Extracellular potassium (K⁺) dysregulation distinguishes healthy aging from neurodegeneration. This study used K⁺-sensitive microelectrodes to measure cortical K⁺ levels in awake wild-type mice and neurodegenerative disease models. Aged wild-type mice had lower cortical K⁺ levels than young mice, while Alzheimer's, ALS, and Huntington's disease models showed elevated K⁺ levels. Cortical resting K⁺ correlated inversely with neuronal density and K⁺ buffering rate but positively with neuronal firing rate. Astrocytic potassium channel genes were downregulated in disease models but not in normal aging. Kcnj10 was downregulated in ALS and HD, while Fxyd1 and Slc1a3 were upregulated in Alzheimer's and ALS. Chronic K⁺ elevation and hyperexcitability may drive neuronal loss in neurodegenerative diseases. These findings suggest that dysregulated extracellular K⁺ homeostasis in neurodegenerative diseases is due to aberrant astrocytic K⁺ buffering, highlighting glial dysfunction in neurodegeneration. Normal aging is associated with reduced cortical K⁺ and stable neuronal density, while neurodegenerative diseases show increased K⁺ and neuronal loss. Astrocytic regulators of potassium buffering were misexpressed in disease models, contributing to elevated extracellular K⁺. These results indicate that extracellular K⁺ dysregulation is a key factor in neurodegenerative disease pathology.Extracellular potassium (K⁺) dysregulation distinguishes healthy aging from neurodegeneration. This study used K⁺-sensitive microelectrodes to measure cortical K⁺ levels in awake wild-type mice and neurodegenerative disease models. Aged wild-type mice had lower cortical K⁺ levels than young mice, while Alzheimer's, ALS, and Huntington's disease models showed elevated K⁺ levels. Cortical resting K⁺ correlated inversely with neuronal density and K⁺ buffering rate but positively with neuronal firing rate. Astrocytic potassium channel genes were downregulated in disease models but not in normal aging. Kcnj10 was downregulated in ALS and HD, while Fxyd1 and Slc1a3 were upregulated in Alzheimer's and ALS. Chronic K⁺ elevation and hyperexcitability may drive neuronal loss in neurodegenerative diseases. These findings suggest that dysregulated extracellular K⁺ homeostasis in neurodegenerative diseases is due to aberrant astrocytic K⁺ buffering, highlighting glial dysfunction in neurodegeneration. Normal aging is associated with reduced cortical K⁺ and stable neuronal density, while neurodegenerative diseases show increased K⁺ and neuronal loss. Astrocytic regulators of potassium buffering were misexpressed in disease models, contributing to elevated extracellular K⁺. These results indicate that extracellular K⁺ dysregulation is a key factor in neurodegenerative disease pathology.