GFAP and multiple sclerosis: This hyperbranched phenotype reflects the transition from physiological astrocyte activation to pathological gliosis, as observed in neuroinflammatory conditions such as multiple sclerosis and traumatic brain injury.[59] Finally, at supraphysiological concentrations (100 ng mL−1), PHAs adopted a profoundly reactive phenotype, with GFAP+ networks spanning longer distances (∗∗∗∗p < 0.0001 vs control; Figure 8B) and dense branch counts (∗∗p < 0.01 vs control; Figure 8B).