Kim N Green

Summary

Affiliation: University of California
Country: USA

Publications

  1. pmc Nicotinamide restores cognition in Alzheimer's disease transgenic mice via a mechanism involving sirtuin inhibition and selective reduction of Thr231-phosphotau
    Kim N Green
    Department of Neurobiology and Behavior, University of California, Irvine, Irvine, California 92697 4545, USA
    J Neurosci 28:11500-10. 2008
  2. doi Linking calcium to Abeta and Alzheimer's disease
    Kim N Green
    Department of Neurobiology and Behavior and Institute for Brain Aging and Dementia, University of California, Irvine, Irvine, CA 92697 4545, USA
    Neuron 59:190-4. 2008
  3. doi ST101 induces a novel 17 kDa APP cleavage that precludes Aβ generation in vivo
    Kim N Green
    From the Department of Neurobiology and Behavior Institute for Memory Impairments and Neurological Disorders, University of California at Irvine, Irvine, CA 92697 4545, USA
    Ann Neurol 69:831-44. 2011
  4. doi Calcium in the initiation, progression and as an effector of Alzheimer's disease pathology
    Kim N Green
    Department of Neurobiology and Behavior, University of California, Irvine, Irvine, CA 92697 4545, USA
    J Cell Mol Med 13:2787-99. 2009
  5. ncbi M1 receptors play a central role in modulating AD-like pathology in transgenic mice
    Antonella Caccamo
    Department of Neurobiology and Behavior, University of California, Irvine, Irvine, California 92697, USA
    Neuron 49:671-82. 2006
  6. pmc Age-dependent sexual dimorphism in cognition and stress response in the 3xTg-AD mice
    Lani K Clinton
    Department of Neurobiology and Behavior, 1109 Gillespie Neuroscience Research Facility, University of California, Irvine, Irvine, CA 92697 4545, USA
    Neurobiol Dis 28:76-82. 2007
  7. pmc Neural stem cells improve cognition via BDNF in a transgenic model of Alzheimer disease
    Mathew Blurton-Jones
    Department of Neurobiology and Behavior and Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, CA 92697, USA
    Proc Natl Acad Sci U S A 106:13594-9. 2009
  8. pmc Memantine improves cognition and reduces Alzheimer's-like neuropathology in transgenic mice
    Hilda Martinez-Coria
    Department of Neurobiology and Behavior, University of California, Irvine, 3400A Biological Sciences III, Irvine, CA 92697 4545, USA
    Am J Pathol 176:870-80. 2010
  9. ncbi Glucocorticoids increase amyloid-beta and tau pathology in a mouse model of Alzheimer's disease
    Kim N Green
    Department of Neurobiology and Behavior, and Center for the Neurobiology of Learning and Memory, University of California, Irvine, Irvine, California 92697 4545, USA
    J Neurosci 26:9047-56. 2006
  10. doi Reductions in amyloid-beta-derived neuroinflammation, with minocycline, restore cognition but do not significantly affect tau hyperphosphorylation
    Anna Parachikova
    Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, CA 92697 4545, USA
    J Alzheimers Dis 21:527-42. 2010

Collaborators

Detail Information

Publications42

  1. pmc Nicotinamide restores cognition in Alzheimer's disease transgenic mice via a mechanism involving sirtuin inhibition and selective reduction of Thr231-phosphotau
    Kim N Green
    Department of Neurobiology and Behavior, University of California, Irvine, Irvine, California 92697 4545, USA
    J Neurosci 28:11500-10. 2008
    ..These preclinical findings suggest that oral nicotinamide may represent a safe treatment for AD and other tauopathies, and that phosphorylation of tau at Thr231 may regulate tau stability...
  2. doi Linking calcium to Abeta and Alzheimer's disease
    Kim N Green
    Department of Neurobiology and Behavior and Institute for Brain Aging and Dementia, University of California, Irvine, Irvine, CA 92697 4545, USA
    Neuron 59:190-4. 2008
    ..Finally, new studies have elucidated the role by which presenilins modulate calcium signaling, including effects on SERCA2b and gating of the IP(3) receptor, and lead to Abeta production...
  3. doi ST101 induces a novel 17 kDa APP cleavage that precludes Aβ generation in vivo
    Kim N Green
    From the Department of Neurobiology and Behavior Institute for Memory Impairments and Neurological Disorders, University of California at Irvine, Irvine, CA 92697 4545, USA
    Ann Neurol 69:831-44. 2011
    ..Here we sought to identify any disease-modifying properties of an azaindolizinone derivative, spiro[imidazo[1,2-a]pyridine-3,2-idan]-2(3H)-one (ST101 or ZSET1446)...
  4. doi Calcium in the initiation, progression and as an effector of Alzheimer's disease pathology
    Kim N Green
    Department of Neurobiology and Behavior, University of California, Irvine, Irvine, CA 92697 4545, USA
    J Cell Mol Med 13:2787-99. 2009
    ....
  5. ncbi M1 receptors play a central role in modulating AD-like pathology in transgenic mice
    Antonella Caccamo
    Department of Neurobiology and Behavior, University of California, Irvine, Irvine, California 92697, USA
    Neuron 49:671-82. 2006
    ..Therefore, selective M1 agonists may be efficacious for the treatment of AD...
  6. pmc Age-dependent sexual dimorphism in cognition and stress response in the 3xTg-AD mice
    Lani K Clinton
    Department of Neurobiology and Behavior, 1109 Gillespie Neuroscience Research Facility, University of California, Irvine, Irvine, CA 92697 4545, USA
    Neurobiol Dis 28:76-82. 2007
    ..Thus, the enhanced corticosterone response of the young female mice likely underlies their poorer performance on stressful tasks...
  7. pmc Neural stem cells improve cognition via BDNF in a transgenic model of Alzheimer disease
    Mathew Blurton-Jones
    Department of Neurobiology and Behavior and Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, CA 92697, USA
    Proc Natl Acad Sci U S A 106:13594-9. 2009
    ..Taken together, our findings demonstrate that neural stem cells can ameliorate complex behavioral deficits associated with widespread Alzheimer disease pathology via BDNF...
  8. pmc Memantine improves cognition and reduces Alzheimer's-like neuropathology in transgenic mice
    Hilda Martinez-Coria
    Department of Neurobiology and Behavior, University of California, Irvine, 3400A Biological Sciences III, Irvine, CA 92697 4545, USA
    Am J Pathol 176:870-80. 2010
    ..These results suggest that the effects of memantine treatment on AD brain include disease modification and prevention of synaptic dysfunction...
  9. ncbi Glucocorticoids increase amyloid-beta and tau pathology in a mouse model of Alzheimer's disease
    Kim N Green
    Department of Neurobiology and Behavior, and Center for the Neurobiology of Learning and Memory, University of California, Irvine, Irvine, California 92697 4545, USA
    J Neurosci 26:9047-56. 2006
    ..These findings suggest that high levels of glucocorticoids, found in AD, are not merely a consequence of the disease process but rather play a central role in the development and progression of AD...
  10. doi Reductions in amyloid-beta-derived neuroinflammation, with minocycline, restore cognition but do not significantly affect tau hyperphosphorylation
    Anna Parachikova
    Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, CA 92697 4545, USA
    J Alzheimers Dis 21:527-42. 2010
    ....
  11. pmc Formulation of a medical food cocktail for Alzheimer's disease: beneficial effects on cognition and neuropathology in a mouse model of the disease
    Anna Parachikova
    Department of Neurobiology and Behavior, Institute for Memory Impairments and Neurological Disorders, University of California Irvine, Irvine, California, United States of America
    PLoS ONE 5:e14015. 2010
    ....
  12. pmc A dynamic relationship between intracellular and extracellular pools of Abeta
    Salvatore Oddo
    Department of Neurobiology and Behavior, University of California, Irvine, 1109 Gillespie Neuroscience Bldg, Irvine, CA 92697 4545, USA
    Am J Pathol 168:184-94. 2006
    ..Taken together, these results provide strong experimental evidence that intraneuronal Abeta may serve as a source for some of the extracellular amyloid deposits...
  13. ncbi Enhanced caffeine-induced Ca2+ release in the 3xTg-AD mouse model of Alzheimer's disease
    Ian F Smith
    Department of Neurobiology and Behavior, University of California, Irvine, California 92697 4545, USA
    J Neurochem 94:1711-8. 2005
    ....
  14. doi Calpain inhibitor A-705253 mitigates Alzheimer's disease-like pathology and cognitive decline in aged 3xTgAD mice
    Rodrigo Medeiros
    Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, California 92697 4545, USA
    Am J Pathol 181:616-25. 2012
    ..Our data provide relevant functional and molecular insights into the beneficial therapeutic effects of inhibiting calpain activation for the management of AD...
  15. pmc Genetically augmenting Abeta42 levels in skeletal muscle exacerbates inclusion body myositis-like pathology and motor deficits in transgenic mice
    Masashi Kitazawa
    Department of Neurobiology and Behavior, 1109 Gillespie Neuroscience Facility, University of California, Irvine, Irvine, CA 92697 4545, USA
    Am J Pathol 168:1986-97. 2006
    ..The data presented here provide experimental evidence that Abeta42 plays a proximal and critical role in the muscle degenerative process...
  16. pmc SERCA pump activity is physiologically regulated by presenilin and regulates amyloid beta production
    Kim N Green
    Department of Neurobiology and Behavior, University of California, Irvine, Irvine, CA 92697, USA
    J Cell Biol 181:1107-16. 2008
    ..Our results point to a physiological role for the presenilins in Ca(2+) signaling via regulation of the SERCA pump...
  17. pmc Presenilin-null cells have altered two-pore calcium channel expression and lysosomal calcium: implications for lysosomal function
    Kara M Neely Kayala
    Department of Neurobiology and Behavior, University of California, Irvine, 3208 Biological Sciences III, Irvine, CA 92697 4545, United States
    Brain Res 1489:8-16. 2012
    ..These data indicate that alterations in lysosomal calcium in the absence of presenilins might be leading to disruptions in autophagy...
  18. ncbi Lipopolysaccharide-induced inflammation exacerbates tau pathology by a cyclin-dependent kinase 5-mediated pathway in a transgenic model of Alzheimer's disease
    Masashi Kitazawa
    Department of Neurobiology and Behavior, University of California Irvine, California 92697 4545, USA
    J Neurosci 25:8843-53. 2005
    ..Therefore, this study clearly demonstrates that microglial activation exacerbates key neuropathological features such as tangle formation...
  19. ncbi Learning decreases A beta*56 and tau pathology and ameliorates behavioral decline in 3xTg-AD mice
    Lauren M Billings
    Department of Neurobiology and Behavior, Center for the Neurobiology of Learning and Memory, University of California, Irvine, Irvine, California 92697 4545, USA
    J Neurosci 27:751-61. 2007
    ..These findings indicate that, in young and middle-aged 3xTg-AD mice, repeated spatial training can significantly delay the development of neuropathology and decline in spatial memory...
  20. ncbi Dietary docosahexaenoic acid and docosapentaenoic acid ameliorate amyloid-beta and tau pathology via a mechanism involving presenilin 1 levels
    Kim N Green
    Department of Neurobiology and Behavior, University of California, Irvine, California 92697 4545, USA
    J Neurosci 27:4385-95. 2007
    ..Collectively, these results suggest that DHA and DPAn-6 supplementations could be a beneficial natural therapy for AD...
  21. pmc Abeta inhibits the proteasome and enhances amyloid and tau accumulation
    Bertrand P Tseng
    Department of Neurobiology and Behavior, University of California, 1109 Gillespie Neuroscience Research Facility, Irvine, CA 92697 4545, USA
    Neurobiol Aging 29:1607-18. 2008
    ..These findings provide further evidence that the proteasome represents a viable target for therapeutic intervention in AD...
  22. pmc Oligemic hypoperfusion differentially affects tau and amyloid-{beta}
    Maya A Koike
    Department of Neurobiology and Behavior, Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, 3212 Biological Sciences III, Irvine, CA 92697 4545, USA
    Am J Pathol 177:300-10. 2010
    ..This finding may have implications for the pathogenesis of AD, as it indicates for the first time that total tau and amyloid-beta are differentially impacted by mild hypoperfusion...
  23. ncbi Intracellular amyloid-beta in Alzheimer's disease
    Frank M LaFerla
    Department of Neurobiology and Behaviour, and Institute for Brain Aging and Dementia, University of California, Irvine, California 92697 4545, USA
    Nat Rev Neurosci 8:499-509. 2007
    ....
  24. doi α7 Nicotinic Receptor Agonist Enhances Cognition in Aged 3xTg-AD Mice with Robust Plaques and Tangles
    Rodrigo Medeiros
    Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, California Department of Neurobiology and Behavior, University of California, Irvine, California
    Am J Pathol 184:520-9. 2014
    ..These novel findings indicate that activating α7 nAChR is a promising treatment for cognitive impairment in AD. ..
  25. pmc Presenilin is necessary for efficient proteolysis through the autophagy-lysosome system in a γ-secretase-independent manner
    Kara M Neely
    Department of Neurobiology and Behavior and Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, Irvine, California 92697 4545, USA
    J Neurosci 31:2781-91. 2011
    ..The role of presenilins in autophagy has many implications for its function in neurological diseases such as AD...
  26. ncbi Intraneuronal Abeta causes the onset of early Alzheimer's disease-related cognitive deficits in transgenic mice
    Lauren M Billings
    Department of Neurobiology and Behavior and Center for the Neurobiology of Learning and Memory, University of California, Irvine, Irvine, CA 92697, USA
    Neuron 45:675-88. 2005
    ..Reemergence of the Abeta pathology again leads to cognitive deficits. This study strongly implicates intraneuronal Abeta in the onset of cognitive dysfunction...
  27. pmc Chronic nicotine administration exacerbates tau pathology in a transgenic model of Alzheimer's disease
    Salvatore Oddo
    Department of Neurobiology and Behavior, University of California, Irvine, CA 92697, USA
    Proc Natl Acad Sci U S A 102:3046-51. 2005
    ..Finally, this study highlights the importance of testing compounds designed to ameliorate AD pathology in a model with both neuropathological lesions because of the differential effects it can have on either Abeta or tau...
  28. pmc IKK phosphorylates Huntingtin and targets it for degradation by the proteasome and lysosome
    Leslie Michels Thompson
    Department of Psychiatry and Human Behavior, University of California, Irvine, 92697, USA
    J Cell Biol 187:1083-99. 2009
    ..Thus, IKK activation may modulate mutant Htt neurotoxicity depending on the cell's ability to degrade the modified species...
  29. doi Endogenous murine tau promotes neurofibrillary tangles in 3xTg-AD mice without affecting cognition
    David Baglietto-Vargas
    Department of Neurobiology and Behavior, Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, CA 92697 4545, USA
    Neurobiol Dis 62:407-15. 2014
    ..These findings provide better understanding about the role of endogenous tau to Alzheimer's disease (AD) pathology and for developing new AD models. ..
  30. pmc Mifepristone alters amyloid precursor protein processing to preclude amyloid beta and also reduces tau pathology
    David Baglietto-Vargas
    Department of Neurobiology and Behavior, University of California, Irvine, USA
    Biol Psychiatry 74:357-66. 2013
    ..Here, we analyzed the effects of the glucocorticoid receptor antagonist mifepristone (RU486) in the 3xTg-AD mouse model at an age where hippocampal damage leads to high circulating corticosterone levels...
  31. ncbi Calcium dysregulation in Alzheimer's disease: recent advances gained from genetically modified animals
    Ian F Smith
    Department of Neurobiology and Behavior, University of California, 1109 Gillespie Neuroscience Building, Irvine CA 92697 4545, USA
    Cell Calcium 38:427-37. 2005
    ..The cause of synaptic dysfunction is unknown but it is likely that amyloid-beta and its ability to disrupt intracellular calcium homeostasis plays a key role in this process...
  32. doi Relevance of transgenic mouse models to human Alzheimer disease
    Debbi A Morrissette
    Department of Neurobiology and Behavior and Institute for Brain Aging and Dementia, University of California, Irvine, California 92697 4545, USA
    J Biol Chem 284:6033-7. 2009
    ..This review discusses the utility of transgenic mice as a research tool and their contributions to our understanding of Alzheimer disease...
  33. pmc Spatial frequency domain imaging of intrinsic optical property contrast in a mouse model of Alzheimer's disease
    Alexander J Lin
    Laser Microbeam and Medical Program, Beckman Laser Institute and Medical Clinic, 1002 Health Sciences Road, Irvine, CA 92612, USA
    Ann Biomed Eng 39:1349-57. 2011
    ..controls, respectively. Our results show that SFDI is capable of revealing quantitative functional contrast in an AD model and may be a useful method for studying dynamic alterations in AD neural tissue composition and physiology...
  34. ncbi Presenilins mediate efficient proteolysis via the autophagosome-lysosome system
    Kara M Neely
    Department of Neurobiology and Behavior, Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, USA
    Autophagy 7:664-5. 2011
    ..We find that wild-type presenilins play a key role in degradation through the autophagy-lysosome system by modulating either fusion of autophagosomes to lysosomes or lysosome function...
  35. ncbi Presenilin regulates capacitative calcium entry dependently and independently of gamma-secretase activity
    Yama Akbari
    Department of Neurobiology and Behavior, University of California, Irvine, CA 92697 4545, USA
    Biochem Biophys Res Commun 322:1145-52. 2004
    ..These data suggest that changes in the structural components of presenilin can modulate CCE independent of its function in gamma-secretase activity and intracellular calcium stores...
  36. ncbi Hypoxic remodelling of Ca2+ mobilization in type I cortical astrocytes: involvement of ROS and pro-amyloidogenic APP processing
    Ian F Smith
    Institute for Cardiovascular Research School of Biomedical Sciences, University of Leeds, Leeds, UK
    J Neurochem 88:869-77. 2004
    ..Our results indicate that chronic hypoxia enhances agonist-evoked rises of [Ca2+]i in cortical astrocytes, and that this can be prevented by antioxidants and appears to be associated with increased AbetaP formation...
  37. ncbi Amyloid peptide-mediated hypoxic regulation of Ca2+ channels in PC12 cells
    Chris Peers
    Institute for Cardiovascular Research, Worsley Medical and Dental Building, University of Leeds, Leeds LS2 9JT, UK
    Adv Exp Med Biol 536:187-92. 2003
  38. ncbi Evaluation of sulfur, selenium and tellurium catalysts with antioxidant potential
    Gregory I Giles
    School of Biological and Chemical Sciences, University of Exeter, Stocker Road, Exeter, UK EX4 4QD
    Org Biomol Chem 1:4317-22. 2003
    ..This compound exhibits a correspondingly high activity with a remarkably low IC50 value of 20 nM, when tested in PC12 cell culture using a bioassay indicative of the early stages of Alzheimer's disease...
  39. ncbi Altered processing of amyloid precursor protein in the human neuroblastoma SH-SY5Y by chronic hypoxia
    Nicola J Webster
    Institute for Cardiovascular Research, University of Leeds, Leeds, UK
    J Neurochem 83:1262-71. 2002
    ..Thus, CH selectively decreases processing of APP by the alpha-secretase pathway, most likely by decreasing levels of ADAM 10...
  40. pmc Hypoxia potentiates exocytosis and Ca2+ channels in PC12 cells via increased amyloid beta peptide formation and reactive oxygen species generation
    Kim N Green
    Institute for Cardiovascular Research, University of Leeds, UK
    J Physiol 541:1013-23. 2002
    ..Our results indicate that the effects of hypoxia require ROS generation from AbetaPs, and suggest that elevated levels of ROS mediate hypoxic and AbetaP-mediated pathological remodelling of Ca2+ homeostasis...
  41. ncbi Altered processing of the amyloid precursor protein and decreased expression of ADAM 10 by chronic hypoxia in SH-SY5Y: no role for the stress-activated JNK and p38 signalling pathways
    Nicola J Webster
    Institute for Cardiovascular Research, Worsley Medical and Dental Building, University of Leeds, Leeds LS2 9JT, United Kingdom
    Brain Res Mol Brain Res 130:161-9. 2004
    ..However, inhibitors of p38 were unable to reverse the loss of sAPPalpha in CH cells, indicating that this increase in activity was not linked to the altered processing of APP...
  42. ncbi Divergent pathways account for two distinct effects of amyloid beta peptides on exocytosis and Ca(2+) currents: involvement of ROS and NF-kappaB
    Kim N Green
    Institute for Cardiovascular Research, University of Leeds, Leeds, UK
    J Neurochem 81:1043-51. 2002
    ....