Recent discoveries implicate the classical complement cascade in normal brain development
and in disease. Complement proteins C1q, C3, and C4 participate in synapse elimination, …

… runs was performed at a particularly low cell concentration (15 cells/μl) and thus high
purity, to evaluate whether results were artifacts of cell-cell doublets or single-cell impurity. We …

Schizophrenia is a heritable brain illness with unknown pathogenic mechanisms.
Schizophrenia’s strongest genetic association at a population level involves variation in the major …

Immune molecules, including complement proteins C1q and C3, have emerged as critical
mediators of synaptic refinement and plasticity. Complement localizes to synapses and refines …

Systemic lupus erythematosus (SLE) is an incurable autoimmune disease characterized by
autoantibody deposition in tissues such as kidney, skin and lungs. Notably, up to 75% of …

Mutations in GPR56, a member of the adhesion G protein-coupled receptor family, cause a
human brain malformation called bilateral frontoparietal polymicrogyria (BFPP). Magnetic …

Amyotrophic lateral sclerosis (ALS) is a fatal neuromuscular disease characterized by motor
neuron (MN) death. Lipid dysregulation manifests during disease; however, it is unclear …

Glia cells are uniquely positioned at synapses, contacting pre-and post-synaptic terminals.
At the Drosophila neuromuscular junction, a novel glia-derived TGF-β ligand has been …

Figure 7d and Supplementary Fig. 10 of this Article reported experiments on synaptic refinement
in the mouse lateral geniculate nucleus (LGN). We identified an error in the description …

In follow-up experiments to this Letter, we have been unable to replicate key aspects of the
original results. Most importantly, the findings from behaviour studies and sequencing of …