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Cortical and basal ganglia beta oscillations and frequency-dependent DBS effects in the A53T Parkinson’s disease rat model
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  • Published: 19 March 2026

Cortical and basal ganglia beta oscillations and frequency-dependent DBS effects in the A53T Parkinson’s disease rat model

  • Laura Kondrataviciute1,2,
  • Minesh Kapadia2,
  • Ivan Skelin2,3,
  • Srdjan Sumarac1,2,
  • Luka Zivkovic1,2,
  • Luis Antonio Franco Vergara1,2,
  • Sabika Jafri2,
  • Cherisse Tan2,4,
  • Hien Chau2,
  • Yuhan Hou5,
  • Savanna Blade5,
  • Xilin Liu3,5,
  • Clement Hamani6,
  • Taufik Valiante1,2,3,7,8,
  • William D. Hutchison2,8,
  • Luka Milosevic1,2,3,7 na1,
  • Lorraine V. Kalia2,9,10 na1 &
  • …
  • Suneil K. Kalia2,3,7,8 na1 

npj Parkinson's Disease , Article number:  (2026) Cite this article

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We are providing an unedited version of this manuscript to give early access to its findings. Before final publication, the manuscript will undergo further editing. Please note there may be errors present which affect the content, and all legal disclaimers apply.

Subjects

  • Neurology
  • Neuroscience

Abstract

Parkinson’s disease (PD) is a movement disorder characterized by alpha-synuclein (a-Syn) aggregation, dopaminergic degeneration, and pathological beta oscillations (13–30 Hz) in the basal ganglia circuit. Deep brain stimulation (DBS) is an effective neurosurgical treatment for the motor symptoms of PD. However, the extent to which mitigation of beta oscillations mediates DBS therapeutic effects remains uncertain. Using an adeno-associated virus-mediated nigral A53T a-Syn overexpression rat model, we examined basal ganglia-thalamo-cortical electrophysiology and the model’s responsiveness to DBS. In vivo recordings revealed early beta emergence in the motor cortex (MCx), spreading to the subthalamic nucleus (STN) and entopeduncular nucleus (EP) with neurodegeneration. This was accompanied by alterations in STN and EP single-unit activity. Awake-state beta oscillations manifested as transient bursts. Low- and high-frequency DBS differentially modulated beta bursts and motor performance. Our results demonstrate that the A53T a-Syn model replicates key PD-like electrophysiological features, providing a platform to investigate DBS mechanisms and optimize therapies targeting aberrant beta activity.

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Data availability

All data generated or analyzed in this study are included in this article and supplementary files, or are available from the corresponding author upon reasonable request. The underlying code for this study is not publicly available but may be made available to qualified researchers on reasonable request from the corresponding author.

Code availability

The underlying code for this study is not publicly available but may be made available to qualified researchers on reasonable request from the corresponding author.

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Acknowledgements

This study was funded by Natural Sciences and Engineering Council (NSERC) RGPIN-2022-05181 (L.M.), the Canadian Institute for Health Research (CIHR) PJT 191880 (L.M., S.K.), Canadian Foundation for Innovation (CFI) Project 42608 (L.M., S.K., T.V.) and the R.R. Tasker Chair in Stereotactic and Functional Neurosurgery (S.K.).

Author information

Author notes

  1. These authors contributed equally: Luka Milosevic, Lorraine V. Kalia, Suneil K. Kalia.

Authors and Affiliations

  1. Institute of Biomedical Engineering, University of Toronto, Toronto, ON, Canada

    Laura Kondrataviciute, Srdjan Sumarac, Luka Zivkovic, Luis Antonio Franco Vergara, Taufik Valiante & Luka Milosevic

  2. Krembil Research Institute, Toronto Western Hospital, University Health Network, Toronto, ON, Canada

    Laura Kondrataviciute, Minesh Kapadia, Ivan Skelin, Srdjan Sumarac, Luka Zivkovic, Luis Antonio Franco Vergara, Sabika Jafri, Cherisse Tan, Hien Chau, Taufik Valiante, William D. Hutchison, Luka Milosevic, Lorraine V. Kalia & Suneil K. Kalia

  3. CRANIA, University Health Network and University of Toronto, Toronto, ON, Canada

    Ivan Skelin, Xilin Liu, Taufik Valiante, Luka Milosevic & Suneil K. Kalia

  4. Institute of Medical Sciences, University of Toronto, Toronto, ON, Canada

    Cherisse Tan

  5. Department of Electrical & Computer Engineering, University of Toronto, Toronto, ON, Canada

    Yuhan Hou, Savanna Blade & Xilin Liu

  6. Division of Neurosurgery, Sunnybrook Health Sciences Centre, University of Toronto, Toronto, ON, Canada

    Clement Hamani

  7. KITE, Toronto Rehabilitation Institute, University Health Network, Toronto, ON, Canada

    Taufik Valiante, Luka Milosevic & Suneil K. Kalia

  8. Department of Surgery, University of Toronto, Toronto, ON, Canada

    Taufik Valiante, William D. Hutchison & Suneil K. Kalia

  9. Division of Neurology, Department of Medicine, University of Toronto, Toronto, ON, Canada

    Lorraine V. Kalia

  10. Tanz Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, ON, Canada

    Lorraine V. Kalia

Authors
  1. Laura Kondrataviciute
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  2. Minesh Kapadia
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  3. Ivan Skelin
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  13. Clement Hamani
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  16. Luka Milosevic
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  17. Lorraine V. Kalia
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  18. Suneil K. Kalia
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Contributions

Conceptualization: L.K., M.K., L.V. K., S.K.K.; Methodology: L.K., M.K., W.D.H.; Formal analysis: L.K., M.K., I.S., W.D.H., S.S., L.Z.; Investigation: L.K.; Resources: S.K.K., L.V.K., L.M., T.V., C.H., X.L.; Data curation: L.K., C.T., S.J., H.C., Y.H., S.B.; Writing–original draft: L.K.; Writing–review & editing: L.K., M.K., S.K.K., L.V.K., W.D.H.; Visualization: L.K.; Supervision: S.K.K., L.V.K., T.V., L.M; Project administration: S.K.K., L.V.K.; Funding acquisition: S.K.K., L.V.K., T.V., L.M. All authors reviewed the manuscript.

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Correspondence to Luka Milosevic, Lorraine V. Kalia or Suneil K. Kalia.

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Kondrataviciute, L., Kapadia, M., Skelin, I. et al. Cortical and basal ganglia beta oscillations and frequency-dependent DBS effects in the A53T Parkinson’s disease rat model. npj Parkinsons Dis. (2026). https://doi.org/10.1038/s41531-026-01304-z

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  • Received: 28 July 2025

  • Accepted: 18 February 2026

  • Published: 19 March 2026

  • DOI: https://doi.org/10.1038/s41531-026-01304-z

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