Prolactin and Neuroendocrine Regulation in Brain Injury: Mechanisms of Adaptive Plasticity and Therapy Strategies.

Background

Acquired Brain Injuries (ABIs) represent a significant worldwide health challenge, with few specific medicines available to enhance recovery. Growing data underscores neuroendocrine dysfunction, especially with prolactin as a relatively overlooked yet potentially alterable element in neuronal regeneration. Hormonal signals regulate synaptic remodeling, neurogenesis, and glial regulation, rendering this a significant and current field of study. METHODOLOGY This review integrates evidence from clinical trials, animal models, and molecular research to assess prolactin's role in post-injury neural adaptation, with an emphasis on astrocyte activation, microglial responses, neuronal survival, and endocrine-neural connections.

Results

Prolactin has a dual function, as suggested by the evidence: a brief elevation may promote neuroprotection, synaptic recovery, and blood-brain barrier integrity, whereas sustained hyperprolactinemia correlates with cognitive deterioration, neuropsychiatric symptoms, and dopaminergic dysfunction. Prolactin receptor signaling appears to be a common feature of neuroinflammatory and glial events.

Discussion

These results illustrate the context-specific action of prolactin and demonstrate the importance of distinguishing between adaptive and maladaptive signaling. The addition of endocrine profiling to neurorehabilitation could open new avenues for individualized treatment.

Conclusion

This review presents prolactin as a potential, though not yet fully confirmed, modulator of ABI recovery. Further clinical research is required to enable the translation of these insights into maximal diagnostic and therapeutic benefit.