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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
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Consistent with previously published data, S-glutathionylation decreased the efficiency of actin polymerization and reduced its cooperativity in binding tropomyosin [145]
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