Review uncovers critical pro-inflammatory mechanisms driving dopaminergic degeneration in Parkinson's disease, highlighting potential immunomodulatory targets to slow progression.
Parkinson's disease (PD) is a progressively advancing neurodegenerative disorder, the pathogenetic mechanisms of which remain poorly understood. The disease is characterized by the degeneration of dopaminergic neurons in the substantia nigra of the midbrain. Given the improvement in the quality of medical care provided to the population, it is projected that the total number of patients diagnosed with PD worldwide will rise to 8.7 million by 2030. This review addresses the fundamental aspects of neuroinflammation in the context of PD pathogenesis. There is no doubt that pro-inflammatory immunological mechanisms play a critical role in the onset and progression of the disease. Neuronal-derived cells, such as microglia and astrocytes, act as inducers of neuroinflammation, affecting the permeability of the blood-brain barrier to peripheral immune-competent cells. Furthermore, cytokine patterns of the immune response in PD appear to exist. Potential therapeutic approaches for mitigating neuroinflammation in PD, which have been studied in experimental and in vitro models, are also discussed.
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Sayfitdinkhuzhaev et al. (2024) studied this question.
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