CHRISTOPHER LINK

Summary

Affiliation: University of Colorado
Country: USA

Publications

  1. ncbi request reprint C. elegans models of age-associated neurodegenerative diseases: lessons from transgenic worm models of Alzheimer's disease
    Christopher D Link
    Institute for Behavioral Genetics, University of Colorado, Boulder, Colorado 80309, USA
    Exp Gerontol 41:1007-13. 2006
  2. pmc Utility of an improved model of amyloid-beta (Aβ₁₋₄₂) toxicity in Caenorhabditis elegans for drug screening for Alzheimer's disease
    Gawain McColl
    The Florey Institute of Neuroscience and Mental Health, University of Melbourne, Victoria 3010, Australia
    Mol Neurodegener 7:57. 2012
  3. pmc Progranulin regulates neuronal outgrowth independent of sortilin
    Jennifer Gass
    Department of Neuroscience, Mayo Clinic College of Medicine, Jacksonville, FL, USA
    Mol Neurodegener 7:33. 2012
  4. pmc A glycine zipper motif mediates the formation of toxic β-amyloid oligomers in vitro and in vivo
    Virginia Fonte
    Institute for Behavioral Genetics, University of Colorado, Boulder, CO 80309, USA
    Mol Neurodegener 6:61. 2011
  5. pmc What have worm models told us about the mechanisms of neuronal dysfunction in human neurodegenerative diseases?
    Dawn Teschendorf
    Institute for Behavioral Genetics, University of Colorado, Boulder, CO, 80309, USA
    Mol Neurodegener 4:38. 2009
  6. pmc The beta amyloid peptide can act as a modular aggregation domain
    Christopher D Link
    Institute for Behavioral Genetics, University of Colorado, Boulder, CO 80309, USA
    Neurobiol Dis 32:420-5. 2008
  7. ncbi request reprint Conversion of green fluorescent protein into a toxic, aggregation-prone protein by C-terminal addition of a short peptide
    Christopher D Link
    Institute for Behavioral Genetics, University of Colorado, Boulder, Colorado 80309, USA
    J Biol Chem 281:1808-16. 2006
  8. pmc Direct observation of stress response in Caenorhabditis elegans using a reporter transgene
    C D Link
    Institute for Behavioral Genetics, University of Colorado Boulder 80309 0447, USA
    Cell Stress Chaperones 4:235-42. 1999
  9. ncbi request reprint Invertebrate models of Alzheimer's disease
    C D Link
    Institute for Behavioral Genetics, University of Colorado, Boulder, CO 80309, USA
    Genes Brain Behav 4:147-56. 2005
  10. ncbi request reprint Visualization of fibrillar amyloid deposits in living, transgenic Caenorhabditis elegans animals using the sensitive amyloid dye, X-34
    C D Link
    Institute for Behavioral Genetics, University of Colorado, Campus Box 447, Boulder, CO 80309, USA
    Neurobiol Aging 22:217-26. 2001

Research Grants

  1. Transgenic C.elegans as Amyloid Disease Model
    CHRISTOPHER LINK; Fiscal Year: 2006
  2. Comparative Modeling of Neurodegenerative Diseases
    CHRISTOPHER LINK; Fiscal Year: 2006
  3. Investigation of TDP-43 Function and Toxicity in C. elegans
    Christopher D Link; Fiscal Year: 2010
  4. TRANSGENIC C. ELEGANS AS AMYLOID DISEASE MODEL
    CHRISTOPHER LINK; Fiscal Year: 2001
  5. TRANSGENIC C. ELEGANS AS AMYLOID DISEASE MODEL
    Christopher D Link; Fiscal Year: 2010

Collaborators

Detail Information

Publications29

  1. ncbi request reprint C. elegans models of age-associated neurodegenerative diseases: lessons from transgenic worm models of Alzheimer's disease
    Christopher D Link
    Institute for Behavioral Genetics, University of Colorado, Boulder, Colorado 80309, USA
    Exp Gerontol 41:1007-13. 2006
    ..In particular, I consider the potential these models have for uncovering common and unique fundamental toxic mechanisms underlying human neurodegenerative diseases...
  2. pmc Utility of an improved model of amyloid-beta (Aβ₁₋₄₂) toxicity in Caenorhabditis elegans for drug screening for Alzheimer's disease
    Gawain McColl
    The Florey Institute of Neuroscience and Mental Health, University of Melbourne, Victoria 3010, Australia
    Mol Neurodegener 7:57. 2012
    ..Ease of culturing and a short life cycle make this animal model well suited to rapid screening of candidate compounds...
  3. pmc Progranulin regulates neuronal outgrowth independent of sortilin
    Jennifer Gass
    Department of Neuroscience, Mayo Clinic College of Medicine, Jacksonville, FL, USA
    Mol Neurodegener 7:33. 2012
    ..We sought to elucidate this relationship to determine what role SORT1, as a regulator of PGRN levels, plays in modulating PGRN's neurotrophic effects...
  4. pmc A glycine zipper motif mediates the formation of toxic β-amyloid oligomers in vitro and in vivo
    Virginia Fonte
    Institute for Behavioral Genetics, University of Colorado, Boulder, CO 80309, USA
    Mol Neurodegener 6:61. 2011
    ..abstract:..
  5. pmc What have worm models told us about the mechanisms of neuronal dysfunction in human neurodegenerative diseases?
    Dawn Teschendorf
    Institute for Behavioral Genetics, University of Colorado, Boulder, CO, 80309, USA
    Mol Neurodegener 4:38. 2009
    ..These studies have given us a variety of insights into the specific disruptions of cellular processes that may underlie human neurodegenerative diseases...
  6. pmc The beta amyloid peptide can act as a modular aggregation domain
    Christopher D Link
    Institute for Behavioral Genetics, University of Colorado, Boulder, CO 80309, USA
    Neurobiol Dis 32:420-5. 2008
    ....
  7. ncbi request reprint Conversion of green fluorescent protein into a toxic, aggregation-prone protein by C-terminal addition of a short peptide
    Christopher D Link
    Institute for Behavioral Genetics, University of Colorado, Boulder, Colorado 80309, USA
    J Biol Chem 281:1808-16. 2006
    ..GFP::degron may serve as an instructive "generic" aggregating control protein for studies of disease-associated aggregating proteins, such as huntingtin, alpha-synuclein, and the beta-amyloid peptide...
  8. pmc Direct observation of stress response in Caenorhabditis elegans using a reporter transgene
    C D Link
    Institute for Behavioral Genetics, University of Colorado Boulder 80309 0447, USA
    Cell Stress Chaperones 4:235-42. 1999
    ..The ability to directly observe the stress response in living animals significantly simplifies the identification of both exogenous treatments and genetic alterations that modulate stress response, and possibly life span, in C. elegans...
  9. ncbi request reprint Invertebrate models of Alzheimer's disease
    C D Link
    Institute for Behavioral Genetics, University of Colorado, Boulder, CO 80309, USA
    Genes Brain Behav 4:147-56. 2005
    ..This review describes the rationale for AD-relevant studies in worms and flies and discusses both what has been learned from these studies and what may be discovered in the future...
  10. ncbi request reprint Visualization of fibrillar amyloid deposits in living, transgenic Caenorhabditis elegans animals using the sensitive amyloid dye, X-34
    C D Link
    Institute for Behavioral Genetics, University of Colorado, Campus Box 447, Boulder, CO 80309, USA
    Neurobiol Aging 22:217-26. 2001
    ..In vivo amyloid staining with X-34 may be a useful tool for monitoring anti-amyloidic treatments in real time or screening for genetic alterations that affect amyloid formation...
  11. ncbi request reprint Transgenic invertebrate models of age-associated neurodegenerative diseases
    C D Link
    Institute for Behavioral Genetics, University of Colorado, Campus Box 447, Boulder, CO 80309, USA
    Mech Ageing Dev 122:1639-49. 2001
    ..This review considers what has been learned from these invertebrate models, and speculates what further insight may be gained from them...
  12. ncbi request reprint Gene expression analysis in a transgenic Caenorhabditis elegans Alzheimer's disease model
    Christopher D Link
    Institute for Behavioral Genetics, University of Colorado, Campus Box 447, Boulder, CO 80309, USA
    Neurobiol Aging 24:397-413. 2003
    ..elegans model. Both CRYAB and TNFAIP1 show increased transcript levels in AD brains, supporting the validity of this approach...
  13. pmc AIP-1 ameliorates beta-amyloid peptide toxicity in a Caenorhabditis elegans Alzheimer's disease model
    Wail M Hassan
    Institute for Behavioral Genetics, University of Colorado at Boulder, Boulder, CO 80303, USA
    Hum Mol Genet 18:2739-47. 2009
    ..Our results implicate AIP-1 in the regulation of protein turnover and protection against Abeta toxicity and point at AIRAPL as the functional mammalian homologue of AIP-1...
  14. ncbi request reprint Suppression of in vivo beta-amyloid peptide toxicity by overexpression of the HSP-16.2 small chaperone protein
    Virginia Fonte
    Institute for Behavioral Genetics, University of Colorado, Boulder, Colorado 80309, USA
    J Biol Chem 283:784-91. 2008
    ....
  15. pmc Interaction of intracellular beta amyloid peptide with chaperone proteins
    Virginia Fonte
    Institute for Behavioral Genetics, University of Colorado, Boulder, CO 80309, USA
    Proc Natl Acad Sci U S A 99:9439-44. 2002
    ..These results suggest that chaperone function can play a role in modulating intracellular A beta metabolism and toxicity...
  16. ncbi request reprint Decreased insulin-receptor signaling promotes the autophagic degradation of beta-amyloid peptide in C. elegans
    Maria L Florez-McClure
    Institute for Behavioral Genetics, University of Colorado, Boulder, Colorado 80309, USA
    Autophagy 3:569-80. 2007
    ..Also, Abeta; daf-2(e1370) nematodes contain more lysosomes than either Abeta or control strains. Finally, we demonstrate that decreased insulin-receptor signaling promotes the autophagic degradation of Abeta...
  17. pmc Life-span extension by dietary restriction is mediated by NLP-7 signaling and coelomocyte endocytosis in C. elegans
    Sang Kyu Park
    Institute for Behavioral Genetics, University of Colorado at Boulder, Box 447, Boulder, CO 80303, USA
    FASEB J 24:383-92. 2010
    ..We conclude that two novel pathways, NLP-7 signaling and endocytosis by coelomocytes, are required for life extension under dietary restriction in C. elegans...
  18. ncbi request reprint Compensatory regulation among ER chaperones in C. elegans
    Wadim J Kapulkin
    Institute for Behavioral Genetics, Campus Box 447, University of Colorado, Boulder, CO 80309, USA
    FEBS Lett 579:3063-8. 2005
    ..We show that this compensatory regulation is specific for ER chaperones, not dependent on RNA interference, and required for maintaining viability in worms containing a deletion of the hsp-3 gene...
  19. ncbi request reprint Reporter transgenes for study of oxidant stress in Caenorhabditis elegans
    Christopher D Link
    Institute for Behavioral Genetics, University of Colorado, Boulder, Colorado 80309, USA
    Methods Enzymol 353:497-505. 2002
  20. pmc Identification of a novel cis-regulatory element involved in the heat shock response in Caenorhabditis elegans using microarray gene expression and computational methods
    Debraj GuhaThakurta
    Department of Genetics, Washington University School of Medicine, St Louis, Missouri 63114, USA
    Genome Res 12:701-12. 2002
    ..The contributions of individual sites toward induction of transcription on HS are nonadditive, which indicates interaction and cross-talk between the sites, possibly through the transcription factors (TFs) binding to these sites...
  21. ncbi request reprint A global analysis of Caenorhabditis elegans operons
    Thomas Blumenthal
    Department of Biochemistry and Molecular Genetics, University of Colorado School of Medicine, Box B121, 4200 E 9th Avenue, Denver, Colorado 80262, USA
    Nature 417:851-4. 2002
    ..elegans genes. Numerous examples of co-transcription of genes encoding functionally related proteins are evident. Inspection of the operon list should reveal previously unknown functional relationships...
  22. ncbi request reprint Oxidative stress precedes fibrillar deposition of Alzheimer's disease amyloid beta-peptide (1-42) in a transgenic Caenorhabditis elegans model
    Jennifer Drake
    Department of Chemistry and Center of Membrane Sciences, University of Kentucky, Lexington, KY 40506, USA
    Neurobiol Aging 24:415-20. 2003
    ..These results are discussed with reference to Alzheimer's disease...
  23. ncbi request reprint Amyloid-beta-induced pathological behaviors are suppressed by Ginkgo biloba extract EGb 761 and ginkgolides in transgenic Caenorhabditis elegans
    Yanjue Wu
    Department of Pharmaceutical Sciences, School of Pharmacy, University of Maryland, Baltimore, Maryland 21201, USA
    J Neurosci 26:13102-13. 2006
    ....
  24. pmc Soy isoflavone glycitein protects against beta amyloid-induced toxicity and oxidative stress in transgenic Caenorhabditis elegans
    Astrid Gutierrez-Zepeda
    Department of Biological Sciences, University of Southern Mississippi, Hattiesburg, MS 39406, USA
    BMC Neurosci 6:54. 2005
    ..elegans, that express human beta amyloid (Abeta), were fed with soy derived isoflavones genistein, daidzein and glycitein (100 microg/ml) and then examined for Abeta-induced paralysis and the levels of reactive oxygen species...
  25. ncbi request reprint Proteomic identification of proteins specifically oxidized in Caenorhabditis elegans expressing human Abeta(1-42): implications for Alzheimer's disease
    Debra Boyd-Kimball
    Department of Chemistry, Center of Membrane Sciences, and Sanders Brown Center on Aging, 121 Chemistry Physics Building, University of Kentucky, Lexington, KY 40506 0055, USA
    Neurobiol Aging 27:1239-49. 2006
    ..We identified 16 oxidized proteins involved in energy metabolism, proteasome function, and scavenging of oxidants that are more oxidized compared to control lines. These results are discussed with reference to Alzheimer's disease...
  26. ncbi request reprint Functional analysis of the glutathione S-transferase 3 from Onchocerca volvulus (Ov-GST-3): a parasite GST confers increased resistance to oxidative stress in Caenorhabditis elegans
    Andreas Kampkotter
    Institut fur Genetik, Heinrich Heine Universitat, Universitatsstrasse 1, 40225 Dusseldorf, Germany
    J Mol Biol 325:25-37. 2003
    ..This study also shows the applicability of C.elegans as a model organism for the functional characterization of genes from (parasitic) nematode species which are not accessible to genetic manipulations...
  27. ncbi request reprint Expression of the small heat-shock protein Hsp16-2 in Caenorhabditis elegans is suppressed by Ginkgo biloba extract EGb 761
    Amy Strayer
    Department of Biological Sciences, The University of Southern Mississippi, Hattiesburg 39406 5018, USA
    FASEB J 17:2305-7. 2003
    ..These results support the hypothesis that EGb 761 augments the natural antistress system of C. elegans, thus increasing stress resistance and life span...
  28. ncbi request reprint A stress-responsive glutathione S-transferase confers resistance to oxidative stress in Caenorhabditis elegans
    Britta Leiers
    Institute for Genetics and Biological Medical Research Center, Heinrich Heine University, Dusseldorf, Germany
    Free Radic Biol Med 34:1405-15. 2003
    ..The Ce-GST-p24 was also localized in BL1 C. elegans by confocal laser-scanning microscopy, revealing a wide-spread distribution profile...
  29. pmc A pilot proteomic study of amyloid precursor interactors in Alzheimer's disease
    Barbara A Cottrell
    Buck Institute for Age Research, Novato, CA 94945, USA
    Ann Neurol 58:277-89. 2005
    ..In agreement with previous studies, our results are compatible with an involvement of APP in axonal transport and vesicular trafficking, and with a potential association of APP with cellular protein folding/protein degradation systems...

Research Grants20

  1. Transgenic C.elegans as Amyloid Disease Model
    CHRISTOPHER LINK; Fiscal Year: 2006
    ..The role of specific genes and gene products in Abeta toxicity will be investigated using double-stranded RNA inhibition (RNAi) and Green Fluorescent Protein (GFP)-based transgenic reporter constructs. ..
  2. Comparative Modeling of Neurodegenerative Diseases
    CHRISTOPHER LINK; Fiscal Year: 2006
    ..elegans to manipulate these molecular responses to determine their role in disease protein toxicity. These studies will directly test whether there is a common underlying toxic mechanism for these neurodegenerative diseases. ..
  3. Investigation of TDP-43 Function and Toxicity in C. elegans
    Christopher D Link; Fiscal Year: 2010
    ..In this project we will use model systems to determine the functions of TDP-43 and how its deposition may cause neurodegeneration. ..
  4. TRANSGENIC C. ELEGANS AS AMYLOID DISEASE MODEL
    CHRISTOPHER LINK; Fiscal Year: 2001
    ..abstract_text> ..
  5. TRANSGENIC C. ELEGANS AS AMYLOID DISEASE MODEL
    Christopher D Link; Fiscal Year: 2010
    ..The proposed study seeks to determine the cellular and molecular basis of -amyloid peptide toxicity. Understanding the toxic mechanism of this protein make be critical for developing therapeutics for Alzheimer's disease. ..