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Parkinson's disease (PD) is a neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons in the substantia nigra, leading to motor and cognitive impairments. Recent research has highlighted the significant role of aging-related inflammation and stem cell exhaustion in the pathogenesis of PD.
Aging is associated with a chronic, low-grade inflammatory state known as inflammaging, which is characterized by increased levels of pro-inflammatory cytokines and immune cell activation. In PD, this inflammation is primarily mediated by microglia, the resident immune cells of the central nervous system. Activated microglia release pro-inflammatory cytokines such as TNF-α and IL-1β, which can exacerbate neuronal damage and contribute to the neurodegenerative process
Stem cell exhaustion refers to the decline in the regenerative capacity of stem cells with age, which can impair tissue repair and maintenance. In the context of PD, the depletion of neural stem cells in the brain can hinder the replacement of lost dopaminergic neurons. This exhaustion is exacerbated by the inflammatory environment, which can further impair stem cell function and promote neurodegeneration .
The interplay between inflammation and stem cell exhaustion creates a vicious cycle that accelerates neurodegeneration in PD. Inflammatory cytokines can inhibit the proliferation and differentiation of neural stem cells, while the loss of these cells reduces the brain's ability to repair itself, leading to further neuronal loss and increased inflammation .
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