Intrinsic thalamocortical connectivity varies in the age of onset subtypes in major depressive disorder.
age of onset
cortex
depression
neuroimaging
resting-state fMRI
thalamus
Journal
Neuropsychiatric disease and treatment
ISSN: 1176-6328
Titre abrégé: Neuropsychiatr Dis Treat
Pays: New Zealand
ID NLM: 101240304
Informations de publication
Date de publication:
2019
2019
Historique:
entrez:
8
1
2019
pubmed:
8
1
2019
medline:
8
1
2019
Statut:
epublish
Résumé
Differences in the thalamocortical system have been shown in patients with major depressive disorder (MDD). Given prior evidence of phenotypic heterogeneity by the age of onset in MDD, we examined whether differences in thalamocortical connectivity could identify biological subtypes of MDD defined by the age of illness onset. A total of 94 subjects including 20 early-onset (EO) MDD (onset, 18 years), 34 adult-onset (AO) MDD, and 40 healthy controls (HCs) underwent resting-state functional MRI. Blood-oxygen-level-dependent time courses were extracted from six cortical regions of interest (ROIs) consisting of frontal, temporal, parietal, and occipital lobes and precentral and postcentral gyri. Each ROI's time course was then correlated with each voxel in thalamus, while covarying out signal from every other ROI. The analysis of variance results showed significant main effects of group in frontal and temporal connectivity with thalamus. Group contrasts showed a right fronto-thalamic hypo-connectivity only in AO-MDD, but not in EO-MDD, when compared to HCs. However, direct comparison between EO-MDD and AO-MDD showed no differences. Furthermore, there was a right temporal-thalamic hyperconnectivity in both EO-MDD and AO-MDD patients relative to HCs. These results were not accounted for by sex, age, or illness burden. The age of illness onset may be a source of heterogeneity in fronto-thalamic intrinsic connectivity in MDD.
Sections du résumé
BACKGROUND
BACKGROUND
Differences in the thalamocortical system have been shown in patients with major depressive disorder (MDD). Given prior evidence of phenotypic heterogeneity by the age of onset in MDD, we examined whether differences in thalamocortical connectivity could identify biological subtypes of MDD defined by the age of illness onset.
METHODS
METHODS
A total of 94 subjects including 20 early-onset (EO) MDD (onset, 18 years), 34 adult-onset (AO) MDD, and 40 healthy controls (HCs) underwent resting-state functional MRI. Blood-oxygen-level-dependent time courses were extracted from six cortical regions of interest (ROIs) consisting of frontal, temporal, parietal, and occipital lobes and precentral and postcentral gyri. Each ROI's time course was then correlated with each voxel in thalamus, while covarying out signal from every other ROI.
RESULTS
RESULTS
The analysis of variance results showed significant main effects of group in frontal and temporal connectivity with thalamus. Group contrasts showed a right fronto-thalamic hypo-connectivity only in AO-MDD, but not in EO-MDD, when compared to HCs. However, direct comparison between EO-MDD and AO-MDD showed no differences. Furthermore, there was a right temporal-thalamic hyperconnectivity in both EO-MDD and AO-MDD patients relative to HCs. These results were not accounted for by sex, age, or illness burden.
CONCLUSION
CONCLUSIONS
The age of illness onset may be a source of heterogeneity in fronto-thalamic intrinsic connectivity in MDD.
Identifiants
pubmed: 30613149
doi: 10.2147/NDT.S184425
pii: ndt-15-075
pmc: PMC6306066
doi:
Types de publication
Journal Article
Langues
eng
Pagination
75-82Déclaration de conflit d'intérêts
Disclosure This work was supported by investigator initiated grant by Astra Zeneca to Dr. Rajamannar Ramasubbu. The authors report no other conflicts of interest in this work.
Références
Br J Psychiatry. 2001 Oct;179:330-4
pubmed: 11581113
Nat Neurosci. 2003 Jul;6(7):750-7
pubmed: 12808459
Neuroimage. 2003 Jul;19(3):1233-9
pubmed: 12880848
J Neurosci. 1992 Nov;12(11):4501-9
pubmed: 1331362
Biol Psychiatry. 2003 Dec 15;54(12):1399-405
pubmed: 14675804
J Chem Neuroanat. 2003 Dec;26(4):317-30
pubmed: 14729134
J Neurosci. 1992 Sep;12(9):3628-41
pubmed: 1527602
Neuroimage. 2004;23 Suppl 1:S208-19
pubmed: 15501092
Psychiatry Res. 2004 Dec 15;129(2):127-40
pubmed: 15590040
Neurobiol Aging. 2005 Oct;26(9):1261-70; discussion 1275-8
pubmed: 16005549
Biol Psychiatry. 2007 Sep 1;62(5):429-37
pubmed: 17210143
Brain Res Bull. 2007 Mar 30;71(6):601-9
pubmed: 17292803
J Neurophysiol. 2008 Oct;100(4):1740-8
pubmed: 18701759
Neuropsychopharmacology. 2010 Jan;35(1):192-216
pubmed: 19693001
Cereb Cortex. 2010 May;20(5):1187-94
pubmed: 19729393
Am J Psychiatry. 2011 Jun;168(6):642-8
pubmed: 21362744
Psychol Med. 2012 Apr;42(4):671-81
pubmed: 21910935
J Affect Disord. 2012 May;138(3):268-76
pubmed: 22377511
J Neurol. 2013 Feb;260(2):386-96
pubmed: 22854887
Soc Cogn Affect Neurosci. 2013 Feb;8(2):123-33
pubmed: 23051902
Nat Rev Neurosci. 2013 Apr;14(4):278-91
pubmed: 23511908
J Affect Disord. 2013 Sep 5;150(2):703-6
pubmed: 23769291
J Psychiatry Neurosci. 2014 May;39(3):170-7
pubmed: 24119793
Neuroimage Clin. 2013 Dec 11;4:209-31
pubmed: 24455472
Am J Psychiatry. 2014 May;171(5):564-71
pubmed: 24577365
Biomed Res Int. 2014;2014:410472
pubmed: 24734233
Psychiatry Clin Neurosci. 2014 Dec;68(12):812-820
pubmed: 24773595
Psychol Med. 2014 Oct;44(13):2833-43
pubmed: 25066703
Clin Neurophysiol. 2015 Jul;126(7):1331-7
pubmed: 25487911
Psychol Aging. 2015 Jun;30(2):475-85
pubmed: 26030776
J Affect Disord. 2017 Aug 1;217:125-131
pubmed: 28407555
Biol Psychiatry. 2018 Apr 15;83(8):648-656
pubmed: 29275841
Br J Soc Clin Psychol. 1967 Dec;6(4):278-96
pubmed: 6080235
Br J Psychiatry. 1994 Mar;164(3):342-8
pubmed: 8199787