Dale E Bredesen

Summary

Affiliation: Buck Institute for Age Research
Country: USA

Publications

  1. ncbi request reprint Receptors that mediate cellular dependence
    D E Bredesen
    The Buck Institute for Age Research, Novato, CA 94945, USA
    Cell Death Differ 12:1031-43. 2005
  2. pmc Key note lecture: toward a mechanistic taxonomy for cell death programs
    Dale E Bredesen
    Buck Institute for Age Research, CA 94945, USA
    Stroke 38:652-60. 2007
  3. pmc Valosin-containing protein gene mutations: cellular phenotypes relevant to neurodegeneration
    Karen S Poksay
    The Buck Institute for Research on Aging, 8001 Redwood Blvd, Novato, CA 94945, USA
    J Mol Neurosci 44:91-102. 2011
  4. pmc A novel motif identified in dependence receptors
    Gabriel Del Rio
    Buck Institute for Age Research, Novato, California, United States of America
    PLoS ONE 2:e463. 2007
  5. pmc Next generation therapeutics for Alzheimer's disease
    Dale E Bredesen
    Buck Institute for Research on Aging, Novato, CA, USA
    EMBO Mol Med 5:795-8. 2013
  6. pmc mCiRNA-synaptic crystal ball?
    Dale Bredesen
    The Buck Institute for Research on Aging, Novato, CA 94945, USA
    Aging (Albany NY) 4:732-3. 2012
  7. ncbi request reprint APP-based neuroprotective strategies
    Dale E Bredesen
    Buck Institute for Age Research and University of California, San Francisco, USA
    Curr Alzheimer Res 4:541-3. 2007
  8. ncbi request reprint Apoptosis and dependence receptors: a molecular basis for cellular addiction
    Dale E Bredesen
    The Buck Institute for Age Research, 8001 Redwood Blvd, Novato, CA 94945, USA
    Physiol Rev 84:411-30. 2004
  9. ncbi request reprint The non-existent aging program: how does it work?
    Dale E Bredesen
    Buck Institute for Age Research, University of California, San Francisco, 8001 Redwood Blvd, Novato, CA 94949, USA
    Aging Cell 3:255-9. 2004
  10. ncbi request reprint Rebuttal to Austad: 'Is aging programmed?
    Dale E Bredesen
    Buck Institute for Age Research, University of California, San Francisco, 8001 Redwood Blvd, Novato, CA 94949, USA
    Aging Cell 3:261-2. 2004

Collaborators

Detail Information

Publications80

  1. ncbi request reprint Receptors that mediate cellular dependence
    D E Bredesen
    The Buck Institute for Age Research, Novato, CA 94945, USA
    Cell Death Differ 12:1031-43. 2005
    ..Cellular dependence receptors, considered in the aggregate, may thus form a system of molecular integration, analogous to the electrical integration system provided by dendritic arbors in the nervous system...
  2. pmc Key note lecture: toward a mechanistic taxonomy for cell death programs
    Dale E Bredesen
    Buck Institute for Age Research, CA 94945, USA
    Stroke 38:652-60. 2007
    ..Both anti-pcd and pro-pcd modulators play prominent roles in development and disease, including ischemic cerebrovascular disease. The purpose of this article is therefore to review the basics of programmed cell death...
  3. pmc Valosin-containing protein gene mutations: cellular phenotypes relevant to neurodegeneration
    Karen S Poksay
    The Buck Institute for Research on Aging, 8001 Redwood Blvd, Novato, CA 94945, USA
    J Mol Neurosci 44:91-102. 2011
    ....
  4. pmc A novel motif identified in dependence receptors
    Gabriel Del Rio
    Buck Institute for Age Research, Novato, California, United States of America
    PLoS ONE 2:e463. 2007
    ..To date, we have not identified a function for this putative domain. We speculate that the DART motif may be involved in protein processing, interaction with other proteins or lipids, or homomultimerization...
  5. pmc Next generation therapeutics for Alzheimer's disease
    Dale E Bredesen
    Buck Institute for Research on Aging, Novato, CA, USA
    EMBO Mol Med 5:795-8. 2013
    ..In searching for new approaches that may succeed where previous ones have failed, it may be instructive to consider the successful therapeutic developments for other chronic illnesses such as cancer and human immunodeficiency virus...
  6. pmc mCiRNA-synaptic crystal ball?
    Dale Bredesen
    The Buck Institute for Research on Aging, Novato, CA 94945, USA
    Aging (Albany NY) 4:732-3. 2012
    ..Comment on: Sheinerman KS, Tsivinsky VG, Crawford F, Mullan MJ, Abdullah L, Umansky SR. Plasma microRNA biomarkers for detection of mild cognitive impairment. Aging (Albany NY). 2012; 4:590-605...
  7. ncbi request reprint APP-based neuroprotective strategies
    Dale E Bredesen
    Buck Institute for Age Research and University of California, San Francisco, USA
    Curr Alzheimer Res 4:541-3. 2007
    ..Here we discuss the possibility that APP-mediated signal transduction, downstream from amyloid-beta peptide production itself, may be an appropriate therapeutic target in Alzheimer's disease...
  8. ncbi request reprint Apoptosis and dependence receptors: a molecular basis for cellular addiction
    Dale E Bredesen
    The Buck Institute for Age Research, 8001 Redwood Blvd, Novato, CA 94945, USA
    Physiol Rev 84:411-30. 2004
    ..Thus these receptors may serve in caspase amplification, and in so doing create cellular states of dependence on their respective ligands...
  9. ncbi request reprint The non-existent aging program: how does it work?
    Dale E Bredesen
    Buck Institute for Age Research, University of California, San Francisco, 8001 Redwood Blvd, Novato, CA 94949, USA
    Aging Cell 3:255-9. 2004
    ....
  10. ncbi request reprint Rebuttal to Austad: 'Is aging programmed?
    Dale E Bredesen
    Buck Institute for Age Research, University of California, San Francisco, 8001 Redwood Blvd, Novato, CA 94949, USA
    Aging Cell 3:261-2. 2004
  11. pmc Cell death in the nervous system
    Dale E Bredesen
    Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, California 94945, USA
    Nature 443:796-802. 2006
    ..Surprisingly, although the cell death itself may occur relatively late in the course of the degenerative process, the mediators of the underlying cell-death pathways have shown promise as potential therapeutic targets...
  12. ncbi request reprint Toward a mechanistic taxonomy of cell death programs
    Dale E Bredesen
    Buck Institute and UCSF, USA
    J Alzheimers Dis 6:S3-6. 2004
  13. ncbi request reprint Apoptosis: overview and signal transduction pathways
    D E Bredesen
    Buck Institute for Age Research, Novato, California, USA
    J Neurotrauma 17:801-10. 2000
    ..Activated caspases are the executioners of the apoptotic program, and carry out this function by cleaving specific cellular substrates. Modulation of this process holds promise as a therapeutic approach in neurotrauma...
  14. pmc Importance of the caspase cleavage site in amyloid-β protein precursor
    Dale E Bredesen
    Buck Institute for Age Research, Novato, CA 94945, USA
    J Alzheimers Dis 22:57-63. 2010
    ..Here we review the results and implications of these studies for the understanding of Alzheimer's disease pathophysiology and the potential development of therapeutics that target this site in AβPP...
  15. pmc Neurodegeneration in Alzheimer's disease: caspases and synaptic element interdependence
    Dale E Bredesen
    Buck Institute for Age Research, 8001 Redwood Blvd, Novato, CA USA 94945
    Mol Neurodegener 4:27. 2009
    ..Here we review the effects and implications of this cleavage event, and propose a model of Alzheimer's disease that focuses on the critical nature of this cleavage and its downstream effects...
  16. ncbi request reprint Programmed cell death mechanisms in neurological disease
    Dale E Bredesen
    Buck Institute for Age Research, 8001 Redwood Blvd, Novato, California 94945, USA
    Curr Mol Med 8:173-86. 2008
    ....
  17. pmc Selective vulnerability in Alzheimer's disease: amyloid precursor protein and p75(NTR) interaction
    Joanna Fombonne
    The Buck Institute for Age Research, Novato, CA 94945, USA
    Ann Neurol 65:294-303. 2009
    ..However, the relation between amyloid precursor protein (APP) and p75(NTR) has not been described previously...
  18. pmc Long-term prevention of Alzheimer's disease-like behavioral deficits in PDAPP mice carrying a mutation in Asp664
    Veronica Galvan
    Buck Institute for Age Research, 8001 Redwood Blvd, Novato, CA 94945, USA
    Behav Brain Res 191:246-55. 2008
    ..Our results thus further demonstrate that the D664A mutation either completely precludes, or markedly delays (beyond 13 mo) the appearance of AD-like deficits in this mouse model of AD...
  19. pmc Interaction of ASK1 and the beta-amyloid precursor protein in a stress-signaling complex
    Veronica Galvan
    Buck Institute for Age Research, 8001 Redwood Blvd, Novato, CA 94945, USA
    Neurobiol Dis 28:65-75. 2007
    ..Thus, ASK1 may be the apical MAPKKK in a signaling complex assembled with APP as a response to stress...
  20. ncbi request reprint Alternative, nonapoptotic programmed cell death: mediation by arrestin 2, ERK2, and Nur77
    Susana Castro-Obregon
    Buck Institute for Age Research, Novato, California 94945 1400, USA
    J Biol Chem 279:17543-53. 2004
    ..These results suggest that Nur77, which is regulated by a MAPK pathway activated via arrestin 2, modulates NK(1)R-mediated nonapoptotic pcd...
  21. pmc C-terminal cleavage of the amyloid-beta protein precursor at Asp664: a switch associated with Alzheimer's disease
    Surita Banwait
    Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945, USA
    J Alzheimers Dis 13:1-16. 2008
    ....
  22. ncbi request reprint Molecular components of a cell death pathway activated by endoplasmic reticulum stress
    Rammohan V Rao
    The Buck Institute for Age Research, Novato, California 94945, USA
    J Biol Chem 279:177-87. 2004
    ..Our data identify two molecules, valosin-containing protein and apoptosis-linked gene-2 (ALG-2), that appear to play a role in mediating ER stress-induced cell death...
  23. pmc Endoplasmic reticulum stress-induced cell death in dopaminergic cells: effect of resveratrol
    Shankar J Chinta
    The Buck Institute for Age Research, 8001 Redwood Blvd, Novato, CA 94945, USA
    J Mol Neurosci 39:157-68. 2009
    ....
  24. pmc The small chaperone protein p23 and its cleaved product p19 in cellular stress
    Karen S Poksay
    The Buck Institute for Research on Aging, 8001 Redwood Blvd, Novato, CA 94945, USA
    J Mol Neurosci 46:303-14. 2012
    ....
  25. pmc Novel mediators of amyloid precursor protein signaling
    Andrzej Swistowski
    Buck Institute for Age Research, Novato, California 94945, USA
    J Neurosci 29:15703-12. 2009
    ..These results define new mediators of the signal transduction network mediated by APP...
  26. pmc Coupling endoplasmic reticulum stress to the cell death program: role of the ER chaperone GRP78
    Rammohan V Rao
    Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945 1400, USA
    FEBS Lett 514:122-8. 2002
    ..These results define a novel protective role for GRP78 in preventing ER stress-induced cell death...
  27. pmc Differential regulation of the intrinsic pathway of apoptosis in brain and liver during ageing
    Veronika Stoka
    Buck Institute for Age Research, 8001 Redwood Blvd, Novato, CA 94945, USA
    FEBS Lett 580:3739-45. 2006
    ..These results suggest that a decrease in apoptosis activation during ageing is not tissue-specific, but rather displays a complex dependence on species and strains of animals...
  28. ncbi request reprint Caspase cleavage of members of the amyloid precursor family of proteins
    Veronica Galvan
    Buck Institute for Age Research, Novato, California 94945 1400, USA
    J Neurochem 82:283-94. 2002
    ..Our results suggest that even though APLP1 and APLP2 cannot generate Abeta, they may potentially contribute to the pathology of AD by generating peptide fragments whose toxicity is comparable to that of APPC31...
  29. pmc Neuroprotective Sirtuin ratio reversed by ApoE4
    Veena Theendakara
    The Buck Institute for Research on Aging, Novato, CA 94945
    Proc Natl Acad Sci U S A 110:18303-8. 2013
    ....
  30. pmc Signal transduction in Alzheimer disease: p21-activated kinase signaling requires C-terminal cleavage of APP at Asp664
    Thuy Vi V Nguyen
    Buck Institute for Age Research, Novato, California 94945, USA
    J Neurochem 104:1065-80. 2008
    ..These findings are compatible with previous suggestions that PAK may be involved in the pathophysiology of AD, and demonstrate that both early activation and late inactivation in the murine AD model require the cleavage of APP at Asp664...
  31. pmc Reversal of learning deficits in hAPP transgenic mice carrying a mutation at Asp664: a role for early experience
    Junli Zhang
    Buck Institute for Age Research, 8001 Redwood Blvd, Novato, CA 94945, United States
    Behav Brain Res 206:202-7. 2010
    ..Our results suggest that early experience reduces the contribution of non-cognitive components of behaviour to performance, and may contribute to the restoration of learning at later ages in PDAPP(D664A) mice...
  32. pmc AβPP-selective BACE inhibitors (ASBI): novel class of therapeutic agents for alzheimer's disease
    Olivier Descamps
    Buck Institute for Research on Aging, Novato, CA, USA
    J Alzheimers Dis 37:343-55. 2013
    ..ASBIs represent a novel class of candidate therapeutic agents for Alzheimer's disease. ..
  33. pmc Coupling endoplasmic reticulum stress to the cell death program in dopaminergic cells: effect of paraquat
    Shankar J Chinta
    The Buck Institute for Age Research, 8001 Redwood Blvd, Novato, CA 94945, USA
    Neuromolecular Med 10:333-42. 2008
    ..Our results indicate a protective role for p23 in PD-related programmed cell death. The data also underscore the involvement of ER, caspases, and the proteasomal system in ER stress-induced cell death process...
  34. pmc Reversal of Alzheimer's-like pathology and behavior in human APP transgenic mice by mutation of Asp664
    Veronica Galvan
    Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945, USA
    Proc Natl Acad Sci U S A 103:7130-5. 2006
    ..These results suggest that Asp-664 plays a critical role in the generation of Alzheimer-related pathophysiological and behavioral changes in human APP transgenic mice, possibly as a cleavage site or via protein-protein interactions...
  35. ncbi request reprint Tau phosphorylation in Alzheimer's disease: potential involvement of an APP-MAP kinase complex
    Alyson L Peel
    Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945, USA
    Neuromolecular Med 5:205-18. 2004
    ..2003), these results suggest a model of AD in which Abeta peptide dimerizes APP directly, leading to the activation of ASK1, MKK6, and p38, with subsequent phosphorylation of tau at sites characteristic of AD...
  36. ncbi request reprint PLAIDD, a type II death domain protein that interacts with p75 neurotrophin receptor
    Harald Frankowski
    Buck Institute for Age Research, Novato, CA 94945 1400, USA
    Neuromolecular Med 1:153-70. 2002
    ..Both isoforms of PLAIDD could be co-immunoprecipitated with p75NTR, suggesting an interaction between these molecules...
  37. 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...
  38. pmc The small co-chaperone p23 overexpressing transgenic mouse
    Junli Zhang
    The Buck Institute for Research on Aging, 8001 Redwood Blvd, Novato, CA 94945, USA
    J Neurosci Methods 212:190-4. 2013
    ..These mice should prove useful for studying the role of p23 and/or uncleavable p23 in cellular stress-induced cell death...
  39. pmc Many neuronal and behavioral impairments in transgenic mouse models of Alzheimer's disease are independent of caspase cleavage of the amyloid precursor protein
    Julie A Harris
    Gladstone Institute of Neurological Disease and Department of Neurology, University of California, San Francisco, San Francisco, California 94158, USA
    J Neurosci 30:372-81. 2010
    ..Thus, caspase cleavage of APP at position D664 and generation of C31 do not play a critical role in the development of these abnormalities...
  40. ncbi request reprint Atypical recognition consensus of CIN85/SETA/Ruk SH3 domains revealed by target-assisted iterative screening
    Alexei V Kurakin
    Buck Institute for Age Research, Novato, California 94945, USA
    J Biol Chem 278:34102-9. 2003
    ..A direct interaction of synaptojanin 1 and PAK2 with CIN85 SH3 domains was confirmed by Far Western blotting...
  41. pmc The PDZ domain as a complex adaptive system
    Alexei Kurakin
    The Buck Institute for Age Research, Novato, California, USA
    PLoS ONE 2:e953. 2007
    ..The generalization of this reconceptualization in regard to other protein interaction modules and specific protein associations is consistent with the image of the cell as a complex adaptive macromolecular system as opposed to clockwork...
  42. pmc Misfolded proteins, endoplasmic reticulum stress and neurodegeneration
    Rammohan V Rao
    Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, California 94945 1400, USA
    Curr Opin Cell Biol 16:653-62. 2004
    ..Dissecting these pathways should be valuable in understanding the pathogenesis of, and ultimately in designing therapy for, neurodegenerative diseases that feature misfolded proteins...
  43. pmc Altering APP proteolysis: increasing sAPPalpha production by targeting dimerization of the APP ectodomain
    Clare A Peters Libeu
    Buck Institute for Research on Aging, Novato, California, United States of America
    PLoS ONE 7:e40027. 2012
    ..These compounds provide a rationale for the development of a new class of therapeutics for Alzheimer's disease...
  44. pmc Paradoxical effect of TrkA inhibition in Alzheimer's disease models
    Qiang Zhang
    Buck Institute for Research on Aging, Novato, CA, USA
    J Alzheimers Dis 40:605-17. 2014
    ..The results also suggest that one component of an optimal therapy for Alzheimer's disease may be a TrkA inhibitor. ..
  45. doi request reprint Signaling via amyloid precursor-like proteins APLP1 and APLP2
    Mark E Orcholski
    Buck Institute for Age Research, Novato, CA 94945, USA
    J Alzheimers Dis 23:689-99. 2011
    ..APLP1 displayed much lower transactivation levels compared to AβPP and APLP2. These results indicate that all three AβPP family members are capable of activating gene transcription via Mint3-Taz and Mint3-Yap...
  46. doi request reprint Identification of new modulators and protein alterations in non-apoptotic programmed cell death
    Sabina Sperandio
    Buck Institute for Age Research, Novato, California 94945, USA
    J Cell Biochem 111:1401-12. 2010
    ..Identification of specific paraptotic changes will ultimately lead to tools to detect this type of programmed cell death in in vivo systems and allow for its further characterization...
  47. pmc Mechanism of cytotoxicity mediated by the C31 fragment of the amyloid precursor protein
    Sun Ah Park
    Department of Neurosciences, University of California, San Diego, La Jolla, CA 92093, USA
    Biochem Biophys Res Commun 388:450-5. 2009
    ....
  48. pmc An unconventional IAP-binding motif revealed by target-assisted iterative screening (TAIS) of the BIR3-cIAP1 domain
    Alexei Kurakin
    The Buck Institute for Age Research, 8001 Redwood Blvd, Novato, CA 94945, USA
    J Mol Recognit 20:39-50. 2007
    ..A 'two-pocket' model of BIR domain recognition mechanism is proposed as the basis of differential BIR domain interactions with different IBMs...
  49. ncbi request reprint Coupling endoplasmic reticulum stress to the cell death program. An Apaf-1-independent intrinsic pathway
    Rammohan V Rao
    Buck Institute for Age Research, Novato, California 94945 and the Department of Medicine III, Johannes Gutenberg University, Mainz D 55101, Germany
    J Biol Chem 277:21836-42. 2002
    ..Thus, ER stress-induced programmed cell death defines a novel, mitochondrial and Apaf-1-independent, intrinsic apoptotic pathway...
  50. pmc No consistent bioenergetic defects in presynaptic nerve terminals isolated from mouse models of Alzheimer's disease
    Sung W Choi
    Buck Institute Research on Aging, Novato, California 94945, USA
    J Neurosci 32:16775-84. 2012
    ..Our results support the conclusion that the intrinsic bioenergetic capacities of presynaptic nerve terminals are maintained in these symptomatic AD mouse models...
  51. pmc The multi-functional drug tropisetron binds APP and normalizes cognition in a murine Alzheimer's model
    Patricia Spilman
    Buck Institute for Research on Aging, 8001 Redwood Blvd, Novato, CA 94945, USA
    Brain Res 1551:25-44. 2014
    ....
  52. ncbi request reprint Proteolytic cleavage of ataxin-7 by caspase-7 modulates cellular toxicity and transcriptional dysregulation
    Jessica E Young
    Buck Institute for Age Research, Novato, California, 94945, USA
    J Biol Chem 282:30150-60. 2007
    ..Our results, thus, suggest that proteolytic processing of ataxin-7 by caspase-7 may contribute to SCA7 disease pathogenesis...
  53. ncbi request reprint An artificially designed pore-forming protein with anti-tumor effects
    H Michael Ellerby
    Program on Cancer and Aging, The Buck Institute, Novato, California 94945, USA
    J Biol Chem 278:35311-6. 2003
    ..We propose and validate a mechanism for the selectivity of SGP toward cell membranes in tumors. SGP is the prototype for a new class of artificial proteins designed for therapeutic applications...
  54. ncbi request reprint Caspase cleavage of the amyloid precursor protein modulates amyloid beta-protein toxicity
    Daniel C Lu
    Department of Neurosciences, University of California, San Diego, La Jolla 92093, USA
    J Neurochem 87:733-41. 2003
    ..These findings link C31 generation and its potential cell death activity to Abeta cytotoxicity, the leading mechanism proposed for neuronal death in AD...
  55. pmc Differential regulation of Smac/DIABLO and Hsp-70 during brain maturation
    Veronika Stoka
    Buck Institute for Age Research, 8001 Redwood Blvd, Novato, CA 94945, USA
    Neuromolecular Med 9:255-63. 2007
    ..These results indicate that the activation pattern of the intrinsic pathway of apoptosis undergoes a marked shift during postnatal maturation...
  56. pmc Enhanced neurogenesis in Alzheimer's disease transgenic (PDGF-APPSw,Ind) mice
    Kunlin Jin
    Buck Institute for Age Research, Novato, CA 94945, USA
    Proc Natl Acad Sci U S A 101:13363-7. 2004
    ..Enhanced neurogenesis in AD and animal models of AD suggests that neurogenesis may be a compensatory response and that measures to enhance neurogenesis further could have therapeutic potential...
  57. pmc Improved prediction of critical residues for protein function based on network and phylogenetic analyses
    Boris Thibert
    Buck Institute for Age Research, 8001 Redwood Blvd, Novato, CA 94945, USA
    BMC Bioinformatics 6:213. 2005
    ....
  58. pmc Structural and functional alterations in amyloid-β precursor protein induced by amyloid-β peptides
    Clare Peters Libeu
    Buck Institute for Age Research, Novato, CA 94945, USA
    J Alzheimers Dis 25:547-66. 2011
    ..Our data provide the first structural evidence for Aβ-AβPP binding and suggest a mechanism for differential modulation of AβPP processing and cell death signaling by Aβ dimers versus conformationally-specific larger oligomers...
  59. ncbi request reprint Neurogenesis in the adult brain: implications for Alzheimer's disease
    Veronica Galvan
    Buck Institute for Age Research, 8001 Redwood Blvd, Novato, CA 94945, USA
    CNS Neurol Disord Drug Targets 6:303-10. 2007
    ....
  60. pmc Developmental shift in the apostat: comparison of neurones and astrocytes
    Veronika Stoka
    Buck Institute for Age Research, Novato, CA 94945, USA
    FEBS Lett 579:6147-50. 2005
    ....
  61. ncbi request reprint Target-assisted iterative screening of phage surface display cDNA libraries
    Alexei Kurakin
    Buck Institute for Age Research, Novato, CA, USA
    Methods Mol Biol 264:47-60. 2004
    ..The described application is a method of choice for the researchers interested in the identification and characterization of novel protein-protein interactions mediated by peptide recognition domains...
  62. ncbi request reprint Target-assisted iterative screening reveals novel interactors for PSD95, Nedd4, Src, Abl and Crk proteins
    Alexei Kurakin
    Buck Institute for Age Research, 8001 Redwood Blvd, Novato, CA 94945, USA
    J Biomol Struct Dyn 19:1015-29. 2002
    ..The novel screening format, dubbed TAIS (target-assisted iterative screening), is discussed as an alternative platform to existing technologies for a pair-wise characterization of protein-protein interactions...
  63. ncbi request reprint Activation of the cell stress kinase PKR in Alzheimer's disease and human amyloid precursor protein transgenic mice
    Alyson L Peel
    Buck Institute for Age Research, Novato, CA, USA
    Neurobiol Dis 14:52-62. 2003
    ..These findings support a role for PKR activation in the pathogenesis of AD...
  64. pmc Ayurvedic medicinal plants for Alzheimer's disease: a review
    Rammohan V Rao
    The Buck Institute for Research on Aging, 8001 Redwood Boulevard, Novato, CA 94945, USA
    Alzheimers Res Ther 4:22. 2012
    ....
  65. ncbi request reprint Induction of the C-terminal proteolytic cleavage of AβPP by statins
    Olivier Descamps
    Buck Institute for Age Research, Novato, CA 94945, USA
    J Alzheimers Dis 25:51-7. 2011
    ....
  66. ncbi request reprint Type 1 insulin-like growth factor receptor (IGF-IR) signaling inhibits apoptosis signal-regulating kinase 1 (ASK1)
    Veronica Galvan
    Buck Institute for Age Research, Novato, California 94945 1400, USA
    J Biol Chem 278:13325-32. 2003
    ....
  67. pmc Efficient identification of critical residues based only on protein structure by network analysis
    Michael P Cusack
    Buck Institute for Age Research, Novato, California, United States of America
    PLoS ONE 2:e421. 2007
    ..A unique feature of the method is the inclusion of the conformational diversity of proteins in the prediction, thus reproducing a basic feature of the structure/function relationship of proteins...
  68. ncbi request reprint Ten years on: mediation of cell death by the common neurotrophin receptor p75(NTR)
    Shahrooz Rabizadeh
    The Buck Institute for Age Research, 8001 Redwood Blvd, Novato, CA 94945 1400, USA
    Cytokine Growth Factor Rev 14:225-39. 2003
    ..Results to date suggest that these functions are mediated through different underlying mechanisms, and that their respective signaling pathways are cell type and co-receptor dependent...
  69. pmc Inhibition of mTOR by rapamycin abolishes cognitive deficits and reduces amyloid-beta levels in a mouse model of Alzheimer's disease
    Patricia Spilman
    Department of Physiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America
    PLoS ONE 5:e9979. 2010
    ..Whether inhibition of the mTOR pathway would delay or prevent age-associated disease such as AD remained to be determined...
  70. pmc Science fact and the SENS agenda. What can we reasonably expect from ageing research?
    Huber Warner
    Buck Institute for Age Research, Novato, CA, USA
    EMBO Rep 6:1006-8. 2005
  71. ncbi request reprint Deficits in synaptic transmission and learning in amyloid precursor protein (APP) transgenic mice require C-terminal cleavage of APP
    Michael J Saganich
    Salk Institute for Biological Studies, La Jolla, California 92037, USA
    J Neurosci 26:13428-36. 2006
    ..These results indicate that cleavage of APP may play a critical role in the development of synaptic and behavioral dysfunction in APP transgenic mice...
  72. ncbi request reprint Molecular characterization of neurohybrid cell death induced by Alzheimer's amyloid-beta peptides via p75NTR/PLAIDD
    Yuichi Hashimoto
    Department of Pharmacology, Keio University School of Medicine, Shinanomachi, Tokyo, Japan
    J Neurochem 90:549-58. 2004
    ..In addition, we found that HN, ADNF, IGF-I, or bFGF inhibits both pathways of Abeta-induced neurotoxicity mediated by p75NTR...
  73. ncbi request reprint Amyloid beta protein toxicity mediated by the formation of amyloid-beta protein precursor complexes
    Daniel C Lu
    Department of Neurosciences, University of California San Diego, 9500 Gilman Drive, Mail Code 0691, La Jolla, CA 92093 0691, USA
    Ann Neurol 54:781-9. 2003
    ....
  74. pmc Coupling endoplasmic reticulum stress to the cell death program in mouse melanoma cells: effect of curcumin
    Jason Bakhshi
    Terra Linda High School, 320 Nova Albion Way, San Rafael, CA 94903, USA
    Apoptosis 13:904-14. 2008
    ..Our studies demonstrate that curcumin triggers ER stress and the activation of specific cell death pathways that feature caspase cleavage and activation, p23 cleavage, and downregulation of the anti-apoptotic Mcl-1 protein...
  75. doi request reprint Hunter-killer peptide (HKP) for targeted therapy
    H Michael Ellerby
    College of Pharmacy, Touro University, Mare Island, Vallejo, California 94592, USA
    J Med Chem 51:5887-92. 2008
  76. ncbi request reprint siRNA-based inhibition specific for mutant SOD1 with single nucleotide alternation in familial ALS, compared with ribozyme and DNA enzyme
    Takanori Yokota
    Department of Neurology, Tokyo Medical and Dental University, Tokyo, Japan
    Biochem Biophys Res Commun 314:283-91. 2004
    ..Our results support the feasibility of utilizing siRNA-based gene therapy of familial ALS with mutant SOD1...
  77. ncbi request reprint Meeting report: cellular dependence--old concept, new mechanisms
    Patrick Mehlen
    Centre Genetique Moleculaire et Cellulaire, Equipe Labellisée La Ligue, CNRS UMR5534, University of Lyon, Lyon, France
    Sci STKE 2003:pe55. 2003
    ..With several of the receptors implicated in various human developmental disorders or disease states, gaining an understanding of the molecular mechanisms controlling dependence receptor-mediated cell death has clear clinical relevance...
  78. ncbi request reprint Neurological manifestations of the acquired immunodeficiency syndrome (AIDS): experience at UCSF and review of the literature. 1985
    Robert M Levy
    J Neurosurg 107:1253-73; discussion 1251. 2007
  79. ncbi request reprint Netrin-1 controls colorectal tumorigenesis by regulating apoptosis
    Laetitia Mazelin
    Apoptosis Differentiation Laboratory Equipe labellisée La Ligue Molecular and Cellular Genetic Center, CNRS UMR 5534, University of Lyon, 69622 Villeurbanne, France
    Nature 431:80-4. 2004
    ..These data demonstrate that netrin-1 can promote intestinal tumour development, probably by regulating cell survival. Thus, a netrin-1 receptor or receptors function as conditional tumour suppressors...
  80. pmc Targeting the prostate for destruction through a vascular address
    Wadih Arap
    Cancer Research Center, The Burnham Institute, La Jolla, CA 92037, USA
    Proc Natl Acad Sci U S A 99:1527-31. 2002
    ..These results suggest that it may be possible to develop an alternative to surgical prostate resection and that such a treatment may also reduce future cancer risk...

Research Grants28

  1. Development and Improvement of an Animal Resource Core
    Dale Bredesen; Fiscal Year: 2007
    ....
  2. Mechanism of apoptosis induction by the receptor DCC
    Dale Bredesen; Fiscal Year: 2005
    ..abstract_text> ..
  3. MECHANISM OF INHIBITION OF NEURODEGENERATION AND AGING
    Dale Bredesen; Fiscal Year: 2005
    ....
  4. Mechanism of apoptosis induction by the receptor DCC
    Dale Bredesen; Fiscal Year: 2007
    ..abstract_text> ..
  5. Buck Institute--Pharmacology of Lifespan Extension
    Dale Bredesen; Fiscal Year: 2005
    ..To bring together academic and commercial researchers to discuss their goals and explore opportunities for collaboration. ..
  6. Novel apoptotic pathway activated by misfolded proteins
    Dale Bredesen; Fiscal Year: 2007
    ..abstract_text> ..
  7. Center for Integrative Studies of Aging
    Dale Bredesen; Fiscal Year: 2004
    ....
  8. Mechanism of apoptosis induction by the receptor DCC
    Dale Bredesen; Fiscal Year: 2004
    ..abstract_text> ..
  9. Novel apoptotic pathway activated by misfolded proteins
    Dale Bredesen; Fiscal Year: 2003
    ..abstract_text> ..
  10. MECHANISM OF INHIBITION OF NEURODEGENERATION AND AGING
    Dale Bredesen; Fiscal Year: 2003
    ....
  11. Mechanism of apoptosis induction by the receptor DCC
    Dale Bredesen; Fiscal Year: 2003
    ..abstract_text> ..
  12. Basic Mechanisms in Aging and Age Related Disease
    Dale Bredesen; Fiscal Year: 2007
    ....
  13. MECHANISM OF INHIBITION OF NEURODEGENERATION AND AGING
    Dale Bredesen; Fiscal Year: 2001
    ....
  14. MECHANISM OF INHIBITION OF NEURODEGENERATION AND AGING
    Dale Bredesen; Fiscal Year: 2001
    ....
  15. Training in Age-Related Disease and Aging Research
    Dale Bredesen; Fiscal Year: 2006
    ..abstract_text> ..
  16. Novel Prionic Mechanism Underlying Alzheimer?s Disease
    Dale Bredesen; Fiscal Year: 2009
    ..We have provided evidence that the prevailing view of Alzheimer's disease is incorrect, and have developed a new model that offers insight into the mechanism and potential treatment of this important and common disease. ..
  17. Novel apoptotic pathway activated by misfolded proteins
    Dale Bredesen; Fiscal Year: 2006
    ..abstract_text> ..
  18. MECHANISM OF INHIBITION OF NEURODEGENERATION AND AGING
    Dale Bredesen; Fiscal Year: 1999
    ..The potential findings have important implications for the process of aging and degenerative disease. ..
  19. Novel apoptotic pathway activated by misfolded proteins
    Dale Bredesen; Fiscal Year: 2004
    ..abstract_text> ..
  20. MECHANISM OF INHIBITION OF NEURODEGENERATION AND AGING
    Dale Bredesen; Fiscal Year: 2004
    ....
  21. MECHANISM OF INHIBITION OF NEURODEGENERATION AND AGING
    Dale Bredesen; Fiscal Year: 2002
    ....
  22. Novel Prionic Mechanism Underlying Alzheimer?s Disease
    Dale E Bredesen; Fiscal Year: 2010
    ..We have provided evidence that the prevailing view of Alzheimer's disease is incorrect, and have developed a new model that offers insight into the mechanism and potential treatment of this important and common disease. ..
  23. Mechanism of apoptosis induction by the receptor DCC
    Dale Bredesen; Fiscal Year: 2006
    ..abstract_text> ..
  24. Novel apoptotic pathway activated by misfolded proteins
    Dale Bredesen; Fiscal Year: 2005
    ..abstract_text> ..