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Cellular and molecular pathophysiology in the progression of Parkinson’s disease

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Abstract

Parkinson’s disease (PD) is a neurodegenerative disorder etiologically linked to the loss of substantia nigra (SN) dopaminergic neurons in the mid-brain. The etiopathology of sporadic PD is still unclear; however, the interaction of extrinsic and intrinsic factors may play a critical role in the onset and progression of the disease. Studies in animal models and human post-mortem tissue have identified distinct cellular and molecular changes in the diseased brain, suggesting complex interactions between different glial cell types and various molecular pathways. Small changes in the expression of specific genes in a single pathway or cell type possibly influence others at the cellular and system levels. These molecular and cellular signatures like neuroinflammation, oxidative stress, and autophagy have been observed in PD patients’ brain tissue. While the etiopathology of PD is still poorly understood, the interplay between glial cells and molecular events may play a crucial role in disease onset and progression.

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Acknowledgements

This work was supported in part by funding from Veterans Administration (1I01BX002349-01, 2I01 BX001262-05, 1I01 BX004269-01), NIH-NINDS (R01 NS62327 and 1R21NS118393-01), and the South Carolina State Spinal Cord Research Fund (SCIRF-2015P-01, SCIRF-2015P-04, SCIRF-2015-I-01, SCIRF-2016 I-03, and SCIRF #2018 I-01).

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Vandana Zaman conceived, designed, wrote the manuscript, and drew the figures. Donald Shields, Ramsha Shams, Kelsey Drasites, and Denise Matzelle edited the manuscript. Azizul Haque and Naren Banik conceived, designed, and edited the manuscript. All authors reviewed and approved the final version of the manuscript.

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Correspondence to Azizul Haque or Narendra L. Banik.

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Zaman, V., Shields, D.C., Shams, R. et al. Cellular and molecular pathophysiology in the progression of Parkinson’s disease. Metab Brain Dis 36, 815–827 (2021). https://doi.org/10.1007/s11011-021-00689-5

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