Objective: To study LTP-like plasticity in M1 in Parkinson’s disease (PD) patients affected responders to external auditory cueing strategies.
Background: Neural plasticity in the primary motor cortex (M1) has been shown to be impaired in PD with a lack of LTP-like plasticity in M11. Moreover, PD patients have also shown abnormal beta band activity in sensorimotor areas during movement initiation2, that can be normalized by the use of cues (such as rhythmic auditory cueing – RAC)3. Recent studies have also shown that LTP-like plasticity in M1 might be related to more efficient processes of movement-related beta-band desynchronization during movement execution4. We hypothesize that PD patients responders to RAC (i.e., showing a lower gait variability in cued gait compared to the uncued gait), might have a preserved LTP-like plasticity in M1.
Method: We recruited 11 RAC-responders (Age: 67,6 ± 7,7 y.o.; H&Y: 2,1 ± 0,31) and 11 RAC non-responders (Age: 67,6 ± 7,8 y.o.; H&Y: 2,1 ± 0,40), all affected by PD, that were tested for corticospinal excitability (CSE) via an I/O curve at 80%, 100%, 120%, 140% and 160% of the individual resting motor threshold (RMT), before and after an intermittent theta burst (iTBS) TMS protocol, used to induce LTP-like plasticity mechanisms in M1. The area under the I/O curve (AUC) was also computed. Clinical (MDS-UPDRS part I-IV) and neuropsychological (MoCA questionnaire, BDI, PAS) assessments were also performed.
Results: Our results showed that responders to RAC exhibited an increased corticospinal excitability post-iTBS in terms of increased MEPs post-iTBS protocol at 100% (p=0.008), 120% (p=0.022), 140% (p=0.003), and 160% (p=0.001) of RMT and AUC (p=0.001). No significant differences were found for non-responders. Moreover, a significantly higher AUC (p=0.021) was found in the post-iTBS protocol for responders compared to non-responders, while no differences were found between the two groups at baseline.
Conclusion: These preliminary results suggest that PD responders to RAC might have intact LTP-like plasticity in M1, possibly related to less abnormal synchronized beta-band activity in sensorimotor areas or to a more efficient mechanism of beta desynchronization during externally cued movement execution. This study is part of the broader UNITE-PD project, funded by the EU-JPND program.
References: References:
1. Suppa, A. et al. Lack of LTP-like plasticity in primary motor cortex in Parkinson’s disease. Exp. Neurol. 227, 296–301 (2011).
2. van Wijk, B. C. M., de Bie, R. M. A. & Beudel, M. A systematic review of local field potential physiomarkers in Parkinson’s disease: from clinical correlations to adaptive deep brain stimulation algorithms. J. Neurol. 270, 1162–1177 (2023).
3. Tosserams, A. et al. Cortical Correlates of Gait Compensation Strategies in Parkinson Disease. Ann. Neurol. 91, 329–341 (2022).
4. Ghilardi, M. F., Tatti, E. & Quartarone, A. Beta power and movement-related beta modulation as hallmarks of energy for plasticity induction: Implications for Parkinson’s disease. Park. Relat. Disord. 88, 136–139 (2021).
5. Tosserams, A. et al. Evaluation of Compensation Strategies for Gait Impairment in Patients with Parkinson Disease. Neurology 99, E2253–E2263 (2022).
To cite this abstract in AMA style:
L. Avanzino, A. Botta, V. Romano, J. Nonnekes, M. Gilat, I. Maidan, E. Pelosin. Preserved neuroplasticity in patients affected by Parkinson’s disease responders to auditory cueing strategies [abstract]. Mov Disord. 2025; 40 (suppl 1). https://www.mdsabstracts.org/abstract/preserved-neuroplasticity-in-patients-affected-by-parkinsons-disease-responders-to-auditory-cueing-strategies/. Accessed October 5, 2025.« Back to 2025 International Congress
MDS Abstracts - https://www.mdsabstracts.org/abstract/preserved-neuroplasticity-in-patients-affected-by-parkinsons-disease-responders-to-auditory-cueing-strategies/