Several studies implicate A1-like and AD astrocytes in synaptic loss through the upregulation of complement component (C3 and C1q), synapse elimination through phagocytosis and synaptotoxicity due to impaired glutamate transport and signaling in neurodegenerative diseases including Alzheimer’s disease, amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS) (Wu et al., 2019; Dalakas et al., 2020; Hulshof et al., 2022). The gene discussed is C3; the disease is Alzheimer disease.