The role of BDNF as a mediator of neurobiological and clinical improvements in Parkinson’s disease patients following HIIT: A comprehensive review.

Oliwia Zuzanna Gańska; Agata Sochocka; Dominika Janik; Nina Nowicka; Martyna Szepietowska; Zuzanna Zapart; Jakub Bundyra; Emil Mian; Alicja Sikorska; Julia Parda

doi:10.12775/QS.2026.56.72621

Authors

Oliwia Zuzanna Gańska Warszawski Uniwersytet Medyczny https://orcid.org/0009-0007-9024-0209
Agata Sochocka Medical University of Warsaw https://orcid.org/0009-0004-5384-2014
Dominika Janik Warszawski Uniwersytet Medyczny https://orcid.org/0009-0000-8527-7428
Nina Nowicka Medical University of Warsaw https://orcid.org/0009-0004-1942-0045
Martyna Szepietowska Medical University of Warsaw, Żwirki i Wigury 61, 02-091 Warsaw, Poland https://orcid.org/0009-0000-2423-4563
Zuzanna Zapart Medical University of Warsaw https://orcid.org/0009-0007-0466-4508
Jakub Bundyra Medical University of Warsaw https://orcid.org/0009-0008-7042-1990
Emil Mian Medical University of Warsaw https://orcid.org/0009-0006-1538-7190
Alicja Sikorska Medical University of Warsaw https://orcid.org/0009-0009-6274-6944
Julia Parda Medical University of Warsaw https://orcid.org/0009-0006-9079-5936

DOI:

https://doi.org/10.12775/QS.2026.56.72621

Keywords

HIIT, Parkinson's disease, BDNF, neuroplasticity, MDS-UPDRS, neurorehabilitation

Abstract

Background. Parkinson’s disease (PD) is characterized by progressive dopaminergic neurodegeneration and significantly reduced levels of Brain-Derived Neurotrophic Factor (BDNF). High-Intensity Interval Training (HIIT) has emerged as a critical non-pharmacological strategy to stimulate neuroplasticity via the muscle-brain axis.

Aim. This review evaluates the role of BDNF as the primary biological mediator of the neurobiological and clinical improvements observed in PD patients following HIIT interventions.

Material and methods. A structured analysis was performed on 28 scientific publications (2008–2026) sourced from PubMed. The methodology synthesized molecular signaling pathways with standardized clinical outcome measures.

Results. HIIT-induced elevations in blood lactate and irisin trigger the PGC-1α/BDNF pathway, crossing the blood-brain barrier to enhance mitochondrial quality control and neuronal survival. Clinical evidence demonstrates a 21.6% mean reduction in MDS-UPDRS Part III scores, alongside significant improvements in gait economy, executive functions, and respiratory mechanics. HIIT further mitigates depressive symptoms through BDNF-modulated neurotransmission.

Conclusions. BDNF is the central driver of the multi-systemic benefits associated with HIIT. Providing a more robust neurotrophic stimulus than moderate-intensity exercise, HIIT acts as a potent disease-modifying therapy. Early implementation of individualized HIIT protocols is essential for optimizing long-term psychomotor resilience.

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The role of BDNF as a mediator of neurobiological and clinical improvements in Parkinson’s disease patients following HIIT: A comprehensive review.

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