TY - JOUR
T1 - High γ-Aminobutyric Acid Content Within the Medial Prefrontal Cortex Is a Functional Signature of Somatic Symptoms Disorder in Patients With Parkinson's Disease
AU - Delli Pizzi, Stefano
AU - Franciotti, Raffaella
AU - Ferretti, Antonio
AU - Edden, Richard A.E.
AU - Zöllner, Helge J.
AU - Esposito, Roberto
AU - Bubbico, Giovanna
AU - Aiello, Claudia
AU - Calvanese, Francesco
AU - Sensi, Stefano L.
AU - Tartaro, Armando
AU - Onofrj, Marco
AU - Bonanni, Laura
N1 - Funding Information:
Dr. Stefano Delli Pizzi serves as academic editor of , , and . Prof. Marco Onofrj has served on the scientific advisory boards of GlaxoSmithKline, Novartis, Lundbeck, Eisai, Valeant, Medtronic, and Newron; has received speaker honoraria from Zambon, the World Parkinson Congress, the Movement Disorder Society, and the Atypical Dementias congress; publishing royalties from Springer; was an invited guest and lecturer for the Mental Disorders in Parkinson Disease Congress; serves on the editorial board of ; has been employed as a speaker for Boehringer Ingelheim, GlaxoSmithKline, UCB, and Zambon; and has received research support from the Italian Ministry of Health and the Italian Ministry of Education. Prof. Stefano Sensi serves as associate editor of , , , and and is supported by nonprofit agencies (the Italian Ministry of Health, the AIRAlzh Onlus), European Union's Horizon 2020 research and innovation program under the Marie Skłodowska‐Curie grant agreement iMIND–No. 84166, the Alzheimer's Association–Part the Cloud: Translational Research Funding for Alzheimer's Disease (18PTC‐19‐602325) and the Alzheimer's Association–GAAIN Exploration to Evaluate Novel Alzheimer's Queries (GEENA‐Q‐19‐596282). Prof. Laura Bonanni has received research support from the Italian Ministry of Health, the European Community, and from Mentis cura srl, Oslo and serves as an editorial board member for the '. Scientific Reports Behavioral and Brain Functions Medicine Medicine (Baltimore) and Frontiers in Neurology Frontiers in Neuroscience Frontiers in Psychiatry PloS One Scientific Reports Journal of Alzheimer s Disease
Funding Information:
This study is not industry sponsored. This work was supported by the Italian Ministry of Health (Grant GR‐2010‐2313418). This study applies tools developed under the National Institutes of Health (Grants NIH R01 EB016089 and P41 EB015909). Richard A. E. Edden also receives salary support from these grants. Funding agency:
Publisher Copyright:
© 2020 International Parkinson and Movement Disorder Society
PY - 2020/12
Y1 - 2020/12
N2 - Background: The dysfunctional activity of the medial prefrontal cortex has been associated with the appearance of the somatic symptom disorder, a key feature of the Parkinson's disease (PD) psychosis complex. Objectives: The objectives of this study were to investigate whether the basal contents of inhibitory γ-aminobutyric acid and excitatory glutamate plus glutamine neurotransmitter levels are changed in the medial prefrontal cortex of patients with PD with somatic symptom disorder and whether this alteration represents a marker of susceptibility of PD to somatic symptom disorder, thus representing a signature of psychosis complex of PD. Methods: Levels of the γ-aminobutyric acid and glutamate plus glutamine were investigated, at rest, with proton magnetic resonance spectroscopy. Total creatine was used as an internal reference. The study cohort included 23 patients with somatic symptom disorder plus PD, 19 patients with PD without somatic symptom disorder, 19 healthy control subjects, and 14 individuals with somatic symptom disorder who did not show other psychiatric or neurological disorders. Results: We found that, compared with patients with PD without somatic symptom disorder or healthy control individuals, patients with somatic symptom disorder, with or without PD, show increased γ-aminobutyric acid/total creatine levels in the medial prefrontal cortex. The medial prefrontal cortex contents of glutamate plus glutamine/total creatine levels or γ-aminobutyric acid/glutamate plus glutamine were not different among groups. Conclusions: Our findings highlight a crucial pathophysiologic role played by high γ-aminobutyric acid within the medial prefrontal cortex in the production of somatic symptom disorder. This phenomenon represents a signature of psychosis complex in patients with PD.
AB - Background: The dysfunctional activity of the medial prefrontal cortex has been associated with the appearance of the somatic symptom disorder, a key feature of the Parkinson's disease (PD) psychosis complex. Objectives: The objectives of this study were to investigate whether the basal contents of inhibitory γ-aminobutyric acid and excitatory glutamate plus glutamine neurotransmitter levels are changed in the medial prefrontal cortex of patients with PD with somatic symptom disorder and whether this alteration represents a marker of susceptibility of PD to somatic symptom disorder, thus representing a signature of psychosis complex of PD. Methods: Levels of the γ-aminobutyric acid and glutamate plus glutamine were investigated, at rest, with proton magnetic resonance spectroscopy. Total creatine was used as an internal reference. The study cohort included 23 patients with somatic symptom disorder plus PD, 19 patients with PD without somatic symptom disorder, 19 healthy control subjects, and 14 individuals with somatic symptom disorder who did not show other psychiatric or neurological disorders. Results: We found that, compared with patients with PD without somatic symptom disorder or healthy control individuals, patients with somatic symptom disorder, with or without PD, show increased γ-aminobutyric acid/total creatine levels in the medial prefrontal cortex. The medial prefrontal cortex contents of glutamate plus glutamine/total creatine levels or γ-aminobutyric acid/glutamate plus glutamine were not different among groups. Conclusions: Our findings highlight a crucial pathophysiologic role played by high γ-aminobutyric acid within the medial prefrontal cortex in the production of somatic symptom disorder. This phenomenon represents a signature of psychosis complex in patients with PD.
KW - Parkinson's disease
KW - medial prefrontal cortex
KW - proton magnetic resonance spectroscopy
KW - somatic symptoms disorder
KW - γ-aminobutyric acid
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U2 - 10.1002/mds.28221
DO - 10.1002/mds.28221
M3 - Article
C2 - 32744357
AN - SCOPUS:85088815692
SN - 0885-3185
VL - 35
SP - 2184
EP - 2192
JO - Movement Disorders
JF - Movement Disorders
IS - 12
ER -