PTSD and appetite dysregulation: mTOR-dependent modulation of fear memory and satiety circuits

The mechanistic target of rapamycin (mTOR) has emerged as a central hub linking these pathways involved in synaptic plasticity, memory consolidation, metabolic and satiety adaptation. This review explores the multifaceted role of mTOR in PTSD, highlighting its involvement in fear memory persistence, neurotransmission, neuroinflammation, and satiety.

Dysregulated mTOR signalling has been linked to aberrant fear extinction, heightened synaptic plasticity, and altered brain metabolism, contributing to PTSD symptoms. mTOR's role in regulating protein synthesis, neuronal excitability, and glucose metabolism underscores its importance as a therapeutic target. Pharmacological modulation of mTOR, through inhibitors such as rapamycin, has shown promise in clinical and animal models for mitigating PTSD-like behaviours and promoting adaptive fear extinction and warrants further translation research for human trials.