Theory of mind (ToM) deficit is a frequent finding in subjects with neurological and psychiatric conditions. While a number of brain regions play a role in ToM, to date the contribution of the diffuse projection systems is less understood. Here, we explored the topographical and neurochemical bases of ToM using multi-tracer molecular imaging and quantitative electroencephalography (qEEG) in a group of 30 drug-naïve, de novo Parkinson's Disease (PD) patients (mean age 73.39 ± 8.93 years, 11 females). ToM was assessed using the “Reading the Mind in the Eyes Task” (RMET), while general cognition with the MMSE. We acquired FDG-PET images (as a marker of regional neurodegeneration), I-123 Ioflupane Single Photon Emission Computed Tomography (123 I-FP-CIT-SPECT, as a marker of dopaminergic impairment in the basal ganglia and in the cortex and as a proxy marker of serotoninergic deafferentation in the thalamus), and qEEG recordings (using the Theta/Alpha power ratio as marker of cholinergic deafferentation). PD presented with a significantly worse RMET score compared to 60 controls (20.7 ± 5.5 vs 27.5 ± 3.0 p = .001) while there was no difference between the two groups in age, education or MMSE. The voxel-wise analysis of total RMET score and regional metabolism showed a positive correlation in the superior temporal gyrus and in the insula. Among the proxy markers of dopaminergic degeneration, serotoninergic and cholinergic deafferentation, ToM presented only an inverse correlation with 123 I-FP-CIT thalamic specific binding ratio (SBR) values -a proxy serotoninergic marker-which remained significant after correction for FDG metabolism in the areas associated with ToM. On the other hand, MMSE only correlated with qEEG posterior Theta/Alpha power. These findings point to the presence of a specific cortical and neurochemical signature of ToM in PD, to the independence of ToM from general cognition, and suggest possible therapeutic targets to treat social cognition deficits.

Anatomical and neurochemical bases of theory of mind in de novo Parkinson's Disease

Orso B.;Arnaldi D.;Fama F.;Girtler N.;Brugnolo A.;Doglione E.;Filippi L.;Massa F.;Peira E.;Bauckneht M.;Morbelli S.;Nobili F.;Pardini M.
2020

Abstract

Theory of mind (ToM) deficit is a frequent finding in subjects with neurological and psychiatric conditions. While a number of brain regions play a role in ToM, to date the contribution of the diffuse projection systems is less understood. Here, we explored the topographical and neurochemical bases of ToM using multi-tracer molecular imaging and quantitative electroencephalography (qEEG) in a group of 30 drug-naïve, de novo Parkinson's Disease (PD) patients (mean age 73.39 ± 8.93 years, 11 females). ToM was assessed using the “Reading the Mind in the Eyes Task” (RMET), while general cognition with the MMSE. We acquired FDG-PET images (as a marker of regional neurodegeneration), I-123 Ioflupane Single Photon Emission Computed Tomography (123 I-FP-CIT-SPECT, as a marker of dopaminergic impairment in the basal ganglia and in the cortex and as a proxy marker of serotoninergic deafferentation in the thalamus), and qEEG recordings (using the Theta/Alpha power ratio as marker of cholinergic deafferentation). PD presented with a significantly worse RMET score compared to 60 controls (20.7 ± 5.5 vs 27.5 ± 3.0 p = .001) while there was no difference between the two groups in age, education or MMSE. The voxel-wise analysis of total RMET score and regional metabolism showed a positive correlation in the superior temporal gyrus and in the insula. Among the proxy markers of dopaminergic degeneration, serotoninergic and cholinergic deafferentation, ToM presented only an inverse correlation with 123 I-FP-CIT thalamic specific binding ratio (SBR) values -a proxy serotoninergic marker-which remained significant after correction for FDG metabolism in the areas associated with ToM. On the other hand, MMSE only correlated with qEEG posterior Theta/Alpha power. These findings point to the presence of a specific cortical and neurochemical signature of ToM in PD, to the independence of ToM from general cognition, and suggest possible therapeutic targets to treat social cognition deficits.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11567/1022902
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