[Anhedonia: from clinical practice to biomarkers].
Medecine sciences : M/S – May 01, 2025
Source: PubMed
Summary
Pleasure and motivation are fundamental to human experience, yet some people lose the ability to feel joy. This reduced capacity, known as anhedonia, goes beyond simple sadness. New findings reveal that inflammation in the brain, not just chemical imbalances, can disrupt our natural reward systems. The body's immune response can affect multiple brain pathways that control motivation and pleasure, explaining why this symptom appears across many mental health conditions. Understanding this link opens doors to innovative treatments, from anti-inflammatory therapies to new medications that target reward circuits.
Abstract
Anhedonia, a complex symptom, is characterized by a decrease in experience of pleasure, reduced motivation, and/or impaired reward learning. Although these aspects are often linked to dopaminergic pathways, recent research shows that immuno-inflammatory alterations present in psychiatric disorders may also play a role, affecting dopaminergic, glutamatergic, and opioid pathways, as well as cellular immune responses (such as the mTOR pathway). These perturbations, through inflammation in the central nervous system, affect reward and motor circuits, contributing to the anhedonia and the psychomotor slowing that are often-associated. Animal models show that chronic inflammation can reduce motivation, providing a preclinical model for anhedonia. This dysfunction is not specific to a single pathology but is common to a variety ofpsychiatric disorders, including psychotic, mood, and neurodevelopmental disorders. These common dimensions of anhedonia across different pathologies open up perspects for targeted treatments, including dopaminergic treatments, glutamatergic treatments (such as ketamine), anti-inflammatory therapies, and the development of new molecules.