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Linda Scoriels

Laboratoire de physiopathologie des maladies psychiatriques, Institut de psychiatrie et neuroscience de Paris, Inserm U1266, Université Paris Cité, France - GHU Paris psychiatrie et neurosciences, Hôpital Sainte Anne, Paris, France - Laboratoire de psychologie du développement et de l'éducation de l'enfant, CNRS, Université Paris Cité, Paris, France.

2 papers in the library · 3 citations · publishing 2024-2025

Papers

Impact of minimal self disorders on naturalistic episodic memory in first-episode psychosis and parallels in healthy individuals with schizotypal traits.

Frontiers in psychiatry January 1, 2024 Delphine Yeh, Sylvain Penaud, Alexandre Gaston-Bellegarde et al. 3 citations

Disturbances in the minimal Self—the basic, pre-reflective sense of embodied experience—are linked to episodic memory impairments in first-episode psychosis (FEP). In a pilot study using immersive virtual reality, 10 FEP patients and 35 matched healthy controls experienced a full-body illusion with either synchronous or asynchronous visuomotor stimulation to induce strong or weak embodiment. Under strong embodiment, FEP patients performed significantly worse than controls in recognizing contextual information, though their retrieval phenomenology ratings were similar. Under weak embodiment, FEP patients performed similarly to controls in contextual recognition but rated retrieval phenomenology significantly lower. Higher schizotypy in controls correlated with a diminished sense of Self and poorer episodic memory. The findings suggest that targeting minimal Self-disorders may improve episodic memory and psychosocial outcomes in schizophrenia spectrum disorders.

[Anhedonia: from clinical practice to biomarkers].

Medecine sciences : M/S May 1, 2025 Antoine Yrondi, Romain Rey, Linda Scoriels et al.

Anhedonia involves reduced pleasure, motivation, and reward learning, and while traditionally linked to dopamine, recent evidence indicates that immune-inflammatory changes in psychiatric disorders also contribute. Inflammation affects dopamine, glutamate, and opioid pathways, plus cellular immune responses like mTOR signaling, disrupting reward and motor circuits in the brain. This leads to anhedonia and psychomotor slowing. Animal models confirm that chronic inflammation lowers motivation, modeling anhedonia. These disruptions occur across psychotic, mood, and neurodevelopmental disorders, not just one condition. This shared dimension suggests targeted treatments may include dopaminergic drugs, glutamatergic agents like ketamine, anti-inflammatory therapies, and novel molecules.