Parkinson’s disease (PD) is the second most common neurodegenerative disorder
among the elderly population, and it is depicted by the degeneration of dopaminergic neurons
in the midbrain which is progressive. Up to the present time, the precise cause remains illdefined
and the mechanism of neurons death indeterminate. It is typically considered as a
disease of central nervous system (CNS). Nevertheless, numerous evidences have been accumulated
in several past years testifying undoubtedly about the principal role of neuroinflammation
in the progression of PD.
Neuroinflammation is associated with the presence of activated microglia in the brain and
elevated levels of cytokine levels in CNS.
Nevertheless, active participation of immune system as well has been noted, such as elevated
levels of cytokines in peripheral blood, as well as, the presence of autoantibodies. In addition,
the infiltration of T cell in CNS has been reported. Moreover, infiltration and
reactivation of those T cells could exacerbate neuroinflammation to greater neurotoxic levels.
Hence, peripheral inflammation is able to prime microglia into pro-inflammatory phenotype,
which can trigger a stronger response in CNS further perpetuating the on-going neurodegenerative
In the present review, the interplay between neuroinflammation and the peripheral immune
response in the pathobiology of PD will be discussed.
First of all, an overview of the regulation of microglial activation and neuroinflammation is
summarized and discussed. Afterwards, we try to collectively analyze changes that occur in
the peripheral immune system of PD patients and trying to link them to the potential exacerbation
of the neuroinflammation and hence the symptoms of the disease. In the end, we
summarize some of the proposed immunotherapies for the treatment of PD.