful to augment therapeutic approaches...
  37. ncbi request reprint Dietary supplementation with 3-deaza adenosine, N-acetyl cysteine, and S-adenosyl methionine provide neuroprotection against multiple consequences of vitamin deficiency and oxidative challenge: relevance to age-related neurodegeneration
    Flaubert Tchantchou
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, Lowell, MA 01854, USA
    Neuromolecular Med 6:93-103. 2004
    ..These findings support combinatorial treatments with agents that compensate for differential insults in age-related neurodegenerative disorders...
  38. ncbi request reprint Restriction of microM-calcium-requiring calpain activation to the plasma membrane in human neuroblastoma cells: evidence for regionalized influence of a calpain activator protein
    T B Shea
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts at Lowell, 01854, USA
    J Neurosci Res 48:543-50. 1997
    ....
  39. ncbi request reprint S-adenosyl methionine: A connection between nutritional and genetic risk factors for neurodegeneration in Alzheimer's disease
    F Tchantchou
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, UMassLowell, One University Avenue, Lowell, MA 01854, USA
    J Nutr Health Aging 10:541-4. 2006
    ....
  40. doi request reprint Dietary supplementation with a combination of alpha-lipoic acid, acetyl-L-carnitine, glycerophosphocoline, docosahexaenoic acid, and phosphatidylserine reduces oxidative damage to murine brain and improves cognitive performance
    James Suchy
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, Lowell, MA 01854, USA
    Nutr Res 29:70-4. 2009
    ..These findings add to the growing body of research indicating that key dietary supplementation may delay the progression of age-related cognitive decline...
  41. ncbi request reprint Supplementation with apple juice can compensate for folate deficiency in a mouse model deficient in methylene tetrahydrofolate reductase activity
    A Chan
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, Lowell, MA 01854, USA
    J Nutr Health Aging 15:221-5. 2011
    ....
  42. ncbi request reprint Selective accumulation of the high molecular weight neurofilament subunit within the distal region of growing axonal neurites
    J T Yabe
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts-Lowell, MA 01854, USA
    Cell Motil Cytoskeleton 50:1-12. 2001
    ..Selective NF-H accumulation into existing cytoskeletal structures within the distal-most region may provide de novo cytoskeletal stability for continued axon extension and/or stabilization...
  43. ncbi request reprint Microtubule motors, phosphorylation and axonal transport of neurofilaments
    T B Shea
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts, Lowell, MA 01854, USA
    J Neurocytol 29:873-87. 2000
    ..This review juxtaposes older and more recent findings on NF dynamics, and speculates on the organization of axonal NFs as suggested by real-time analyses of NF transport...
  44. pmc Dietary deficiency increases presenilin expression, gamma-secretase activity, and Abeta levels: potentiation by ApoE genotype and alleviation by S-adenosyl methionine
    Amy Chan
    Department of Biological Sciences and Health and Clinical Sciences, Center for Cellular Neurobiology and Neurodegeneration Research, University of Massachusetts, Lowell, Massachusets 01854, USA
    J Neurochem 110:831-6. 2009
    ..Abeta increased only in E4 mice maintained under the complete diet, and was alleviated by SAM supplementation. These findings suggest dietary compromise can potentiate latent risk factors for AD...
  45. ncbi request reprint Supplementation with apple juice attenuates presenilin-1 overexpression during dietary and genetically-induced oxidative stress
    Amy Chan
    Department of Biological Sciences, Center for Cellular Neurobiology and Neurodegeneration Research, University of Massachusetts, Lowell, MA 01854, USA
    J Alzheimers Dis 10:353-8. 2006
    ....
  46. ncbi request reprint Folate and vitamin E deficiency impair cognitive performance in mice subjected to oxidative stress: differential impact on normal mice and mice lacking apolipoprotein E
    Shelia M Mihalick
    Center for Cellular Neurobiology and Neurodegeneration Research Department of Biological Sciences, University of Massachusetts, Lowell, MA 01854, USA
    Neuromolecular Med 4:197-202. 2003
    ..They further leave open the possibility that one or more risk factors may remain latent, and neurodegeneration may ensue only following augmentation by one or more additional traumatic events or conditions...
  47. ncbi request reprint Triton-soluble phosphovariants of the heavy neurofilament subunit in developing and mature mouse central nervous system
    T B Shea
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts, Lowell 08154, USA
    J Neurosci Res 48:515-23. 1997
    ....
  48. ncbi request reprint Neurofilaments consist of distinct populations that can be distinguished by C-terminal phosphorylation, bundling, and axonal transport rate in growing axonal neurites
    J T Yabe
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts-Lowell, Lowell, Massachusetts 01854, USA
    J Neurosci 21:2195-205. 2001
    ..Inhibition of phosphatase activities increased NF-NF interactions within living cells. These findings collectively suggest that C-terminal phosphorylation and NF-NF interactions are responsible for slowing NF axonal transport...
  49. ncbi request reprint Monitoring thiobarbituric acid-reactive substances (TBARs) as an assay for oxidative damage in neuronal cultures and central nervous system
    Maria Dawn-Linsley
    Department of Biological Sciences, Center for Cellular Neurobiology and Neurodegeneration Research, University of Massachusetts Lowell, Lowell, MA 01854, USA
    J Neurosci Methods 141:219-22. 2005
    ....
  50. ncbi request reprint Dietary and genetically-induced oxidative stress alter tau phosphorylation: influence of folate and apolipoprotein E deficiency
    Amy Chan
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, One University Avenue, Lowell, MA 01854, USA
    J Alzheimers Dis 9:399-405. 2006
    ....
  51. ncbi request reprint Inhibition of neurite outgrowth following intracellular delivery of anti-GAP-43 antibodies depends upon culture conditions and method of neurite induction
    T B Shea
    Laboratory for Molecular Neuroscience, Mailman Research Center, McLean Hospital, Belmont, Massachusetts, USA
    J Neurosci Res 41:347-54. 1995
    ....
  52. ncbi request reprint A vitamin/nutriceutical formulation improves memory and cognitive performance in community-dwelling adults without dementia
    A Chan
    Center for Cell Neurobiology and Neurodegeneration Research, University of Massachusetts, Lowell, Lowell MA 01854, USA
    J Nutr Health Aging 14:224-30. 2010
    ..These findings support the benefit of nutritional supplements for cognitive performance and suggest that additional supplementation may be required for the elderly...
  53. ncbi request reprint Phospholipids alter tau conformation, phosphorylation, proteolysis, and association with microtubules: implication for tau function under normal and degenerative conditions
    T B Shea
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts at Lowell, 01854, USA
    J Neurosci Res 50:114-22. 1997
    ..These data further suggest that disruption of the normal association of tau with phospholipids may foster accumulation of tau and, in doing so, render tau more susceptible to hyperphosphorylation...
  54. pmc Dietary supplementation with S-adenosyl methionine was associated with protracted reduction of seizures in a line of transgenic mice
    Sheryl Perry
    Center for Cellular Neurobiology and Neurodegeneration Research, University of Massachusetts Lowell, Lowell, Massachusetts, USA
    Comp Med 58:604-6. 2008
    ....
  55. ncbi request reprint Folate, vitamin E, and acetyl-L-carnitine provide synergistic protection against oxidative stress resulting from exposure of human neuroblastoma cells to amyloid-beta
    Sirikarnt Dhitavat
    Center for Cellular Neurobiology and Neurodegeneration Research, University of Massachusetts Lowell, Lowell, MA 01854, USA
    Brain Res 1061:114-7. 2005
    ..These findings support a combinatorial approach in Alzheimer's therapy...
  56. ncbi request reprint Arsenic inhibits neurofilament transport and induces perikaryal accumulation of phosphorylated neurofilaments: roles of JNK and GSK-3beta
    Jason DeFuria
    Department of Biological Sciences and Biochemistry, Center Cell Neurobiology and Neurodegeneration Research, University of Massachusetts Lowell, Lowell MA 01854, USA
    Brain Res 1181:74-82. 2007
    ..These latter findings suggest that this environmental neurotoxin could contribute to peripheral neuropathy by perturbing NF dynamics...
  57. ncbi request reprint Folate deprivation induces neurodegeneration: roles of oxidative stress and increased homocysteine
    Pei I Ho
    Center for Cellular Neurobiology and Neurodegeneration Research, University of Massachusetts Lowell, Lowell, MA 01854, USA
    Neurobiol Dis 14:32-42. 2003
    ..These findings underscore the importance of folate metabolism in neuronal homeostasis and suggest that folate deficiency may augment AD neuropathology by increasing ROS and excitotoxicity via HC generation...
  58. ncbi request reprint Folate deficiency and homocysteine induce toxicity in cultured dorsal root ganglion neurons via cytosolic calcium accumulation
    Lindsay Tjiattas
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, Lowell, MA 01854, USA
    Aging Cell 3:71-6. 2004
    ..These findings support the idea that folate deprivation and HC treatment can compromise the health of DRG neurons by perturbing calcium homeostasis...
  59. ncbi request reprint Neurofilament subunits undergo more rapid translocation within retinas than in optic axons
    Cheolwha Jung
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, One University Avenue, Lowell, MA 01854, USA
    Brain Res Mol Brain Res 122:188-92. 2004
    ..These findings provide additional support for the notion that phosphorylation regulates NF axonal transport...
  60. ncbi request reprint Expression and activity of methionine cycle genes are altered following folate and vitamin E deficiency under oxidative challenge: modulation by apolipoprotein E-deficiency
    Flaubert Tchantchou
    Department of Biological Sciences, Center for Cellular Neurobiology and Neurodegeneration Research, University of Massachusetts Lowell, Lowell, MA 01854, USA
    Nutr Neurosci 9:17-24. 2006
    ..They further support the notion that latent genetic deficiencies, including those of methionine cycle, may contribute to Alzheimer's disease, especially in concert with age-related nutritional deficiencies...
  61. ncbi request reprint Apple juice concentrate prevents oxidative damage and impaired maze performance in aged mice
    Flaubert Tchantchou
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, Lowell, MA 01854, USA
    J Alzheimers Dis 8:283-7. 2005
    ..These findings also support the efficacy of antioxidant supplementation, including consumption of antioxidant-rich foods such as apples, in preventing the decline in cognitive performance that accompanies normal aging...
  62. doi request reprint Dietary supplementation with apple juice decreases endogenous amyloid-beta levels in murine brain
    Amy Chan
    Department of Biological Sciences, University of Massachusetts Lowell, Lowell, MA, USA
    J Alzheimers Dis 16:167-71. 2009
    ..These findings provide further evidence linking nutritional and genetic risk factors for age-related neurodegeneration, and underscore that dietary supplementation may be useful to augment therapeutic approaches...
  63. ncbi request reprint Potentiation of arsenic neurotoxicity by folate deprivation: protective role of S-adenosyl methionine
    Maya Dubey
    Department of Biological Sciences, Center for Cellular Neurobiology and Neurodegeneration Research, University of Massachusetts, Lowell, MA 01854, USA
    Nutr Neurosci 10:199-204. 2007
    ..These findings demonstrate how key nutritional deficiencies can potentiate the impact of enrivonmental neurotoxins...
  64. doi request reprint Deprivation of folate and B12 increases neurodegeneration beyond that accompanying deprivation of either vitamin alone
    Lydia Kifle
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, MA 01854, USA
    J Alzheimers Dis 16:533-40. 2009
    ....
  65. doi request reprint Dietary deficiency in folate and vitamin E under conditions of oxidative stress increases phospho-tau levels: potentiation by ApoE4 and alleviation by S-adenosylmethionine
    Amy Chan
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, Lowell, MA 01854, USA
    J Alzheimers Dis 17:483-7. 2009
    ..Since neurofibrillary tangles are comprised of phospho-tau, investigation of the impact of dietary deficiency and S-adenosyl methionine supplementation on neurofibrillary tangle formation are warranted...
  66. doi request reprint Dietary supplementation with S-adenosyl methionine delays the onset of motor neuron pathology in a murine model of amyotrophic lateral sclerosis
    James Suchy
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, Lowell, MA 01854, USA
    Neuromolecular Med 12:86-97. 2010
    ..SAM did not increase survival time. These preliminary findings, using a single concentration of SAM, suggest that SAM supplementation maybe useful as part of a comprehensive therapeutic approach for ALS...
  67. ncbi request reprint Homocysteine, folate deprivation and Alzheimer neuropathology
    Thomas B Shea
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, Department of Health and Clinical Sciences, Department of Biochemistry, UMass, Lowell, Lowell, MA 01854, USA
    J Alzheimers Dis 4:261-7. 2002
    ..The potential contribution of folate deficiency and resultant increases in HC to neurodegeneration in AD, and therapeutic approaches to alleviate their impact, is discussed...
  68. ncbi request reprint Multiple aspects of homocysteine neurotoxicity: glutamate excitotoxicity, kinase hyperactivation and DNA damage
    Pei I Ho
    Center for Cellular Neurobiology and Neurodegeneration Research, University of Massachusetts, Lowell, MA 01854, USA
    J Neurosci Res 70:694-702. 2002
    ..These findings indicate that HC compromises neuronal homeostasis by multiple, divergent routes...
  69. doi request reprint Folate deprivation increases tau phosphorylation by homocysteine-induced calcium influx and by inhibition of phosphatase activity: Alleviation by S-adenosyl methionine
    Amy Y Chan
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, One University Avenue, Lowell, MA 01854, USA
    Brain Res 1199:133-7. 2008
    ....
  70. ncbi request reprint 17 beta-estradiol alleviates synergistic oxidative stress resulting from folate deprivation and amyloid-beta treatment
    Thomas B Shea
    Center for Cellular Neurobiology and Neurodegeneration Research Department of Biological Sciences University of Massachusetts, Lowell Lowell, MA 01854, USA
    J Alzheimers Dis 5:323-7. 2003
    ..These findings suggest that therapeutic approaches utilizing antioxidants may be particularly important in conditions such as AD, where multiple factors, including compromises in endogenous antioxidants, promote oxidative stress...
  71. ncbi request reprint N-acteyl cysteine alleviates oxidative damage to central nervous system of ApoE-deficient mice following folate and vitamin E-deficiency
    Flaubert Tchantchou
    Center for Cellular Neurobiology and Neurodegeneration Research Departments of University of Massachusetts Lowell Lowell, MA 01854, USA
    J Alzheimers Dis 7:135-8; discussion 173-80. 2005
    ..These data support the administration of antioxidant precursors to buffer oxidative damage in neurodegenerative disorders...
  72. ncbi request reprint Apple juice prevents oxidative stress and impaired cognitive performance caused by genetic and dietary deficiencies in mice
    E J Rogers
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, One University Avenue, Lowell, MA 01854, USA
    J Nutr Health Aging 8:92-7. 2004
    ..In addition, we demonstrate that this protective effect is not derived from the sugar content of the concentrate...
  73. ncbi request reprint Apple juice prevents oxidative stress induced by amyloid-beta in culture
    Daniela Ortiz
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, Lowell, MA 01854, USA
    J Alzheimers Dis 6:27-30. 2004
    ..AJC also prevented Abeta-induced calcium influx and apoptosis, each of which results in part due to increased ROS. These findings suggest that the antioxidant potential of apple products can prevent Abeta-induced oxidative damage...
  74. doi request reprint Aluminum induces neurofilament aggregation by stabilizing cross-bridging of phosphorylated c-terminal sidearms
    Jacob Kushkuley
    Center for Cellular Neurobiology and Neurodegeneration Research, Departments of Biological Sciences and Biochemistry, University of Massachusetts Lowell, Lowell, MA 01854, USA
    Brain Res 1322:118-23. 2010
    ..These findings are consistent with the notion that prolonged interactions induced among phospho-NFs by the trivalent aluminum impairs axonal transport and promotes perikaryal aggregation...
  75. doi request reprint The glutamate-rich region of the larger lamprey neurofilament sidearm is essential for proper neurofilament architecture
    Sangmook Lee
    Center for Cellular Neuroscience and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, Lowell, MA 01854, USA
    Brain Res 1231:1-5. 2008
    ..We present evidence that, like mammalian NFs, the glutamate-rich region of NF-180 sidearm plays a critical role in NF architecture...
  76. ncbi request reprint S-adenosylmethionine mediates glutathione efficacy by increasing glutathione S-transferase activity: implications for S-adenosyl methionine as a neuroprotective dietary supplement
    Flaubert Tchantchou
    Department of Biological Sciences, Center for Cellular Neurobiology and Neurodegeneration Research, UMASS Lowell, One University Avenue, Lowell, MA 01854, USA
    J Alzheimers Dis 14:323-8. 2008
    ..Since Alzheimer's disease is accompanied by reduced GST activity, diminished SAM and increased SAH, these findings underscore the critical role of SAM in maintenance of neuronal health...
  77. ncbi request reprint The high and middle molecular weight neurofilament subunits regulate the association of neurofilaments with kinesin: inhibition by phosphorylation of the high molecular weight subunit
    Cheolwha Jung
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts, Lowell, One University Avenue, Lowell, MA 01854, USA
    Brain Res Mol Brain Res 141:151-5. 2005
    ..They further indicate that phosphorylation of NF-H dissociates NFs from kinesin and provides a mechanism by which NF-H phosphorylation can contribute to the slowing of NF axonal transport...
  78. ncbi request reprint Cdk5 inhibits anterograde axonal transport of neurofilaments but not that of tau by inhibition of mitogen-activated protein kinase activity
    Catherine M Moran
    Center for Cell Neurobiology and Neurodegeneration Research, University of Massachusetts Lowell, Lowell, MA 01854, USA
    Brain Res Mol Brain Res 134:338-44. 2005
    ..These findings suggest that axonal transport of tau and NFs is under the control of distinct kinase cascades, and that cdk5 inhibits NF transport at least in part by inhibiting MAPk...
  79. ncbi request reprint Tau inhibits anterograde axonal transport and perturbs stability in growing axonal neurites in part by displacing kinesin cargo: neurofilaments attenuate tau-mediated neurite instability
    Maya Dubey
    Center for Cell Neurobiology and Neurodegeneration Research, University of Massachusetts Lowell, Lowell, Massachusetts 01854, USA
    Cell Motil Cytoskeleton 65:89-99. 2008
    ....
  80. ncbi request reprint Kinesin, dynein and neurofilament transport
    T B Shea
    Center for Cellular Neurobiology and Neurodegeneration Research, Dept of Biological Sciences, University of Massachusetts Lowell, 01854
    Trends Neurosci 24:644-8. 2001
    ..In addition, these findings unify both certain aspects of axonal transport and neurofilament biology. We discuss these data herein in the context of both older and more recent studies of neurofilament dynamics...
  81. doi request reprint Neurofilament cross-bridging competes with kinesin-dependent association of neurofilaments with microtubules
    Jacob Kushkuley
    Center for Cellular Neurobiology and Neurodegeneration Research, Departments of Biological Sciences and Biochemistry, University of Massachusetts Lowell, Lowell, MA 01854, USA
    J Cell Sci 122:3579-86. 2009
    ..These findings confirm that bundling competes with NF-MT association, and provide a mechanism by which C-terminal NF phosphorylation might indirectly contribute to the observed slowing in axonal transport of phospho-NFs...
  82. ncbi request reprint Growth cones contain a dynamic population of neurofilament subunits
    Walter K H Chan
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, MA 01854, USA
    Cell Motil Cytoskeleton 54:195-207. 2003
    ....
  83. ncbi request reprint Increased transcription and activity of glutathione synthase in response to deficiencies in folate, vitamin E, and apolipoprotein E
    Flaubert Tchantchou
    Center for Cellular Neurobiology and Neurodegeneration Research, University of Massachusetts Lowell, Massachusetts 01854, USA
    J Neurosci Res 75:508-15. 2004
    ....
  84. ncbi request reprint Regulation of the transition from vimentin to neurofilaments during neuronal differentiation
    Jason T Yabe
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, MA 01854, USA
    Cell Motil Cytoskeleton 56:193-205. 2003
    ....
  85. ncbi request reprint Okadaic acid mediates tau phosphorylation via sustained activation of the L-voltage-sensitive calcium channel
    Fatma J Ekinci
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, 1 University Avenue, Lowell, MA 01854, USA
    Brain Res Mol Brain Res 117:145-51. 2003
    ..These findings underscore that divergent and convergent kinase and phosphatase activities regulate tau phosphorylation...
  86. ncbi request reprint Mitogen-activated protein kinase regulates neurofilament axonal transport
    Walter Kong Ho Chan
    Center Cell Neurobiology and Neurodegeneration Research, University of Massachusetts, Lowell, MA 01854, USA
    J Cell Sci 117:4629-42. 2004
    ..These data suggest that p42/44 MAP kinase regulates NF anterograde transport by NF C-terminal phosphorylation. MAP kinase may therefore stabilize developing axons by promoting the accumulation of NFs within growing axonal neurites...
  87. ncbi request reprint Divergent effects of the MEKK-1/JNK pathway on NB2a/d1 differentiation: some activity is required for outgrowth and stabilization of neurites but overactivation inhibits both phenomena
    Jason DeFuria
    Departments of Biological Sciences and Biochemistry, Center Cell Neurobiology and Neurodegeneration Research, University of Massachusetts, Lowell, Lowell, MA 01854, USA
    Brain Res 1123:20-6. 2006
    ..Finally, both caMEKK-1 and dnMEKK-1 prevented initial neuritogenesis. These findings indicate that the MEKK-1/JNK pathway regulates critical aspects of initial outgrowth, and subsequent stabilization of axonal neurites...
  88. doi request reprint Efficacy of a vitamin/nutriceutical formulation for early-stage Alzheimer's disease: a 1-year, open-label pilot study with an 16-month caregiver extension
    Amy Chan
    Center for Cell Neurobiology and Neurodegeneration Research, University of Massachusetts Lowell, MA, USA
    Am J Alzheimers Dis Other Demen 23:571-85. 2008
    ..This formulation holds promise for treatment of early-stage Alzheimer's disease prior to and/or as a supplement for pharmacological approaches. A larger, placebo-controlled trial is warranted...
  89. doi request reprint Efficacy of a vitamin/nutriceutical formulation for moderate-stage to later-stage Alzheimer's disease: a placebo-controlled pilot study
    Ruth Remington
    Department of Nursing, University of Massachusetts Lowell, Lowell, Massachusetts, USA
    Am J Alzheimers Dis Other Demen 24:27-33. 2009
    ..A larger trial is warranted...
  90. ncbi request reprint Inhibition of dynein but not kinesin induces aberrant focal accumulation of neurofilaments within axonal neurites
    Jennifer Motil
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, One University Avenue, Lowell, MA 01854, USA
    Brain Res 1164:125-31. 2007
    ..These findings are consistent with studies indicating that perturbations in dynein activity can contribute to the aberrant accumulations of neurofilaments that accompany ALS/motor neuron disease...
  91. ncbi request reprint Folate and homocysteine metabolism in neural plasticity and neurodegenerative disorders
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, National Institutes of Health, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Trends Neurosci 26:137-46. 2003
    ..A better understanding of the roles of folate and homocysteine in neuronal homeostasis throughout life is revealing novel approaches for preventing and treating neurological disorders...
  92. pmc Role of phosphorylation on the structural dynamics and function of types III and IV intermediate filaments
    Ram K Sihag
    Laboratory of Neurochemistry, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Bldg 49 Room 2A28, MD 20892, USA
    Exp Cell Res 313:2098-109. 2007
    ..The role of IF phosphorylation in disease pathobiology is discussed...
  93. ncbi request reprint Neurofilaments can undergo axonal transport and cytoskeletal incorporation in a discontinuous manner
    Walter K H Chan
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, One University Avenue Lowell, Massachusetts 01854, USA
    Cell Motil Cytoskeleton 62:166-79. 2005
    ..These findings provide a mechanism by which some NFs exhibit extended residence time within axons, which lessens the metabolic burden of cytoskeletal turnover...
  94. ncbi request reprint Neurofilament transport is dependent on actin and myosin
    Cheolwha Jung
    Center for Cellular Neurobiology and Neurodegeneration Research, Departments of Biological Sciences and Biochemistry, University of Massachusetts Lowell, Lowell, Massachusetts 01854, USA
    J Neurosci 24:9486-96. 2004
    ..These findings suggest that some NF subunits may undergo axonal transport via myosin-mediated interactions with the actin cortex...
  95. ncbi request reprint Reexpression of vimentin in differentiated neuroblastoma cells enhances elongation of axonal neurites
    Maya Dubey
    Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts Lowell, Lowell, Massachusetts 01854, USA
    J Neurosci Res 78:245-9. 2004
    ....
  96. ncbi request reprint Homocysteine and dementia
    Thomas B Shea
    N Engl J Med 346:2007; author reply 2008. 2002

Research Grants4

  1. Nanospheres as Vehicles for Treatment of Neuroblastoma
    Thomas Shea; Fiscal Year: 2004
    ..Resulting data will indicate whether or not nanospheres represent useful delivery agents for cancer therapy. ..
  2. Is S-adenosyl Methionine a Nutrition: Genetic Link in AD?
    Thomas Shea; Fiscal Year: 2007
    ..Our proposed studies will further underscore crucial deleterious interplay between nutritional and genetic compromise in AD and may point towards the development of therapeutic approaches using dietary SAM. ..