Microglia are an important population of helper cells whose primary function is to act as resident immune cells within the brain. They function like a 'special force', linked to the body's immune system. They deal with injury/infection in the brain and communicate with the immune system about how best to deal with an emerging condition. When microglia sense trouble in the brain, they will start to evaluate whether the affected cells need to be killed off or nurtured back to health.

Researchers at the Van Andel Institute in Grand Rapids (Michigan, USA) recently published a report demonstrating that microglia are critically involved in the cell-to-cell transfer of the protein alpha-synuclein. This Parkinson's-associated protein is believed to pass from one cell to another, and during this passage the alpha-synuclein begin to clump or aggregate within the cells. This process is how researchers believe the progressive nature of Parkinson's is manifesting itself within the brain.

The Van Andel Institute researchers reported that the removal of microglia from the brain resulted in greater aggregation of alpha-synuclein, as did the hyperactivation of the microglia when a chemical used to induce inflammation was introduced. Their results suggest that under normal resting or 'non-inflammatory' conditions, microglia play an important role in modulating the transfer of alpha-synuclein in models of Parkinson's.

The researchers concluded that drugs regulating microglia and neuroinflammation could represent a future avenue for limiting the progression of Parkinson's - by reducing the spread of alpha-synuclein in the brain. Neuroinflammation is an important target for our international Linked Clinical Trials (LCT) programme because we have several LCT studies designed to specifically test the effect of inflammation in Parkinson's, which are hopefully starting very soon.

Read the full paper which is open access -

Microglia affect α-synuclein cell-to-cell transfer in a mouse model of Parkinson’s disease - Brundin et al. Molecular Neurodegeneration volume 14, Article number: 34 (2019)