article · The Egyptian Journal of Neurology Psychiatry and Neurosurgery
Stroke causes widespread mortality and long-term disability, driving the search for more effective rehabilitation strategies. Astrocytes interact closely with neurons to regulate neural plasticity after injury. They maintain chemical balance through glutamate uptake and D-serine release, deliver metabolic support, and promote neuronal survival by producing neurotrophic factors like BDNF and GDNF. Astrocytes also modulate post-stroke neuroinflammation via communication with microglia. While reactive astrocytes build protective glial scars, these formations can also obstruct axonal regeneration. Potential therapies targeting astrocytes include pharmacological agents such as minocycline and celastrol, non-invasive neuromodulation including transcranial direct current stimulation and repetitive transcranial magnetic stimulation, stem cell transplantation, and cellular reprogramming. Overcoming key challenges, including imperfect translational models, imaging constraints, and difficulties isolating astrocyte-specific actions, will require emerging methods such as single-cell transcriptomics.
Stroke is a principal cause of long-term disability globally, yet existing clinical treatments offer incomplete recovery for many survivors. Exploring how non-neuronal cells such as astrocytes influence repair mechanisms opens new paths to restore damaged brain networks. Understanding their dual role in shielding brain tissue while potentially blocking regrowth helps guide more precise interventions to optimise functional rehabilitation.
This research outlines targets for developers of neuroprotective pharmaceuticals, stem cell therapies, and non-invasive brain stimulation devices aimed at stroke rehabilitation. Target end-users would ultimately be clinical neurologists and rehabilitation therapists. Given the reliance on early-stage mechanistic findings, experimental models, and unresolved hurdles around cellular heterogeneity, these approaches remain at an early research stage and distant from direct clinical deployment.
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Abstract Stroke remains a leading cause of global mortality and disability, necessitating innovative rehabilitation strategies to enhance recovery. Interactions between astrocytes and neurons modulate neural plasticity. This review synthesizes current evidence on the role of astrocytes in stroke recovery, focusing on their contributions to neural plasticity through neurotransmitter homeostasis, gliotransmission, neurotrophic factor release, metabolic support, modulation of inflammation, and extracellular matrix remodeling. Astrocytes regulate synaptic function via glutamate uptake and D-serine release, support neuronal survival through brain-derived neurotrophic factor (BDNF) and glial cell-derived neurotrophic factor (GDNF), and shape the neuroinflammatory response via crosstalk with microglia. While reactive astrocytes form protective glial scars, they also pose barriers to axonal regeneration. We explore astrocyte-targeted therapeutic strategies, including pharmacological interventions (minocycline, celastrol), non-invasive neuromodulation (tDCS, rTMS), stem cell therapy, and cellular reprogramming, highlighting their potential to enhance plasticity and recovery. Challenges such as limited translational models, difficulties isolating astrocyte-specific effects, and methodological constraints in imaging are discussed, alongside future directions involving single-cell transcriptomics to address astrocyte heterogeneity. By elucidating the multifaceted roles of astrocytes, this review highlights their therapeutic potential in stroke rehabilitation and advocates targeted interventions to optimize neuroprotection and circuit rewiring.
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DOI: 10.1186/s41983-026-01216-y
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