Our findings suggest potential links of such responses to neurodegenerative conditions such as Alzheimer’s disease, in which astrocyte loss-of-functions and gain-of-functions may contribute to disease progression68 and in which the top 30 most consistently upregulated proteins across multiple studies included at least 11 molecules identified here not only as upregulated by, but also enriched in, wound repair astrocytes: Cd44, S100a6, Padi2, Prdx6, C3, Gpx1, Hsbp1, Gpnmb, Clu, Vim and Gfap69. This evidence concerns the gene GPNMB and early-onset autosomal dominant Alzheimer disease.