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| Format: | Recurso digital |
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Zenodo
2026
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| Matèries: | |
| Accés en línia: | https://doi.org/10.5281/zenodo.18365964 |
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Taula de continguts:
- <p><span lang="EN-US">Parkinson's disease (PD) is characterized by progressive neurodegeneration but is also defined by a dynamic and sustained neuroplastic response within the central nervous system. This review explores the dualistic role of neuroplasticity in PD, operating along a continuum from physiological adaptation to pathological dysfunction. Initially, adaptive (compensatory) neuroplasticity—mediated by presynaptic dopaminergic upregulation, postsynaptic receptor super sensitivity, and long-term potentiation (LTP)—preserves motor function, underpinning the prolonged clinical "honeymoon period." However, as neurodegeneration advances and with chronic, pulsatile dopaminergic therapy, these same plastic mechanisms veer into maladaptive (aberrant) territory. Characterized by impaired LTP, enhanced long-term depression (LTD), and pathological circuit reorganization, this shift leads to levodopa-induced dyskinesias, freezing of gait, and other refractory symptoms. Modern neurorehabilitation must therefore strategically guide this inherent plastic potential. This requires adherence to evidence-based principles—specificity, salience, intensity, repetition, and progressive challenge—operationalized through modalities such as aerobic exercise, skill-based training (e.g., LSVT BIG, dance), dual-task practice, and adjunctive technologies (e.g., non-invasive brain stimulation). Effective intervention necessitates a personalized, plasticity-centric paradigm that matches rehabilitation strategies to disease stage, clinical phenotype, and medication state, supported by a multidisciplinary team. Future directions include the development of biomarkers to monitor neuroplasticity, the application of AI for personalization, and novel therapies targeting maladaptive plasticity. Ultimately, a deep understanding of neuroplasticity transforms PD management, positioning targeted rehabilitation not merely as symptomatic care but as a fundamental strategy to promote adaptive rewiring, mitigate pathological dysfunction, and potentially modify disease course.</span></p>