Convergence of Neuroinflammation, Microbiota, and Parkinson's Disease: Therapeutic Insights and Prospects

Abstract

Parkinson's disease (PD) is a complex neurodegenerative disorder. Recent evidence reveals connections between neuroinflammatory processes and intestinal microbiota alterations in the progression of this pathology. This comprehensive review explores the intricate relationships between them, highlighting their combined impact on PD. Neuroinflammation, characterized by immune activation in the central nervous system, is increasingly acknowledged as a critical factor in the development of PD. Concurrently, alterations in the gut microbiota composition have been linked to PD, suggesting a potential modulatory role in disease progression. Thus, bidirectional communication along the gut-brain axis has become pivotal in comprehending the pathogenesis of PD. Furthermore, we explore emerging therapeutic strategies that target these interconnected pathways, providing insights into potential avenues for PD treatment. The elucidation of these intricate relationships establishes a promising foundation for innovative therapeutic strategies aimed at altering disease progression and improving the quality of life for individuals affected by PD.

Keywords: Parkinson’s disease; microbiota; neuroinflammation; therapeutic interventions.

Figure 1

Comparison of pathophysiological features between Parkinson’s disease (PD) murine models and the different interventions studied. TNF-α: Tumor Necrosis Factor α; IL-1β: Interleukin-1β; IL-6: Interleukin-6; IL-8: Interleukin-8; Iba-1: Ionized Calcium-binding Adaptor Molecule 1; GFAP: Glial Fibrillary Acidic Protein; α-syn: α-Synuclein; TH: Tyrosine Hydroxylase; DAT: Dopamine Transporter.

Figure 2

Comparison of the microbiota and short-chain fatty acids (SCFAs) between Parkinson’s disease (PD) murine models and the different interventions studied.