Role of immune system in synapse loss in Alzheimer’s

Complement protein C1q deposition in Alzheimer’s disease and its contribution to synaptic loss is well documented although the mechanism is not well studied. 

The researchers in this study demonstrate that neuronal hyperactivity triggers C1q protein deposition at synaptic targeting sites accompanied by accumulation of B cells, resulting in the loss of synaptic components.

The authors show that dampening neuronal hyperactivity in AD models lowered C1q deposition and partially restored loss of synaptic components.

They also show that B cell–derived immunoglobulin M also played a role in activity-dependent synapse loss. 

https://www.science.org/doi/10.1126/science.adv1219

https://www.cell.com/trends/pharmacological-sciences/fulltext/S0165-6147(26)00233-6

https://sciencemission.com/B-cells-enter-the-synaptic-conversation