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Review
. 2022 Nov 30;23(23):14997.
doi: 10.3390/ijms232314997.

Neuroinflammation and Autophagy in Parkinson's Disease-Novel Perspectives

Danail Minchev  1   2 , Maria Kazakova  1   2 , Victoria Sarafian  1   2
Affiliations
Review

Neuroinflammation and Autophagy in Parkinson's Disease-Novel Perspectives

Danail Minchev et al. Int J Mol Sci. .

Abstract

Parkinson's disease (PD) is the second most prevalent neurodegenerative disorder. It is characterized by the accumulation of α-Synuclein aggregates and the degeneration of dopaminergic neurons in substantia nigra in the midbrain. Although the exact mechanisms of neuronal degeneration in PD remain largely elusive, various pathogenic factors, such as α-Synuclein cytotoxicity, mitochondrial dysfunction, oxidative stress, and pro-inflammatory factors, may significantly impair normal neuronal function and promote apoptosis. In this context, neuroinflammation and autophagy have emerged as crucial processes in PD that contribute to neuronal loss and disease development. They are regulated in a complex interconnected manner involving most of the known PD-associated genes. This review summarizes evidence of the implication of neuroinflammation and autophagy in PD and delineates the role of inflammatory factors and autophagy-related proteins in this complex condition. It also illustrates the particular significance of plasma and serum immune markers in PD and their potential to provide a personalized approach to diagnosis and treatment.

Keywords: Parkinson’s disease (PD); autophagy; neurodegeneration; neuroinflammation.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The complex interplay between cellular and molecular factors in PD-related neuroinflammation.
See this image and copyright information in PMC

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