Neuroplasticity and Functional Recovery in Stroke Models

Stroke induces a spectrum of neurological deficits through focal or global cerebral ischaemia, triggering cell death, inflammation and disruption of neural networks. Neuroplasticity—the capacity of the brain to reorganise its structure, function and connections—underpins spontaneous and therapy-driven recovery. Key mechanisms include synaptic plasticity, whereby existing synapses are strengthened or weakened; neurogenesis in neurogenic niches that supplies new neurons; and angiogenesis that restores perfusion to hypoxic tissue. Beyond intrinsic regeneration, the post-stroke milieu can be shaped by environmental, pharmacological and rehabilitative interventions. Enriched environments comprising multisensory, cognitive and social stimuli augment dendritic complexity, upregulate neurotrophic factors and temper neuroinflammation. Targeted molecules, such as growth factors and signalling pathways (for example sonic hedgehog), can further enhance axonal sprouting and synaptic remodelling. Advances in neuroimaging and behavioural assays in animal models have refined our understanding of the temporal and regional dynamics of plasticity. A translational focus on combining environmental enrichment with neuromodulation, biomaterials or pharmacotherapy promises to accelerate functional recovery and improve quality of life for stroke survivors worldwide.

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Neuroplasticity and Functional Recovery in Stroke Models publication trend

The graph below shows the total number of articles in neuroplasticity and functional recovery in stroke models across all publications each year (not limited to Nature Index journals).

Technical terms

Neuroplasticity: The brain’s ability to reorganise neural circuits and form new connections after injury.

Enriched environment (EE): A housing paradigm providing enhanced sensory, cognitive and social stimulation to promote recovery.

Synaptic plasticity: The modification of synaptic strength through changes in receptor density or neurotransmitter release.

Neurogenesis: The generation of new neurons from neural progenitor cells, primarily in the hippocampus and subventricular zone.

Angiogenesis: The formation of new blood vessels to restore perfusion to ischaemic brain regions.

Brain-derived neurotrophic factor (BDNF): A neurotrophin essential for neuronal survival, growth and synaptic modulation.

Middle cerebral artery occlusion (MCAO): A widely used surgical method to induce focal cerebral ischaemia in animal models.

References

1. Enriched environment remodels the central immune environment and improves the prognosis of acute ischemic stroke in elderly mice with chronic ischemia. Frontiers in Immunology (2023).
2. Combination of fMRI and PET reveals the beneficial effect of three‐phase enriched environment on post‐stroke memory deficits by enhancing plasticity of brain connectivity between hippocampus and peri‐hippocampal cortex. CNS Neuroscience & Therapeutics (2023).
3. Total saponins from Trillium tschonoskii Maxim promote neurological recovery in model rats with post-stroke cognitive impairment. Frontiers in Pharmacology (2023).
4. Enriched environment-induced neuroplasticity in ischemic stroke and its underlying mechanisms. Frontiers in Cellular Neuroscience (2023).
5. The three-phase enriched environment paradigm promotes neurovascular restorative and prevents learning impairment after ischemic stroke in rats. Neurobiology of Disease (2020).