In Alzheimer’s disease (AD), astrocytic pathology is characterized by dysregulated calcium signaling, impaired glutamate clearance due to downregulation and dysfunction of excitatory amino acid transporter 2 (EAAT2/GLT-1), and mislocalization of aquaporin-4 (AQP4) channels in perivascular endfeet, leading to glymphatic system impairment and neurovascular uncoupling [40,41,42]. Here, SLC1A2 is linked to early-onset autosomal dominant Alzheimer disease.