Decreased levels of N-Acetylaspartyglutamate, myo-inositol, and syllo-inositol, in cortical brain regions of women exposed to adverse childhood experiences
School authors:
author photo
Pablo Irarrázaval
External authors:
  • Rocio Artigas ( Pontificia Universidad Catolica de Chile )
  • Sergio Ruiz ( Pontificia Universidad Catolica de Chile )
  • Cristian Montalba ( Pontificia Universidad Catolica de Chile )
  • Claudio Penafiel ( Pontificia Universidad Catolica de Chile )
  • Rodrigo Figueroa ( Pontificia Universidad Catolica de Chile )
Abstract:

Adverse Childhood Experiences (ACE), including abuse and neglect, can have lasting negative effects on health, decreasing lifespan and increasing the risk of chronic diseases. While research on ACE's impact on brain biochemistry is limited, Magnetic Resonance Spectroscopy (MRS) provides a non-invasive way to study these alterations. This study aims to identify neurochemical patterns linked to ACE exposure using J-edited MRS methods. 43 female participants (18 Low-ACE and 25 High-ACE), aged 19 to 31, were recruited. ACE exposure was assessed using the Maltreatment and Abuse Chronology of Exposure (MACE) test. MRS was conducted on a 3.0 T scanner, with J-edited single-voxel 1H-MRS from the Anterior Cingulate Cortex (ACC), Pre-Frontal Cortex (PFC), and hippocampus. Metabolite quantification was carried out using the Osprey pipeline and analyzed using univariate and multivariate methods. Univariate analysis showed reduced N-Acetylaspartyglutamate (NAAG) and syllo-Inositol (sI) levels in the ACC (p = 0.06) and PFC (p = 0.057), respectively, among High-ACE participants. Logistic Regression identified lower NAAG, GABA, glutathione (GSH), and myo-Inositol (mI) in the ACC, and differences in sI, lactate, NAAG, and GSH in the PFC, within the High-ACE group. Random Forest and Support Vector Machines confirmed NAAG, mI, and sI as possible ACE biomarkers. Throughout this study, cortical regions consistently showed reduced levels of NAAG, mI, and sI in the HighACE group, suggesting a potential link to ACE. These findings improve our understanding of neurochemical changes associated with ACE, aiding in the identification of at-risk individuals and in the development of strategies to prevent long-term health effects.

UT WOS:001676804700001
Number of Citations 0
Type
Pages
ISSUE
Volume 128
Month of Publication MAY
Year of Publication 2026
DOI https://doi.org/10.1016/j.mri.2026.110621
ISSN
ISBN