Research points to a new early target for Parkinson’s treatment

Inflammatory cells in the brain may offer a new early target for the treatment of early Parkinson’s disease, say researchers from Neuroscience Research Australia.

In a review published in the journal Movement Disorders, Professor Glenda Halliday and PhD student Claire Stevens propose that glial cells, which produce inflammation in the brain, play a much more important role in the initiation of Parkinson’s disease than previous thought.

“If we can stop some of this inflammation early on, before symptoms appear, we may actually be able to reduce the risk of the disease progressing at all,” says Ms Stevens.

Glial cells support and protect neurons by supplying nutrients and producing inflammatory factors to protect the brain from harm.

It is already known that glial cells drive the progression of Parkinson’s by releasing an excess of toxic inflammatory factors, which causes the destruction of brain cells.

What the NeuRA team found was evidence that glial cells also have a role in the very earliest stages of the disease, before neurons begin to die and clinical symptoms become apparent.

In particular, a type of glial cell called microglia tries to clear an abnormal accumulation of a protein in the brain called alpha-synuclein. The accumulation of this protein is typical in Parkinson’s disease.

“The microglia can actually consume the debris to get rid of it, but we think that’s where the problem starts,” says Ms Stevens. “Eventually, the volume of protein becomes too much for them and they become dysfunctional, increasing in number and releasing toxic inflammatory factors uncontrollably. They lose the ability to regulate their inflammatory response, which is what we think causes the ongoing neuronal death in Parkinson’s disease.”

The significance of this review, says Ms Stevens, is that it reveals the greater role of glial cells in Parkinson’s disease, and the need to investigate this role further, particularly in the earliest disease stages.

“If we don’t address these early glial changes, we’re not really going to have any success in stopping neuronal death,” says Ms Stevens.

This research also supports the suggestions that anti-inflammatory drugs – possibly targeting glial cells – may make an effective treatment for the disease.