Parkinson disease (PD) is a progressive neurodegenerative disorder traditionally defined by degeneration of dopaminergic neurons in the substantia nigra pars compacta and accumulation of misfolded alpha-synuclein. Increasing evidence indicates that inflammation is not merely a secondary response to neuronal death but an active component of PD pathophysiology. Misfolded alpha-synuclein, mitochondrial injury, impaired autophagy, oxidative stress, and cell-derived danger signals can activate microglia and astrocytes. These responses involve pattern-recognition receptors, nuclear factor kappa B, complement, and inflammasomes such as NLRP3, producing cytokines, reactive oxygen species, and other mediators capable of injuring vulnerable neurons. Peripheral immunity also contributes through altered monocytes, T cells, cytokines, intestinal inflammation, and disruption of blood-brain and gut barriers.
The intensity and consequences of inflammation vary with age, genetic susceptibility, biological sex, metabolic health, infections, pesticide and air-pollution exposure, intestinal dysbiosis, sleep, diet, adiposity, and physical activity. However, these factors are not equally established, and association does not necessarily demonstrate causation. Inflammatory biomarkers are elevated on average in blood and cerebrospinal fluid, but substantial overlap between patients and controls currently limits their diagnostic usefulness. Anti-inflammatory strategies have produced compelling preclinical findings, yet clinical evidence remains inconclusive. Effective treatment may therefore require early intervention, biomarker-guided patient selection, and precise modulation rather than broad suppression of immunity. This paper critically examines the mechanisms connecting inflammation to PD, the factors that modify inflammatory activity, the evidence for biomarkers and interventions, and the principal gaps that must be resolved before immunomodulation can become disease-modifying therapy.
- Arbeit zitieren
- Kunal Kunal (Autor:in), 2026, Neuroinflammation in Parkinson Disease. Mechanisms, Modifying Factors, Biomarkers, and Therapeutic Implications, München, GRIN Verlag, https://www.hausarbeiten.de/document/1774831
