<i>BDNF</i> rs6265 differentially influences neurometabolites in the anterior cingulate of healthy and bipolar disorder subjects

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Tipo de produção
article
Data de publicação
2023
DOI
Scopus
Web of Science
PubMed
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SPRINGER
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Citação
BRAIN IMAGING AND BEHAVIOR, v.17, n.3, p.282-293, 2023
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Brain-derived neurotrophic factor (BDNF) is the most abundant brain neurotrophin and plays a critical role in neuronal growth, survival and plasticity, implicated in the pathophysiology of Bipolar Disorders (BD). The single-nucleotide polymorphism in the BDNF gene (BDNF rs6265) has been associated with decreased hippocampal BDNF secretion and volume in met carriers in different populations, although the val allele has been reported to be more frequent in BD patients. The anterior cingulate cortex (ACC) is a key center integrating cognitive and affective neuronal connections, where consistent alterations in brain metabolites such as Glx (Glutamate + Glutamine) and N-acetylaspartate (NAA) have been consistently reported in BD. However, little is known about the influence of BDNF rs6265 on neurochemical profile in the ACC of Healthy Controls (HC) and BD subjects. The aim of this study was to assess the influence of BDNF rs6265 on ACC neurometabolites (Glx, NAA and total creatine- Cr) in 124 euthymic BD type I patients and 76 HC, who were genotyped for BDNF rs6265 and underwent a 3-Tesla proton magnetic resonance imaging and spectroscopy scan ((1) H-MRS) using a PRESS ACC single-voxel (8cm(3)) sequence. BDNF rs6265 polymorphism showed a significant two-way interaction (diagnosis x genotype) in relation to NAA/Cr and total Cr. While met carriers presented increased NAA/Cr in HC, BD-I subjects with the val allele revealed higher total Cr, denoting an enhanced ACC metabolism likely associated with increased glutamatergic metabolites observed in BD-I val carriers. However, these results were replicated only in men. Therefore, our results support evidences that the BDNF rs6265 polymorphism exerts a complex pleiotropic effect on ACC metabolites influenced by the diagnosis and sex.
Palavras-chave
Creatine, Glx, H-1-MRS, N-acetylaspartate, Pleiotropic effect, Val66Met polymorphism
URI
https://observatorio.fm.usp.br/handle/OPI/58982
Referências
  1. American Psychiatric Association Ed T. & Revision, 2000, DIAGN STAT MAN MENT
  2. Baj G, 2013, FRONT NEUROSCI-SWITZ, V7, DOI 10.3389/fnins.2013.00188
  3. Boulle F, 2012, MOL PSYCHIATR, V17, P584, DOI 10.1038/mp.2011.107
  4. Brown NC, 2014, PSYCHIAT RES, V218, P61, DOI 10.1016/j.psychres.2014.04.005
  5. Buonocore MH, 2015, REV NEUROSCIENCE, V26, P609, DOI 10.1515/revneuro-2015-0010
  6. Camuso S, 2022, NEUROBIOL DIS, V163, DOI 10.1016/j.nbd.2021.105606
  7. Chen ZY, 2004, J NEUROSCI, V24, P4401, DOI 10.1523/JNEUROSCI.0348-04.2004
  8. Clay HB, 2011, INT J DEV NEUROSCI, V29, P311, DOI 10.1016/j.ijdevneu.2010.08.007
  9. Croarkin PE, 2015, BIPOLAR DISORD, V17, P450, DOI 10.1111/bdi.12285
  10. De-Paula VJ, 2016, BIPOLAR DISORD, V18, P692, DOI 10.1111/bdi.12449
  11. Decoster J, 2011, AM J MED GENET B, V156B, P363, DOI 10.1002/ajmg.b.31174
  12. Di Rosa MC, 2021, LIFE-BASEL, V11, DOI 10.3390/life11111256
  13. Egan MF, 2003, CELL, V112, P257, DOI 10.1016/S0092-8674(03)00035-7
  14. Ehrlich A, 2015, PSYCHIAT RES-NEUROIM, V233, P73, DOI 10.1016/j.pscychresns.2015.05.010
  15. First MSR., 1996, Structured clinical interview for DSM-IV axis I disorders, clinical version (SCID-CV)
  16. Frey BN, 2007, NEUROREPORT, V18, P1567, DOI 10.1097/WNR.0b013e3282ef7082
  17. Fukumoto N, 2010, AM J MED GENET B, V153B, P235, DOI 10.1002/ajmg.b.30986
  18. Gallinat J, 2010, NEUROIMAGE, V49, P767, DOI 10.1016/j.neuroimage.2009.08.018
  19. Gasparovic C, 2006, MAGN RESON MED, V55, P1219, DOI 10.1002/mrm.20901
  20. Gruber O, 2012, EUR ARCH PSY CLIN N, V262, P23, DOI 10.1007/s00406-011-0214-6
  21. Hamilton M., 1967, BRIT J SOC CLIN PSYC, V6, P278, DOI [10.1111/j.2044-8260.1967.tb00530.x, DOI 10.1111/J.2044-8260.1967.TB00530.X]
  22. Harrisberger F, 2015, NEUROSCI BIOBEHAV R, V55, P107, DOI 10.1016/j.neubiorev.2015.04.017
  23. Harrisberger F, 2014, NEUROSCI BIOBEHAV R, V42, P267, DOI 10.1016/j.neubiorev.2014.03.011
  24. Harrison PJ, 2021, MOL PSYCHIATR, V26, P4106, DOI 10.1038/s41380-019-0622-y
  25. HIBAR DP, 2017, MOL PSYCHIATR, P1
  26. HOFER M, 1990, EMBO J, V9, P2459, DOI 10.1002/j.1460-2075.1990.tb07423.x
  27. Hosang GM, 2014, BMC MED, V12, DOI 10.1186/1741-7015-12-7
  28. Karaca M, 2015, CELL REP, V13, P365, DOI 10.1016/j.celrep.2015.09.003
  29. Kennedy K. G., 2021, BIPOLAR DISORD, V00, P1
  30. Kowianski Przemyslaw, 2018, Cell Mol Neurobiol, V38, P579, DOI 10.1007/s10571-017-0510-4
  31. Kreis R, 2004, NMR BIOMED, V17, P361, DOI 10.1002/nbm.891
  32. Laing KR, 2012, AGE, V34, P1011, DOI 10.1007/s11357-011-9275-8
  33. LAITINEN J, 1994, BIOTECHNIQUES, V17, P316
  34. Lang UE, 2009, MOL PSYCHIATR, V14, P120, DOI 10.1038/mp.2008.80
  35. Li M, 2016, NEUROSCI BIOBEHAV R, V68, P218, DOI 10.1016/j.neubiorev.2016.05.031
  36. Maletic V, 2014, FRONT PSYCHIATRY, V5, DOI 10.3389/fpsyt.2014.00098
  37. Mandolini GM, 2019, J AFFECT DISORDERS, V243, P552, DOI 10.1016/j.jad.2018.07.054
  38. Markham A, 2014, BRIT J PHARMACOL, V171, P2206, DOI 10.1111/bph.12531
  39. Martens L, 2021, SCI REP-UK, V11, DOI 10.1038/s41598-021-86220-3
  40. Mitchelmore C, 2014, BRAIN RES, V1586, P162, DOI 10.1016/j.brainres.2014.06.037
  41. Mlynárik V, 2001, NMR BIOMED, V14, P325, DOI 10.1002/nbm.713
  42. Neves-Pereira M, 2002, AM J HUM GENET, V71, P651, DOI 10.1086/342288
  43. Nortje G, 2013, J AFFECT DISORDERS, V150, P192, DOI 10.1016/j.jad.2013.05.034
  44. Pagani R, 2019, PSYCHIAT RES, V278, P42, DOI 10.1016/j.psychres.2019.05.036
  45. Paul P, 2021, J PSYCHOPHARMACOL, V35, P1510, DOI 10.1177/02698811211032609
  46. Pedersen CB, 2014, JAMA PSYCHIAT, V71, P573, DOI 10.1001/jamapsychiatry.2014.16
  47. Pereira LP, 2017, NEUROSCI BIOBEHAV R, V79, P87, DOI 10.1016/j.neubiorev.2017.05.002
  48. PROVENCHER SW, 1993, MAGNET RESON MED, V30, P672, DOI 10.1002/mrm.1910300604
  49. Pruunsild P, 2007, GENOMICS, V90, P397, DOI 10.1016/j.ygeno.2007.05.004
  50. Rackayova V, 2017, ANAL BIOCHEM, V529, P144, DOI 10.1016/j.ab.2016.11.007
  51. Scotti-Muzzi E, 2022, EUR NEUROPSYCHOPHARM, V59, P26, DOI 10.1016/j.euroneuro.2022.04.001
  52. Scotti-Muzzi E, 2021, EUR NEUROPSYCHOPHARM, V47, P62, DOI 10.1016/j.euroneuro.2021.01.096
  53. Sheehan DV, 1998, J CLIN PSYCHIAT, V59, P22, DOI 10.4088/JCP.09m05305whi
  54. Sklar P, 2002, MOL PSYCHIATR, V7, P579, DOI 10.1038/sj.mp.4001058
  55. Smedler E, 2021, BRIT J PSYCHIAT, V218, P77, DOI 10.1192/bjp.2019.173
  56. Soeiro-de-Souza MG, 2018, J AFFECT DISORDERS, V241, P192, DOI 10.1016/j.jad.2018.08.039
  57. Soeiro-de-Souza MG, 2018, BIOL PSYCHIAT-COGN N, V3, P985, DOI 10.1016/j.bpsc.2018.02.007
  58. Soeiro-de-Souza MG, 2013, INT J NEUROPSYCHOPH, V16, P1505, DOI 10.1017/S1461145713000047
  59. Stanisz GJ, 2005, MAGNET RESON MED, V54, P507, DOI 10.1002/mrm.20605
  60. Stern AJ, 2008, BIOL PSYCHIAT, V64, P856, DOI 10.1016/j.biopsych.2008.07.009
  61. Stork C, 2005, MOL PSYCHIATR, V10, P900, DOI 10.1038/sj.mp.4001711
  62. Strakowski SM, 2012, BIPOLAR DISORD, V14, P313, DOI 10.1111/j.1399-5618.2012.01022.x
  63. Tsai SJ, 2018, FRONT MOL NEUROSCI, V11, DOI 10.3389/fnmol.2018.00156
  64. Vederine FE, 2011, PROG NEURO-PSYCHOPH, V35, P1820, DOI 10.1016/j.pnpbp.2011.05.009
  65. Walls A. B., 2021, EUR NEUROPSYCHOPHARM, V47, P402
  66. Wei SM, 2019, NEUROPSYCHOPHARMACOL, V44, P223, DOI 10.1038/s41386-018-0223-5
  67. YOUNG RC, 1978, BRIT J PSYCHIAT, V133, P429, DOI 10.1192/bjp.133.5.429
  68. YU AC, 1982, J NEUROCHEM, V39, P954, DOI 10.1111/j.1471-4159.1982.tb11482.x

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Artigos e Materiais de Revistas Científicas - FM/MPS