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Genomes and Genes | Kim N GreenSummaryAffiliation: University of California Country: USA Publications
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Publications
Nicotinamide restores cognition in Alzheimer's disease transgenic mice via a mechanism involving sirtuin inhibition and selective reduction of Thr231-phosphotauKim 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...
Linking calcium to Abeta and Alzheimer's diseaseKim 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...- Calcium in the initiation, progression and as an effector of Alzheimer's disease pathologyKim N Green
Department of Neurobiology and Behavior, University of California, Irvine, Irvine, CA 92697 4545, USA
J Cell Mol Med 13:2787-99. 2009.... - ST101 induces a novel 17 kDa APP cleavage that precludes Aβ generation in vivoKim 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)... 
M1 receptors play a central role in modulating AD-like pathology in transgenic miceAntonella 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...- Age-dependent sexual dimorphism in cognition and stress response in the 3xTg-AD miceLani 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... - Glucocorticoids increase amyloid-beta and tau pathology in a mouse model of Alzheimer's diseaseKim 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... - Memantine improves cognition and reduces Alzheimer's-like neuropathology in transgenic miceHilda 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... - Neural stem cells improve cognition via BDNF in a transgenic model of Alzheimer diseaseMathew 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... - Reductions in amyloid-beta-derived neuroinflammation, with minocycline, restore cognition but do not significantly affect tau hyperphosphorylationAnna Parachikova
Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, CA 92697 4545, USA
J Alzheimers Dis 21:527-42. 2010.... - Formulation of a medical food cocktail for Alzheimer's disease: beneficial effects on cognition and neuropathology in a mouse model of the diseaseAnna 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.... - Enhanced caffeine-induced Ca2+ release in the 3xTg-AD mouse model of Alzheimer's diseaseIan F Smith
Department of Neurobiology and Behavior, University of California, Irvine, California 92697 4545, USA
J Neurochem 94:1711-8. 2005.... - A dynamic relationship between intracellular and extracellular pools of AbetaSalvatore 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... - Calpain inhibitor A-705253 mitigates Alzheimer's disease-like pathology and cognitive decline in aged 3xTgAD miceRodrigo 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... - SERCA pump activity is physiologically regulated by presenilin and regulates amyloid beta productionKim 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... - Genetically augmenting Abeta42 levels in skeletal muscle exacerbates inclusion body myositis-like pathology and motor deficits in transgenic miceMasashi 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... - Lipopolysaccharide-induced inflammation exacerbates tau pathology by a cyclin-dependent kinase 5-mediated pathway in a transgenic model of Alzheimer's diseaseMasashi 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... - Learning decreases A beta*56 and tau pathology and ameliorates behavioral decline in 3xTg-AD miceLauren 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... - Dietary docosahexaenoic acid and docosapentaenoic acid ameliorate amyloid-beta and tau pathology via a mechanism involving presenilin 1 levelsKim 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... - Abeta inhibits the proteasome and enhances amyloid and tau accumulationBertrand 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... - 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... - Intracellular amyloid-beta in Alzheimer's diseaseFrank 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.... - Presenilin is necessary for efficient proteolysis through the autophagy-lysosome system in a γ-secretase-independent mannerKara 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... - Chronic nicotine administration exacerbates tau pathology in a transgenic model of Alzheimer's diseaseSalvatore 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... - Intraneuronal Abeta causes the onset of early Alzheimer's disease-related cognitive deficits in transgenic miceLauren 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... - IKK phosphorylates Huntingtin and targets it for degradation by the proteasome and lysosomeLeslie 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... - Relevance of transgenic mouse models to human Alzheimer diseaseDebbi 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... - Calcium dysregulation in Alzheimer's disease: recent advances gained from genetically modified animalsIan 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... - Spatial frequency domain imaging of intrinsic optical property contrast in a mouse model of Alzheimer's diseaseAlexander 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... - Presenilins mediate efficient proteolysis via the autophagosome-lysosome systemKara 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... - Presenilin-null cells have altered two-pore calcium channel expression and lysosomal calcium: implications for lysosomal functionKara 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... - Presenilin regulates capacitative calcium entry dependently and independently of gamma-secretase activityYama 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... - Hypoxic remodelling of Ca2+ mobilization in type I cortical astrocytes: involvement of ROS and pro-amyloidogenic APP processingIan 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... - Amyloid peptide-mediated hypoxic regulation of Ca2+ channels in PC12 cellsChris 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 - 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 pathwaysNicola 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... - Evaluation of sulfur, selenium and tellurium catalysts with antioxidant potentialGregory 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... - Altered processing of amyloid precursor protein in the human neuroblastoma SH-SY5Y by chronic hypoxiaNicola 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... - Hypoxia potentiates exocytosis and Ca2+ channels in PC12 cells via increased amyloid beta peptide formation and reactive oxygen species generationKim 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... - Divergent pathways account for two distinct effects of amyloid beta peptides on exocytosis and Ca(2+) currents: involvement of ROS and NF-kappaBKim N Green
Institute for Cardiovascular Research, University of Leeds, Leeds, UK
J Neurochem 81:1043-51. 2002....