Neuropsychopharmacology of Depression and Anxiety Disorders

Neuropsychopharmacology of depression and anxiety disorders explores how chemical messengers, receptors and intracellular signalling govern mood regulation, emotional processing and stress resilience. Traditional treatments target monoamine systems, principally serotonin, noradrenaline and dopamine, to restore neurotransmitter balance. Advances in glutamatergic pharmacology have introduced rapid-acting agents that modulate NMDA or AMPA receptors, offering new avenues for treatment-resistant cases. Research now emphasises the interplay between neuroinflammation, neurotrophic support and synaptic plasticity: pro‐inflammatory cytokines can disrupt neurogenesis and dendritic remodelling, while factors such as brain‐derived neurotrophic factor (BDNF) promote synaptic strength and circuit stability. Intracellular pathways—PI3K/AKT/mTOR, Wnt–CamKII and sphingolipid‐mediated autophagy—link metabolic and stress signals to the maintenance of neuronal health. Pharmacological modulation of these pathways, alongside lifestyle and psychosocial interventions, holds promise for more personalised and enduring treatments. Global significance arises from the high prevalence and disability burden of mood and anxiety disorders, and from emerging evidence that peripheral biomarkers may predict treatment response. Together, these findings underscore a shift from simple neurotransmitter replacement towards integrated strategies that target cellular clearance, immune‐neural crosstalk and circuit remodelling.

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Neuropsychopharmacology of Depression and Anxiety Disorders publication trend

The graph below shows the total number of articles in neuropsychopharmacology of depression and anxiety disorders across all publications each year (not limited to Nature Index journals).

Technical terms

Autophagy: A cellular process for degrading and recycling damaged organelles and proteins, essential for neuronal homeostasis and stress adaptation.

Inflammasome: A multiprotein complex that recognises danger signals and induces maturation of pro‐inflammatory cytokines, linking immunity to neuronal function.

Synaptic plasticity: The ability of synapses to strengthen or weaken over time, underpinning learning, memory and mood regulation.

PI3K/AKT/mTOR pathway: An intracellular signalling cascade that regulates cell growth, survival and autophagy in response to growth factors and stress.

Wnt5a–CamKII signalling: A pathway in which the Wnt5a ligand activates CamKII kinase to influence synaptic structure and autophagy in neurons.

Sphingomyelin–ceramide metabolism: The balance between sphingomyelin and ceramide lipids in cellular membranes, which controls autophagy initiation and neuronal resilience.

References

1. Autophagy dysfunction contributes to NLRP1 inflammasome-linked depressive-like behaviors in mice. Journal of Neuroinflammation (2024).
2. Regular exercise ameliorates high-fat diet-induced depressive-like behaviors by activating hippocampal neuronal autophagy and enhancing synaptic plasticity. Cell Death & Disease (2024).
3. Antidepressants act by inducing autophagy controlled by sphingomyelin–ceramide. Molecular Psychiatry (2018).
4. Roles of PI3K/AKT/GSK3/mTOR Pathway in Cell Signaling of Mental Illnesses. Depression Research and Treatment (2012).
5. Brain-derived neurotrophic factor: a bridge between inflammation and neuroplasticity. Frontiers in Cellular Neuroscience (2014).