Parkinson's disease: genetics and neuroinflammatory insights

Parkinson's disease is a fast-growing neurodegenerative disorder that causes dopaminergic neuron loss and build-up of alpha-synuclein. In terms of number of people affected, it has a large effect on society with an approximately 6.1 million people diagnosed till 2023. Two important factors in PD are neuroinflammation and genetic mutations. The build-up of alpha-synuclein activates neuroimmune cells which leads to the release of inflammatory mediators. Problems with immune system can worsen this inflammation, creating a cycle of ongoing nerve damage. This review discusses the complex interlink between neuroinflammation and genetic mutations in PD. The relationship between neuroinflammation and genetic mutation is bidirectional, neuroinflammation can affect gene expression and genomic stability, while mutation in genes can further exacerbate inflammation and neuronal injury. Current therapies primarily focus on relief from symptoms and increasingly target neuroinflammatory pathways. Approaches, such as cytokine inhibitors, Toll-like receptor antagonists, and inflammasome inhibitors, show promise in mitigating neuroinflammation by potentially altering the disease advancement. Exploring the interplay between neuroinflammation, genetic factors and therapeutic interventions is important for the advancement of effective treatments for PD.