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Neuronal calcineurin transcriptional targets parallel changes observed in Alzheimer disease brain

Hopp, Sarah C., Bihlmeyer, Nathan A., Corradi, John P., Vanderburg, Charles, Cacace, Angela M., Das, Sudeshna, Clark, Timothy W., Betensky, Rebecca A., Hyman, Bradley T., Hudry, Eloise·2018·Journal of Neurochemistry
DOI 10.1111/jnc.14469PMC PMC6181788
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Abstract

Synaptic dysfunction and loss are core pathological features in Alzheimer disease (AD). In the vicinity of amyloid‐β plaques in animal models, synaptic toxicity occurs and is associated with chronic activation of the phosphatase calcineurin (CN). Indeed, pharmacological inhibition of CN blocks amyloid‐β synaptotoxicity. We therefore hypothesized that CN‐mediated transcriptional changes may contribute to AD neuropathology and tested this by examining the impact of CN over‐expression on neuronal gene expression in vivo. We found dramatic transcriptional down‐regulation, especially of synaptic mRNA s, in neurons chronically exposed to CN activation. Importantly, the transcriptional profile parallels the changes in human AD tissue. Bioinformatics analyses suggest that both nuclear factor of activated T cells and numerous micro RNA s may all be impacted by CN, and parallel findings are observed in AD. These data and analyses support the hypothesis that at least part of the synaptic failure characterizing AD may result from aberrant CN activation leading to down‐regulation of synaptic genes, potentially via activation of specific transcription factors and expression of repressive micro RNA s. Open science badges: This article has received a badge for *Open Materials* because it provided all relevant information to reproduce the study in the manuscript. The complete Open Science Disclosure form for this article can be found at the end of the article. More information about the Open Practices badges can be found at https://cos.io/our-services/open-science-badges/. image Read the Editorial Highlight for this article on page 8.

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  • PBS serves as an adequate control for these experiments, because the endo-lysosomal pathway targeted here is not greatly affected by AAV-GFP.

    “Our previous work demonstrates that about 400 transcripts, many related to ribosomal processing, are upregulated in AAV-GFP treated hippocampal neurons compared to PBS treated hippocampal neurons (Hopp et al., 2018), suggesting that the endo-lysosomal pathway targeted herein is not greatly affected by AAV-GFP and that PBS can serve as an adequate control for the experiments herein.”

    From Hippocampal TMEM55B overexpression in the 5XFAD mouse model of Alzheimer's disease (2024) · cites this paper as Hopp et al., 2018

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  1. 10.1523/JNEUROSCI.1064-09.2009 · DOI
  2. 10.1016/S0022-2836(05)80360-2 · DOI · Paper page
  3. 10.1186/s13024-017-0169-9 · DOI
  4. 10.1371/journal.pone.0053845 · DOI
  5. 10.1074/jbc.M408741200 · DOI
  6. 10.1016/j.neurobiolaging.2012.11.024 · DOI · Paper page
  7. 10.1016/S0092-8674(00)81816-4 · DOI
  8. 10.1016/j.jchemneu.2011.06.007 · DOI · Paper page
  9. 10.1093/bioinformatics/19.2.185 · DOI
  10. 10.1038/nrn2150 · DOI
  11. 10.1016/j.freeradbiomed.2017.10.001 · DOI · Paper page
  12. 10.3389/fncel.2013.00159 · DOI
  13. 10.1016/j.bbr.2014.06.013 · DOI
  14. 10.3233/JAD-2011-111328 · DOI
  15. 10.1007/s00213-014-3629-8 · DOI
  16. 10.1007/s10571-011-9788-9 · DOI
  17. 10.1021/bi002732 · DOI
  18. 10.1523/JNEUROSCI.1930-15.2016 · DOI
  19. 10.1007/s12640-009-9112-3 · DOI
  20. 10.3389/fncel.2013.00178 · DOI · Paper page
  21. 10.1016/j.expneurol.2009.09.011 · DOI · Paper page
  22. 10.1093/nar/gkn923 · DOI · Paper page
  23. 10.1523/JNEUROSCI.6439-11.2012 · DOI
  24. 10.1093/biostatistics/4.2.249 · DOI · Paper page
  25. 10.4049/jimmunol.1003322 · DOI
  26. 10.1007/s12035-014-9053-6 · DOI
  27. 10.1074/jbc.M113.460287 · DOI
  28. 10.3390/ncrna2020003 · DOI
  29. 10.1016/j.neuron.2008.06.008 · DOI · Paper page
  30. 10.1074/jbc.M901121200 · DOI
  31. 10.1016/j.cels.2015.12.004 · DOI · Paper page
  32. 10.1074/jbc.M507475200 · DOI
  33. 10.1038/sj.gt.3302048 · DOI
  34. 10.1186/1476-511X-11-39 · DOI
  35. 10.1016/S0092-8674(00)80897-1 · DOI
  36. 10.1016/S0143-4160(03)00128-3 · DOI
  37. 10.1038/mt.2008.37 · DOI
  38. 10.1111/j.1474-9726.2010.00645.x · DOI
  39. 10.1016/j.ceb.2010.12.006 · DOI
  40. 10.1016/j.ijdevneu.2007.10.004 · DOI · Paper page
  41. 10.1074/jbc.M109.015719 · DOI
  42. 10.1126/science.1110647 · DOI · Paper page
  43. 10.1523/JNEUROSCI.0365-05.2005 · DOI · Paper page
  44. 10.1006/nbdi.2001.0395 · DOI
  45. 10.1016/j.bbrc.2016.09.053 · DOI
  46. 10.1016/j.bbrc.2016.08.067 · DOI · Paper page
  47. 10.1093/nar/gkv007 · DOI · Paper page
  48. 10.1002/syn.20933 · DOI
  49. 10.3389/fnagi.2015.00199 · DOI
  50. 10.1016/j.neuron.2009.05.007 · DOI · Paper page
  51. 10.3389/fnmol.2016.00149 · DOI
  52. 10.1016/j.neurobiolaging.2013.08.035 · DOI
  53. 10.1002/glia.22797 · DOI
  54. 10.1523/JNEUROSCI.4970-06.2007 · DOI · Paper page
  55. 10.1016/j.ajhg.2011.01.006 · DOI
  56. 10.1523/JNEUROSCI.0877-17.2017 · DOI · Paper page
  57. 10.1016/j.neulet.2010.10.033 · DOI
  58. 10.1016/j.ceca.2009.12.014 · DOI
  59. 10.1002/jnr.22290 · DOI
  60. 10.1074/jbc.M112.448183 · DOI
  61. 10.1007/s12035-014-8758-x · DOI
  62. 10.1126/science.1260419 · DOI · Paper page
  63. 10.1016/j.neures.2014.09.002 · DOI · Paper page
  64. 10.1126/science.1115901 · DOI
  65. 10.1016/S0092-8674(00)80896-X · DOI
  66. 10.1007/978-94-007-2888-2_54 · DOI
  67. 10.1523/JNEUROSCI.4456-09.2010 · DOI · Paper page
  68. 10.1038/nature03441 · DOI · Paper page
  69. 10.1093/nar/gkv1157 · DOI
  70. 10.1093/bioinformatics/btu684 · DOI
  71. 10.1093/hmg/ddx269 · DOI
  72. 10.3389/fcell.2014.00064 · DOI
  73. 10.1074/jbc.M513769200 · DOI

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Metadata

Authors
Hopp, S. C., Bihlmeyer, N. A., Corradi, J. P., Vanderburg, C., Cacace, A. M., Das, S., Clark, T. W., Betensky, R. A., Hyman, B. T., & Hudry, E.
Affiliations
  • Alzheimer's disease Research Laboratory Department of Neurology MassGeneral Institute for Neurodegenerative Disease Massachusetts General Hospital and Harvard Medical School Charlestown Massachusetts USA
  • MIND Informatics MassGeneral Institute for Neurodegenerative Disease Massachusetts General Hospital and Harvard Medical School Cambridge Massachusetts USA
  • Exploratory Biology and Genomics Bristol‐Myers Squibb Wallingford Connecticut USA
  • Department of Biostatistics Harvard T. H. Chan School of Public Health Boston Massachusetts USA
ORCID
Venue
Journal of Neurochemistry
Publisher
Wiley
Published
2018-09-07
Volume
147
Issue
1
Pages
24-39
ISSN
  • 0022-3042
  • 1471-4159
DOI
10.1111/jnc.14469
PMC
PMC6181788
Cited by
20
References
14
Language
en
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Funders
  • National Institute on Aging (1K99AG047336‐01A1)
  • National Institutes of Health (AGR01AG041507)
  • Bristol-Myers Squibb

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