ROLE OF NEURO-INFLAMMATION IN PARKINSON'S DISEASECategory:
UPDATE ON THE ROAD TO THE CURE
A REAL-TIME SCIENCE REPORT
Role of Neuro-inflammation in Parkinson’s disease
Caused by the death of dopaminergic neurons in the Substancia Nigra part of the brain, Parkinson’s disease (PD) is the second most prevalent neurodegenerative disease worldwide that affects approximately 1% of adults above the age of 50. The onset of cellular neuropathology of PD appears decades before the onset of the motor symptoms. Around 30% of the dopaminergic neurons are already lost when the first symptoms of PD occur.
Our brain is made up of two types of cells. These cells are neurons and non-neuron cells called glia. There are many types of glial cells in the brain but the three important glial cell types are oligodendrocytes, microglial, and astrocytes. Oligodendrocytes is a special type of glial cell known as an oligodendrocyte that wraps around the axons of neurons, making up what is known as the myelin sheath. Like insulation around an electrical wire, oligodendrocytes insulate the axon and help neurons pass electrical signals at incredible speed and over long distances. In simple words, oligodendrocytes are the protectors of myelin sheath of axons. The average adult human brain contains approximately 100 billion neurons, and just as many—if not more—glia. Although neurons are the most famous brain cells, both neurons and glial cells are necessary for proper brain function. While neurons are the cells in the brain that send and receive electrical and chemical signals, glia cells support the well-being and well-function of the neurons. It is best to regard glia cells as the security guards for neurons because they mount an attack in the form of an immune response to an insult to the brain which may be in the form of an infection, injury, or protein aggregation. This immune response results in phagocytosis of the invader molecule, resulting in neuro-inflammation. While short-term immune response is neuroprotective, the chronic microglia immune response is implicated in neurodegenerative diseases. That is why, chronic neuro-inflammation is considered as one of the most important processes involved in the pathogenesis of PD and many other diseases of the CNS, including Alzheimer’s, MSA, PSP, ALS, and others.
In vivo evidence of neuro-inflammation comes from the brain of PD animal models. Animals injected with a neurotoxin such as 6-hydroxydopamine (6-OHDA) or 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has an increase in the levels of pro-inflammatory cytokines TNF-α, IF-γ, IL-1β, IL-2, IL-6, and NF-kβ, in parallel with a decrease in the levels of the anti-inflammatory cytokine IL-10 in the striatum of these mice. Importantly, this was reversed when mice were treated with Chrysin, a natural flavonoid known to have neuroprotective effects. Autopsied performed on Parkinson’s patients have likewise shown an increase in the above cytokines.
Thus, there is ample of evidence that chronic brain inflammation could be causative for Parkinson’s disease. Next month, we will tell what La Jolla based ICB International is doing to counteract neuro-inflammation.
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