The upregulation of mGluR1 induces FMRP dephosphorylation and facilitates the local translation of synaptic complement component 1q (C1q) mRNA, the initiator of the classical complement activation pathway promoting microglia-operated synaptic pruning [220,221], consequently increasing the phagocytosis of hippocampal glutamatergic synapses and contributing to cognitive dysfunction in AD rodent models [222]. Here, FMR1 is linked to Alzheimer disease.