Neuroinflamación en la enfermedad de Parkinson

Resumen

Parkinson’s disease is the most common neurodegenerative disorder after Alzheimer’s disease. The origin of the disease is unknown, except some hereditary forms in certain family groups linked to specific genes. However, it is known that Parkinson’s patients have aggregates of α-synuclein protein in the dopaminergic neurons of the substantia nigra pars compacta, mitochondrial dysfunction in these neurons and generalised neuroinflammation. This neuroinflammatory process is mediated by microglia, the cells that form the immune system of the central nervous system. It has been observed that in PD patients, the microglia are activated inducing the release of a variety of proinflammatory cytokines which are indispensable for the elimination of abnormal proteins. Several factors lead to an overactivation of microglia, such as secondary inflammatory events, α-synuclein aggregates, mitochondrial dysfunction or loss of blood-brain barrier integrity. This leads to widespread neuroinflammation in the brain and neuronal death. This review summarises the mechanisms involved in neuroinflammation and presents possible therapeutic options for its treatment.