Neuroinflammation
Neuroinflammation is a bit different than “inflammation”, primarily as a result of the involvement of the immune system cells called the “microglia”. Neuroinflammation is a condition of the central nervous system and takes place beyond the obscuring wall of the blood brain barrier. There is communication across that barrier, however, which results in the triggering of neuroinflammation by ordinary, or peripheral, inflammation.
In both immune responses, the net result is the release of cytokines, a family of communication molecules that allows for the control of that response. Some increase inflammation and some repress it.
One aspect of cytokines that is often overlooked is that they are neuroactive and give the immune system the ability to take control. This is called “sickness behavior” and is most evident when a cold or the flu sends us to our bed.
Neuroinflammation’s severity is determined by individual sensitivity and by the nature of the challenge. Individual sensitivity is determined by a number of factors, such as genetics, epigenetics, prenatal exposure to bacterial toxins, adult infection, etc.
Cytokine induced inflammation does not act alone. The endocrine system has a similar structure as the immune and produces hormones which fill the same roles of communication and coordination.
The single most important thing to realize is that both the immune and endocrine systems respond to stress and stress acts as a sort of Rosetta Stone allowing the two systems to interact with one another. This interaction ultimately triggers the synergistic actions o a feedback loop. The immune component destroys the substantia nigra with its high density of microglia. The endocrine component succumbs to the stress response and accounts for most of the non-motor symptoms.
This view of Parkinson’s Disease as a complex interaction between the endocrine and immune systems damaging the CNS is, while fragmented, supported by the existing literature.
Parkinson's Disease: A Matter of Balance 