Pharmacological Modulation for Post-Stroke Recovery

Pharmacological modulation for post-stroke recovery encompasses the use of drugs to enhance neuroprotection, promote neural repair and foster functional restoration after cerebral ischaemia. Key strategies target excitotoxicity, inflammation and impaired neuroplasticity in the ischaemic penumbra. Agents that elevate monoamine levels, such as selective serotonin reuptake inhibitors (SSRIs), have been shown to enhance synaptic plasticity, stimulate neurogenesis and modulate excitatory–inhibitory balance, thereby improving motor and cognitive recovery. Other classes under investigation include tricyclic antidepressants, neurotrophic factor mimetics, anti-inflammatory compounds and small molecules that stabilise neuronal calcium homeostasis. Preclinical models indicate that certain antidepressants confer direct neuroprotective effects through attenuation of lipid peroxidation, suppression of pro-inflammatory cytokines and upregulation of survival pathways. Clinically, fluoxetine and related compounds have been trialled for their ability to facilitate motor relearning and reduce post-stroke depression, with evidence of improved functional outcomes in selected patient subsets. Ongoing research seeks to optimise timing, dose and patient stratification, while novel pharmacological targets such as GABAergic modulators and agents that enhance angiogenesis are entering early translational studies. Given the global burden of stroke, refined drug-based approaches hold promise for cost-effective adjuncts to rehabilitation programmes worldwide.

Research from Nature Portfolio

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Pharmacological Modulation for Post-Stroke Recovery publication trend

The graph below shows the total number of articles in pharmacological modulation for post-stroke recovery across all publications each year (not limited to Nature Index journals).

Technical terms

Neuroplasticity: The ability of neural circuits to reorganise synaptic connections and functional outputs in response to experience or injury.

Neurogenesis: The process by which new neurons are generated from neural stem or progenitor cells, particularly in the adult hippocampus and subventricular zone.

Excitotoxicity: Neuronal injury and death caused by excessive activation of glutamate receptors, leading to calcium overload and oxidative stress.

Ischaemic penumbra: Tissue surrounding the core infarct that remains viable but functionally impaired due to reduced blood flow.

Long-term potentiation: A sustained increase in synaptic strength following high-frequency stimulation, regarded as a cellular mechanism of learning and memory.

Excitatory–inhibitory balance: The homeostatic ratio of excitatory to inhibitory synaptic inputs that regulates neuronal network stability and plasticity.

References

1. The atypical antidepressant tianeptine confers neuroprotection against oxygen–glucose deprivation. European Archives of Psychiatry and Clinical Neuroscience (2023).
2. SSRI and Motor Recovery in Stroke: Reestablishment of Inhibitory Neural Network Tonus. Frontiers in Neuroscience (2017).
3. Selective serotonin reuptake inhibitors to improve outcome in acute ischemic stroke: possible mechanisms and clinical evidence. Brain and Behavior (2015).
4. Selective serotonin reuptake inhibitors for functional independence and depression prevention in early stage of post-stroke. Medicine (2020).