Longitudinal relationships among depressive symptoms, cortisol, and brain atrophy in the neocortex and the hippocampusVisa övriga samt affilieringar
2018 (Engelska)Ingår i: Acta Psychiatrica Scandinavica, ISSN 0001-690X, E-ISSN 1600-0447, Vol. 167, nr 6, s. 491-502Artikel i tidskrift (Refereegranskat) Published
Abstract [en]
OBJECTIVE: Depression is associated with accelerated aging and age-related diseases. However, mechanisms underlying this relationship remain unclear. The aim of this study was to longitudinally assess the link between depressive symptoms, brain atrophy, and cortisol levels.
METHOD: Participants from the Betula prospective cohort study (mean age = 59 years, SD = 13.4 years) underwent clinical, neuropsychological and brain 3T MRI assessments at baseline and a 4-year follow-up. Cortisol levels were measured at baseline in four saliva samples. Cortical and hippocampal atrophy rates were estimated and compared between participants with and without depressive symptoms (n = 81) and correlated with cortisol levels (n = 49).
RESULTS: Atrophy in the left superior frontal gyrus and right lingual gyrus developed in parallel with depressive symptoms, and in the left temporal pole, superior temporal cortex, and supramarginal cortex after the onset of depressive symptom. Depression-related atrophy was significantly associated with elevated cortisol levels. Elevated cortisol levels were also associated with widespread prefrontal, parietal, lateral, and medial temporal atrophy.
CONCLUSION: Depressive symptoms and elevated cortisol levels are associated with atrophy of the prefrontal and limbic areas of the brain.
Ort, förlag, år, upplaga, sidor
John Wiley & Sons, 2018. Vol. 167, nr 6, s. 491-502
Nyckelord [en]
depressive symptomatology, neuroimaging, superior temporal gyrus, superior frontal gyrus, MRI
Nationell ämneskategori
Omvårdnad Psykiatri
Identifikatorer
URN: urn:nbn:se:umu:diva-146479DOI: 10.1111/acps.12860ISI: 000433560700006PubMedID: 29457245Scopus ID: 2-s2.0-85042120842OAI: oai:DiVA.org:umu-146479DiVA, id: diva2:1196604
2018-04-102018-04-102023-03-24Bibliografiskt granskad