Limited effects of an eIF2α S51A allele on neurological impairments in the 5xFAD mouse model of Alzheimer's disease

Neural Plasticity

Volumn 2015, Issue , 2015, Pages

  Paesler, Katharina ^a   Xie, Kan ^a   Hettich, Moritz M ^a   Siwek, Magdalena E ^b   Ryan, Devon P ^a   Schröder, Susanne ^a   Papazoglou, Anna ^b   Broich, Karl ^b   Müller, Ralf ^c   Trog, Astrid ^d   Garthe, Alexander ^a   Kempermann, Gerd ^a   Weiergräber, Marco ^b   Ehninger, Dan ^a  

^a GERMAN CENTER FOR NEURODEGENERATIVE DISEASES DZNE   (Germany)

^b Federal Institute for Drugs and Medical Devices BfArM   (Germany)

^c UNIVERSITY OF COLOGNE   (Germany)

^d UNIVERSITY OF BONN   (Germany)

Author keywords

[No Author keywords available]

Indexed keywords

ALANINE; CARPROFEN; INITIATION FACTOR 2ALPHA; SERINE; AMYLOID PRECURSOR PROTEIN; INITIATION FACTOR 2; PRESENILIN 1; PSEN1 PROTEIN, HUMAN;

5XFAD MOUSE; ALZHEIMER DISEASE; ANIMAL CELL; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BEHAVIOR ASSESSMENT; BRAIN LEVEL; COGNITIVE DEFECT; CONDITIONING; DISEASE COURSE; ELECTROENCEPHALOGRAM; ENDOPLASMIC RETICULUM STRESS; EPILEPTIC DISCHARGE; GENETIC TRANSCRIPTION; HIPPOCAMPAL CA1 REGION; HYPERACTIVITY; MORRIS WATER MAZE TEST; MOTOR ACTIVITY; MOUSE; NEUROPATHOLOGY; NONHUMAN; OPEN FIELD TEST; POSTOPERATIVE ANALGESIA; POSTOPERATIVE PAIN; PROTEIN FUNCTION; PROTEIN PHOSPHORYLATION; PROTEIN SYNTHESIS; PSYCHOMOTOR DISORDER; TAIL SUSPENSION TEST; TRANSCRIPTOMICS; WIRE HANG TEST; ALLELE; ANIMAL; BRAIN CORTEX; C57BL MOUSE; DISEASE MODEL; FEAR; GENE TARGETING; GENETICS; METABOLISM; PATHOPHYSIOLOGY; PHOSPHORYLATION; PHYSIOLOGY; SEIZURE; TRANSGENIC MOUSE;

ALLELES; ALZHEIMER DISEASE; AMYLOID BETA-PROTEIN PRECURSOR; ANIMALS; CEREBRAL CORTEX; DISEASE MODELS, ANIMAL; EUKARYOTIC INITIATION FACTOR-2; FEAR; GENE KNOCK-IN TECHNIQUES; MICE; MICE, INBRED C57BL; MICE, TRANSGENIC; MOTOR ACTIVITY; PHOSPHORYLATION; PRESENILIN-1; SEIZURES;

EID: 84927139023     PISSN: 20905904     EISSN: 16875443     Source Type: Journal    
DOI: 10.1155/2015/825157     Document Type: Article

References (56)

1. J. J. Palop and L. Mucke, "Amyloid-β-induced neuronal dysfunction in Alzheimers disease: from synapses toward neural networks, " Nature Neuroscience, vol. 13, no. 7, pp. 812-818, 2010.
2. N. S. Langstrom, J. P. And erson, H. G. Lindroos, B. Winbland , and W. C. Wallace, "Alzheimers disease-associated reduction of polysomalmRNA translation, "Molecular Brain Research, vol. 5, no. 4, pp. 259-269, 1989.
3. A. Gamliel, C. Teicher, D. M. Michaelson et al. , "Increased expression of presenilin 2 inhibits protein synthesis, "Molecular and Cellular Neuroscience, vol. 19, no. 1, pp. 111-124, 2002.
4. Q. Ding, W. R. Markesbery, Q. Chen, F. Li, and J. N. Keller, "Ribosome dysfunction is an early event inAlzheimers disease, " Journal of Neuroscience, vol. 25, no. 40, pp. 9171-9175, 2005.
5. R. C. C. Chang, A. K. Y. Wong, H.-K. Ng, and J. Hugon, "Phosphorylation of eukaryotic initiation factor-2α (eIF2α) is associated with neuronal degeneration in Alzheimers disease, " NeuroReport, vol. 13, no. 18, pp. 2429-2432, 2002.
6. H.-S. Kim, Y. Choi, K.-Y. Shin et al. , "Swedish amyloid precursor protein mutation increases phosphorylation of eIF2α in vitro and in vivo, " Journal of Neuroscience Research, vol. 85, no. 7, pp. 1527-1537, 2007.
7. T. OConnor, K. R. Sadleir, E. Maus et al. , "Phosphorylation of the translation initiation factor eIF2α increases BACE1 levels and promotes amyloidogenesis, " Neuron, vol. 60, no. 6, pp. 988-1009, 2008.
8. F. Mouton-Liger, C. Paquet, J. Dumurgier et al. , "Oxidative stress increases BACE1 protein levels through activation of the PKR-eIF2α pathway, " Biochimica et Biophysica Acta, vol. 1822, no. 6, pp. 885-896, 2012.
9. H. P. Harding, Y. Zhang, and D. Ron, "Protein translation and folding are coupled by an endoplasmic-reticulum-resident kinase, " Nature, vol. 397, no. 6716, pp. 271-274, 1999.
10. J. D. Blais, V. Filipenko, M. Bi et al. , "Activating transcription factor 4 is translationally regulated by hypoxic stress, "Molecular and Cellular Biology, vol. 24, no. 17, pp. 7469-7482, 2004.
11. M. Costa-Mattioli, W. S. Sossin, E. Klann, and N. Sonenberg, "Translational control of long-lasting synaptic plasticity and memory, " Neuron, vol. 61, no. 1, pp. 10-26, 2009.
12. E. Klann and T. E. Dever, "Biochemical mechanisms for translational regulation in synaptic plasticity, " Nature Reviews Neuroscience, vol. 5, no. 12, pp. 931-942, 2004.
13. M. Costa-Mattioli, D. Gobert, H. Harding et al. , "Translational control of hippocampal synaptic plasticity and memory by the eIF2α kinase GCN2, " Nature, vol. 436, no. 7054, pp. 1166-1173, 2005.
14. T. Ma, M. A. Trinh, A. J. Wexler et al. , "Suppression of eIF2α kinases alleviates Alzheimers disease-related plasticity and memory deficits, " Nature Neuroscience, vol. 16, no. 9, pp. 1299-1305, 2013.
15. H. Oakley, S. L. Cole, S. Logan et al. , "Intraneuronal β-amyloid aggregates, neurodegeneration, and neuron loss in transgenic mice with five familial Alzheimers disease mutations: potential factors in amyloid plaque formation, " Journal of Neuroscience, vol. 26, no. 40, pp. 10129-10140, 2006.
16. D. Scheuner, B. Song, E. McEwen et al. , "Translational control is required for the unfolded protein response and in vivo glucose homeostasis, " Molecular Cell, vol. 7, no. 6, pp. 1165-1176, 2001.
17. L. Devi and M. Ohno, "Deletion of the eIF2α Kinase GCN2 fails to rescue the memory decline associated with Alzheimers disease, " PLoS ONE, vol. 8, no. 10, Article IDe77335, 2013.
18. A. Garthe, J. Behr, and G. Kempermann, "Adult-generated hippocampal neurons allow the flexible use of spatially precise learning strategies, " PLoS ONE, vol. 4, no. 5, Article ID e5464, 2009.
19. D. Balschun, D. P. Wolfer, P. Gass et al. , "Does cAMP response element-binding protein have a pivotal role in hippocampal synaptic plasticity and hippocampus-dependent memory? Journal of Neuroscience, vol. 23, no. 15, pp. 6304-6314, 2003.
20. M. Weiergräber, M. Henry, J. Hescheler, N. Smyth, and T. Schneider, "Electrocorticographic and deep intracerebral EEG recording in mice using a telemetry system, " Brain Research Protocols, vol. 14, no. 3, pp. 154-164, 2005.
21. D. W. Huang, B. T. Sherman, and R. A. Lempicki, "Systematic and integrative analysis of large gene lists using DAVID bioinformatics resources, " Nature Protocols, vol. 4, no. 1, pp. 44-57, 2009.
22. D. W. Huang, B. T. Sherman, and R. A. Lempicki, "Bioinformatics enrichment tools: paths toward the comprehensive functional analysis of large gene lists, " Nucleic Acids Research, vol. 37, no. 1, pp. 1-13, 2009.
23. K. R. Sadleir, W. A. Eimer, R. J. Kaufman, P. Osten, and R. Vassar, "Genetic inhibition of phosphorylation of the translation initiation factor eIF2α does not block Aβ-dependent elevation of BACE1 and APP levels or reduce amyloid pathology in a mouse model of alzheimers disease, " PLoS ONE, vol. 9, no. 7, Article ID e101643, 2014.
24. C. R. Prostko, M. A. Brostrom, and C. O. Brostrom, "Reversible phosphorylation of eukaryotic initiation factor 2α in response to endoplasmic reticular signaling, " Molecular and Cellular Biochemistry, vol. 127-128, pp. 255-265, 1993.
25. S. Boncristiano, M. E. Calhoun, P. H. Kelly et al. , "Cholinergic changes in the APP23 transgenic mouse model of cerebral amyloidosis, " The Journal of Neuroscience, vol. 22, no. 8, pp. 3234-3243, 2002.
26. A. Bellucci, I. Luccarini, C. Scali et al. , "Cholinergic dysfunction, neuronal damage and axonal loss in TgCRND8 mice, " Neurobiology of Disease, vol. 23, no. 2, pp. 260-272, 2006.
27. S. E. Perez, S. Dar, M. D. Ikonomovic, S. T. DeKosky, and E. J. Mufson, "Cholinergic forebrain degeneration in the APPswe/ PS1DeltaE9 transgenic mouse, " Neurobiology of Disease, vol. 28, no. 1, pp. 3-15, 2007.
28. D. Z. Christensen, T. A. Bayer, and O. Wirths, "Intracellular Aβ triggers neuron loss in the cholinergic systemof the APP/PS1KI mouse model of Alzheimers disease, " Neurobiology of Aging, vol. 31, no. 7, pp. 1153-1163, 2010.
29. L. Devi and M. Ohno, "Phospho-eIF2α level is important for determining abilities of BACE1 reduction to rescue cholinergic neurodegeneration and memory defects in 5XFAD mice, " PLoS ONE, vol. 5, no. 9, Article ID e12974, 2010.
30. I. Q. Whishaw, W. T. OConnor, and S. B. Dunnett, "Disruption of central cholinergic systems in the rat by basal forebrain lesions or atropine: effects on feeding, sensorimotor behaviour, locomotor activity and spatial navigation, " Behavioural Brain Research, vol. 17, no. 2, pp. 103-115, 1985.
31. J. J. Palop and L. Mucke, "Epilepsy and cognitive impairments in alzheimer disease, " Archives of Neurology, vol. 66, no. 4, pp. 435-440, 2009.
32. L. Verret, E. O. Mann, G. B. Hang et al. , "Inhibitory interneuron deficit links altered network activity and cognitive dysfunction in Alzheimer model, " Cell, vol. 149, no. 3, pp. 708-721, 2012.
33. J. F. Loring, X. Wen, J. M. Lee, J. Seilhamer, and R. Somogyi, "A gene expression profile of Alzheimers disease, " DNA and Cell Biology, vol. 20, no. 11, pp. 683-695, 2001.
34. V. Colangelo, J. Schurr, M. J. Ball, R. P. Pelaez, N. G. Bazan, and W. J. Lukiw, "Gene expression profiling of 12633 genes in Alzheimer hippocampal CA1: transcription and neurotrophic factor down-regulation and up-regulation of apoptotic and proinflammatory signaling, " Journal of Neuroscience Research, vol. 70, no. 3, pp. 462-473, 2002.
35. E. M. Blalock, J. W. Geddes, K. C. Chen, N. M. Porter, W. R. Markesbery, and P. W. Land field, "IncipientAlzheimers disease: Microarray correlation analyses reveal major transcriptional and tumor suppressor responses, " Proceedings of the National Academy of Sciences of the United States of America, vol. 101, no. 7, pp. 2173-2178, 2004.
36. W. S. Liang, T. Dunckley, T. G. Beach et al. , "Altered neuronal gene expression in brain regions differentially affected by Alzheimers disease: a reference data set, " Physiological Genomics, vol. 33, no. 2, pp. 240-256, 2008.
37. L. Devi, M. J. Alldred, S. D. Ginsberg, and M. Ohno, "Sexand brain region-specific acceleration of β-amyloidogenesis following behavioral stress in a mouse model of Alzheimers disease, " Molecular Brain, vol. 3, no. 1, article 34, 2010.
38. L. Holcomb, M. N. Gordon, E. Mcgowan et al. , "Accelerated Alzheimer-type phenotype in transgenic mice carrying both mutant amyloid precursor protein and presenilin 1 transgenes, " Nature Medicine, vol. 4, no. 1, pp. 97-100, 1998.
39. J.-C. Dodart, H. Meziane, C. Mathis, A. Ungerer, K. R. Bales, and S. M. Paul, "Behavioral disturbances in transgenic mice overexpressing the V717F beta-amyloid precursor protein, " Behavioral Neuroscience, vol. 113, no. 5, pp. 982-990, 1999.
40. L. A. Holcomb, M. N. Gordon, P. Jantzen, K. Hsiao, K. Duff, and D. Morgan, "Behavioral changes in transgenic mice expressing bothamyloid precursor protein and presenilin-1mutations: lack of association with amyloid deposits, " Behavior Genetics, vol. 29, no. 3, pp. 177-185, 1999.
41. M. Filali, R. Lalonde, and S. Rivest, "Anomalies in social behaviors and exploratory activities in an APPswe/PS1 mouse model of Alzheimers disease, " Physiology & Behavior, vol. 104, no. 5, pp. 880-885, 2011.
42. H. K. White, E. S. McConnell, C. W. Bales, and M. Kuchibhatla, "A 6-month observational study of the relationship between weight loss and behavioral symptoms in institutionalized Alzheimers disease subjects, " Journal of the American Medical Directors Association, vol. 5, no. 2, pp. 89-97, 2004.
43. P. J. Whitehouse, D. L. Price, R. G. Struble, A. W. Clark, J. T. Coyle, and M. R. Delon, "Alzheimers disease and senile dementia: loss of neurons in the basal forebrain, " Science, vol. 215, no. 4537, pp. 1237-1239, 1982.
44. O. J. M. Vogels, C. A. J. Broere, H. J. ter Laak, H. J. tenDonkelaar, R. Nieuwenhuys, and B. P. M. Schulte, "Cell loss and shrinkage in the nucleus basalisMeynert complex in Alzheimers disease, " Neurobiology of Aging, vol. 11, no. 1, pp. 3-13, 1990.
45. R. S. Jope, L. Song, and R. E. Powers, "Cholinergic activation of phosphoinositide signaling is impaired in Alzheimers disease brain, " Neurobiology of Aging, vol. 18, no. 1, pp. 111-120, 1997.
46. K. M. Cullen and G. M. Halliday, "Neurofibrillary degeneration and cell loss in the nucleus basalis in comparison to cortical Alzheimer pathology, " Neurobiology of Aging, vol. 19, no. 4, pp. 297-306, 1998.
47. A. M. Palmer, P. T. Francis, J. S. Benton et al. , "Presynaptic serotonergic dysfunction in patients with Alzheimers disease, " Journal of Neurochemistry, vol. 48, no. 1, pp. 8-15, 1987.
48. C. G. Gottfries, "Disturbance of the 5-hydroxytryptamine metabolism in brains frompatients with Alzheimers dementia, " Journal of Neural Transmission, Supplement, vol. 30, pp. 33-43, 1990.
49. A. J. Nazarali and G. P. Reynolds, "Monoamine neurotransmitters and their metabolites in brain regions in Alzheimers disease: a postmortem study, " Cellular and MolecularNeurobiology, vol. 12, no. 6, pp. 581-587, 1992.
50. D. L. Sparks, J. C. Hunsaker III, J. T. Slevin, S. T. DeKosky, R. J. Kryscio, and W. R. Markesbery, "Monoaminergic and cholinergic synaptic markers in the nucleus basalis of Meynert (nbM): normal age-related changes and the effect of heart disease and Alzheimers disease, " Annals of Neurology, vol. 31, no. 6, pp. 611-620, 1992.
51. M. Garcia-Alloza, W. D. Hirst, C. P. L.-H. Chen, B. Lasheras, P. T. Francis, and M. J. Ramírez, "Differential involvement of 5-HT(1B/1D) and 5-HT6 receptors in cognitive and non-cognitive symptoms in Alzheimers disease, " Neuropsychopharmacology, vol. 29, no. 2, pp. 410-416, 2004.
52. A. J. Cross, "Serotonin in Alzheimer-type dementia and other dementing illnesses, " Annals of the New York Academy of Sciences, vol. 600, pp. 405-417, 1990.
53. M. K. P. Lai, S. W. Y. Tsang, P. T. Francis et al. , "Postmortem serotoninergic correlates of cognitive decline in Alzheimers disease, " NeuroReport, vol. 13, no. 9, pp. 1175-1178, 2002.
54. M. Garcia-Alloza, F. J. Gil-Bea, M. Diez-Ariza et al. , "Cholinergic-serotonergic imbalance contributes to cognitive and behavioral symptoms in Alzheimers disease, " Neuropsychologia, vol. 43, no. 3, pp. 442-449, 2005.
55. J. Mintzer, O. Brawman-Mintzer, D. F. Mirski et al. , "Fenfluramine challenge test as a marker of serotonin activity in patients with Alzheimers dementia and agitation, " Biological Psychiatry, vol. 44, no. 9, pp. 918-921, 1998.
56. W. Adriani, E. Ognibene, E. Heuland , O. Ghirardi, A. Caprioli, and G. Laviola, "Motor impulsivity in APP-SWE mice: a model of Alzheimers disease, " Behavioural Pharmacology, vol. 17, no. 5-6, pp. 525-533, 2006.