ABSTRACT
Parkinson’s disease (PD) is characterized by tremor, rigidity, and slowness of movements and is associated with progressive neuronal loss of the substantia nigra (SN) and other brain structures. Ample evidence of chronic infl ammatory reactions in the brain of PD patients is shown. Neuroinfl ammatory responses in the brain involve diff erent cells of the immune system (e.g., macrophages, mast cells, T and B lymphocytes, dendritic cells), resident cells of the central nervous system (CNS) (e.g., microglia, astrocytes, neurons), many protein components (e.g., complement, adhesion molecules, chemokines, cytokines) and cytotoxic substances (e.g., reactive oxygen and nitrogen species). Soluble molecules or cytokines released by immuno-competent cells may be responsible for the bidirectional communication between cells of the nervous and immune systems. One hypothesis is that infl ammation starts within the CNS, where several infl ammatory products are formed and are quickly removed into the bloodstream. On the other hand, it has also been proposed that infl ammation develops at fi rst in the periphery and then will contribute to brain damage and fi nally neurodegeneration. Elevated levels of pro-infl ammatory cytokines, such as tumour necrosis factor α (TNF-α), interleukin (IL) 1β, IL-6 and the colonystimulating factor, have been demonstrated in the brain and cerebrospinal fl uid (CSF) as well as basal ganglia of PD patients. Peripheral blood mononuclear cells deriving from patients with PD have been reported to have an altered production of TNFα-as well as IL-1α and -1β compared to healthy controls, while IL-2,
IFN-γ, IL-6 and plasma-soluble interleukin-2 receptor (sIL-2R) are no diff erent from healthy controls. Th e identifi cation of biomarkers for neurodegenerative diseases such as PD is required to improve the accuracy of clinical diagnosis and monitor both disease progression and response to treatments.
