Association between spontaneous activity of the default mode network hubs and leukocyte telomere length in late childhood and early adolescence

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Citações na Scopus
1
Tipo de produção
article
Data de publicação
2019
DOI
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Editora
PERGAMON-ELSEVIER SCIENCE LTD
Autores
REBELLO, Keila
MOURA, Luciana M.
XAVIER, Gabriela
SPINDOLA, Leticia M.
CARVALHO, Carolina Muniz
GADELHA, Ary
PICON, Felipe
PAN, Pedro Mario
ZUGMAN, Andre
Citação
JOURNAL OF PSYCHOSOMATIC RESEARCH, v.127, article ID 109864, 5p, 2019
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
The impact of early life stress on mental health and telomere length shortening have been reported. Changes in brain default mode network (DMN) were found to be related to a myriad of psychiatric conditions in which stress may play a role. In this context, family environment and adverse childhood experiences (ACEs) are potential causes of stress. This is a hypothesis-driven study focused on testing two hypotheses: (i) there is an association between telomere length and the function of two main hubs of DMN: the posterior cingulate cortex (PCC) and the medial prefrontal cortex (mPFC); (ii) this association is modulated by family environment and/or ACEs. To the best of our knowledge, this is the first study investigating these hypotheses. Resting-state functional magnetic resonance imaging data and blood sample were collected from 389 subjects (6-15 age range). We assessed DMN fractional amplitude of low-frequency fluctuations (fALFF) and leukocyte telomere length (LTL). We fitted general linear models to test the main effects of LTL on DMN hubs and the interaction effects with Family Environment Scale (FES) and ACEs. The results did not survive a strict Bonferroni correction. However, uncorrected p-values suggest that LTL was positively correlated with fALFF in PCC and a FES interaction between FES and LTL at mPFC. Although marginal, our results encourage further research on the interaction between DMN hubs, telomere length and family environment, which may play a role on the biological embedding of stress.
Palavras-chave
Telomere, Leukocyte telomere length, Default-mode, Resting state, Brain development, Childhood, Adolescence, Stress
URI
https://observatorio.fm.usp.br/handle/OPI/34511
Referências
  1. Amodio DM, 2006, NAT REV NEUROSCI, V7, P268, DOI 10.1038/nrn1884
  2. Asok A, 2013, DEV PSYCHOPATHOL, V25, P577, DOI 10.1017/S0954579413000011
  3. Blackburn EH, 2005, FEBS LETT, V579, P859, DOI 10.1016/j.febslet.2004.11.036
  4. Brown DW, 2009, AM J PREV MED, V37, P389, DOI 10.1016/j.amepre.2009.06.021
  5. Buckner RL, 2008, ANN NY ACAD SCI, V1124, P1, DOI 10.1196/annals.1440.011
  6. Buckner RL, 2007, TRENDS COGN SCI, V11, P49, DOI 10.1016/j.tics.2006.11.004
  7. Cawthon RM, 2009, NUCLEIC ACIDS RES, V37, DOI 10.1093/nar/gkn1027
  8. Coimbra BM, 2017, J PSYCHIATR RES, V92, P47, DOI 10.1016/j.jpsychires.2017.03.023
  9. Conger RD, 2007, ANNU REV PSYCHOL, V58, P175, DOI 10.1146/annurev.psych.58.110405.085551
  10. Delpierre C, 2016, LONGITUD LIFE COURSE, V7, P79, DOI 10.14301/llcs.v7i1.325
  11. Drury SS, 2014, PEDIATRICS, V134, pE128, DOI 10.1542/peds.2013-3415
  12. Epel ES, 2004, P NATL ACAD SCI USA, V101, P17312, DOI 10.1073/pnas.0407162101
  13. Fagundes CP, 2013, BRAIN BEHAV IMMUN, V27, P8, DOI 10.1016/j.bbi.2012.06.014
  14. Fair DA, 2008, P NATL ACAD SCI USA, V105, P4028, DOI 10.1073/pnas.0800376105
  15. Fair DA, 2007, P NATL ACAD SCI USA, V104, P13507, DOI 10.1073/pnas.0705843104
  16. Flannagan KS, 2017, AM J HUM BIOL, V29, DOI 10.1002/ajhb.22942
  17. Fox MD, 2005, P NATL ACAD SCI USA, V102, P9673, DOI 10.1073/pnas.0504136102
  18. Fransson P, 2005, HUM BRAIN MAPP, V26, P15, DOI 10.1002/hbm.20113
  19. Gao W, 2017, NEUROSCIENTIST, V23, P169, DOI 10.1177/1073858416635986
  20. Gao W, 2009, P NATL ACAD SCI USA, V106, P6790, DOI 10.1073/pnas.0811221106
  21. Graham AM, 2015, J CHILD PSYCHOL PSYC, V56, P1212, DOI 10.1111/jcpp.12409
  22. Guo WB, 2014, PROG NEURO-PSYCHOPH, V49, P16, DOI 10.1016/j.pnpbp.2013.10.021
  23. Hamilton JP, 2015, BIOL PSYCHIAT, V78, P224, DOI 10.1016/j.biopsych.2015.02.020
  24. Hanssen LM, 2017, HEALTH PSYCHOL RES, V5, DOI 10.4081/hpr.2017.6378
  25. Heidinger BJ, 2012, P NATL ACAD SCI USA, V109, P1743, DOI 10.1073/pnas.1113306109
  26. Kessler RC, 2012, ARCH GEN PSYCHIAT, V69, P372, DOI 10.1001/archgenpsychiatry.2011.160
  27. Kleckner IR, 2017, NAT HUM BEHAV, V1, DOI 10.1038/s41562-017-0069
  28. Leech R, 2011, J NEUROSCI, V31, P3217, DOI 10.1523/JNEUROSCI.5626-10.2011
  29. Marsland AL, 2017, BRAIN BEHAV IMMUN, V62, P162, DOI 10.1016/j.bbi.2017.01.013
  30. McEwen B.S., 2017, CHRONIC STRESS, V1
  31. McEwen BS, 2013, NEURON, V79, P16, DOI 10.1016/j.neuron.2013.06.028
  32. Miller GE, 2011, PSYCHOL BULL, V137, P959, DOI 10.1037/a0024768
  33. Mitchell C, 2014, P NATL ACAD SCI USA, V111, P5944, DOI 10.1073/pnas.1404293111
  34. Monroe SM, 2008, ANNU REV CLIN PSYCHO, V4, P33, DOI 10.1146/annurev.clinpsy.4.022007.141207
  35. MOOS RH, 1994, FAMILY ENV SCALE MAN
  36. Muscatell KA, 2012, NEUROIMAGE, V60, P1771, DOI 10.1016/j.neuroimage.2012.01.080
  37. Needham BL, 2012, SOC SCI MED, V74, P1948, DOI 10.1016/j.socscimed.2012.02.019
  38. Patriat R, 2016, J AM ACAD CHILD PSY, V55, P319, DOI 10.1016/j.jaac.2016.01.010
  39. Price LH, 2013, BIOL PSYCHIAT, V73, P15, DOI 10.1016/j.biopsych.2012.06.025
  40. Raichle ME, 2001, P NATL ACAD SCI USA, V98, P676, DOI 10.1073/pnas.98.2.676
  41. Rebello K., 2018, CHRONIC STRESS, V2
  42. Robles TF, 2016, PSYCHONEUROENDOCRINO, V63, P343, DOI 10.1016/j.psyneuen.2015.10.018
  43. Roth TL, 2011, J CHILD PSYCHOL PSYC, V52, P398, DOI 10.1111/j.1469-7610.2010.02282.x
  44. Salum GA, 2015, INT J METH PSYCH RES, V24, P58, DOI 10.1002/mpr.1459
  45. Sato JR, 2014, J PSYCHIATR RES, V58, P89, DOI 10.1016/j.jpsychires.2014.07.004
  46. Shalev C, 2013, PSYCHONEUROENDOCRINO, V38, P1835, DOI 10.1016/j.psyneuen.2013.03.010
  47. Shalev I, 2013, MOL PSYCHIATR, V18, P576, DOI 10.1038/mp.2012.32
  48. Shonkoff JP, 2012, PEDIATRICS, V129, pE232, DOI 10.1542/peds.2011-2663
  49. Singh MK, 2014, BIPOLAR DISORD, V16, P678, DOI 10.1111/bdi.12221
  50. Soares JM, 2017, BRAIN STRUCT FUNCT, V222, P101, DOI 10.1007/s00429-016-1203-3
  51. Sripada RK, 2014, NEUROPSYCHOPHARMACOL, V39, P2244, DOI 10.1038/npp.2014.75
  52. Supekar K, 2010, NEUROIMAGE, V52, P290, DOI 10.1016/j.neuroimage.2010.04.009
  53. Teicher MH, 2016, NAT REV NEUROSCI, V17, P652, DOI 10.1038/nrn.2016.111
  54. Theall KP, 2013, SOC SCI MED, V85, P50, DOI 10.1016/j.socscimed.2013.02.030
  55. Thijssen S, 2017, DEV PSYCHOPATHOL, V29, P505, DOI 10.1017/S0954579417000141
  56. Thomason ME, 2017, NEUROSCIENCE, V342, P55, DOI 10.1016/j.neuroscience.2016.02.022
  57. Tyrka AR, 2010, BIOL PSYCHIAT, V67, P531, DOI 10.1016/j.biopsych.2009.08.014
  58. United Nations, 2015, MILL DEV GOALS REP
  59. Utevsky AV, 2014, J NEUROSCI, V34, P932, DOI 10.1523/JNEUROSCI.4227-13.2014
  60. Viana Silva, 2007, VERSAO PORTUGUES FAM
  61. von Zglinicki T, 2005, CURR MOL MED, V5, P197
  62. Washington Stuart D, 2015, Int J Med Biol Front, V21, P207
  63. Whitfield-Gabrieli S, 2012, ANNU REV CLIN PSYCHO, V8, P49, DOI 10.1146/annurev-clinpsy-032511-143049
  64. Wickerhauser H., 1991, CRITERIO ABEP ABIPEM
  65. Xavier G, 2018, J PSYCHIATR RES, V107, P104, DOI 10.1016/j.jpsychires.2018.10.012
  66. Yan CG, 2013, NEUROIMAGE, V76, P183, DOI 10.1016/j.neuroimage.2013.03.004
  67. Yang Z, 2014, NEUROIMAGE, V89, P45, DOI 10.1016/j.neuroimage.2013.10.039
  68. ZAKIAN VA, 1995, SCIENCE, V270, P1601, DOI 10.1126/science.270.5242.1601
  69. Zhang HD, 2016, SCI REP-UK, V6, DOI 10.1038/srep27906
  70. Zhou JS, 2016, BRAIN IMAGING BEHAV, V10, P995, DOI 10.1007/s11682-015-9465-6
  71. Zou QH, 2008, J NEUROSCI METH, V172, P137, DOI 10.1016/j.jneumeth.2008.04.012

Coleções
Artigos e Materiais de Revistas Científicas - FM/MPS
Artigos e Materiais de Revistas Científicas - LIM/23