open access publication

Article, 2024

Impaired striatal glutamate/GABA regulation in violent offenders with antisocial personality disorder and psychopathy

Molecular Psychiatry, ISSN 1359-4184, 10.1038/s41380-024-02437-4

Contributors

Tully J. 0000-0002-5858-3419 (Corresponding author) [1] [2] Pereira A.C. [2] Sethi A. [2] Griem J. 0000-0002-1779-5255 [2] Cross B. [2] Williams S.C.R. 0000-0003-4299-1941 [2] Blair R.J.R. 0000-0002-6377-2361 [3] Murphy D. 0000-0002-6664-7451 [2] Blackwood N. [2]

Affiliations

  1. [1] University of Nottingham
  2. [NORA names: United Kingdom; Europe, Non-EU; OECD];
  3. [2] King's College London
  4. [NORA names: United Kingdom; Europe, Non-EU; OECD];
  5. [3] Capital Region of Denmark
  6. [NORA names: Capital Region of Denmark; Hospital; Denmark; Europe, EU; Nordic; OECD]

Abstract

Men with antisocial personality disorder (ASPD) with or without psychopathy (+/−P) are responsible for most violent crime in society. Development of effective treatments is hindered by poor understanding of the neurochemical underpinnings of the condition. Men with ASPD with and without psychopathy demonstrate impulsive decision-making, associated with striatal abnormalities in functional neuroimaging studies. However, to date, no study has directly examined the potential neurochemical underpinnings of such abnormalities. We therefore investigated striatal glutamate: GABA ratio using Magnetic Resonance Spectroscopy in 30 violent offenders (16 ASPD-P, 14 ASPD + P) and 21 healthy non-offenders. Men with ASPD +/− P had a significant reduction in striatal glutamate : GABA ratio compared to non-offenders. We report, for the first time, striatal Glutamate/GABA dysregulation in ASPD +/− P, and discuss how this may be related to core behavioral abnormalities in the disorders.

Funders

  • King’s College London
  • National Institute for Health Research
  • Autism Research for Europe
  • Wellcome Clinical Research
  • South London and Maudsley NHS Foundation Trust
  • Medical Research Council

Data Provider: Elsevier