Immune system involved in synaptic degeneration



From Stanford University School of Medicine, a group of researchers led by Beth Stevens and Ben Barres refers, in an article in the latest issue of the journal Cell, that they discovered the immune system actively contributes to the development of the brain through the elimination of excess of synaptic connections that characterizes the early stages of developing brain.

The protein C1q label unwanted synapses, following the process of the complement cascade, candidate elimination, and the researchers also found evidence that this process can be reactivated during the course of neuro-degenerative diseases.

Eg After studying mice suffering from glaucoma, the scientists noticed that the complement cascade comes into play in the synapses of the adult cells of the retina from the early stages of disease, leading to a sharp loss.

The authors explain "Our results suggest that a signal produced by immature astrocytes in the developing brain and the retina acts as a switch that regulates the temporal expression of the complement protein C1q, opening a window to the synapse-dependent.

This suggests strongly that the normal mechanism of elimination of synapses mediated by the complement that we have described is reactivated so aberrant central nervous system after injury or the beginning of a degenerative disease. In this case, drugs that block the normal complement cascade may counteract the loss of synapses, not only in the glaucoma, but also in other neurodegenerative diseases like Alzheimer's or multiple sclerosis. "

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