Neuropathological findings further support the strong association between plaques and astrogliosis, with reactive astrocytes following the spatial distribution of Aβ plaques.115 Kamphuis et al. 60 in line with previous observations by Xu et al.116 reported that GFAP-null astrocytes, unlike normal astrocytes, exhibited a delayed and reduced capacity to form tight and extensive boundaries around amyloid aggregates. Here, GFAP is linked to amyloidosis.