Fig. 4

Key features, pathological processes and some candidates for therapeutic intervention in GRN-FTLD, Alzheimer disease and astrocytoma. Illustration presents some molecules expressed by microglia or astrocytes that modulate abnormal pathways activated in AD, GRN-FTLD and astrocytoma and therefore show some promise in treatment strategies. Among them are molecules that target metabolic malfunctions like lipid metabolism and energetic imbalance but also inflammatory factors contributing to neurodegeneration and factors involved in hypoxia, cell cycle, and lifelong immune regulation in cancer. APOE apolipoprotein E, CLU clusterin, ABCA7 ATP-binding cassette subfamily A member 7, LXRa Liver X receptor alpha, TREM2 triggering receptor expressed on myeloid cells 2, TGFβ1 transforming growth factor beta 1, A2AR adenosine A2A receptor, GRN granulin, LRRK2 leucine-rich repeat kinase 2, TBKBP1 TBK1 binding protein 1, SLPI secretory leukocyte protease inhibitor, SORT1 sortilin, RIPK1 receptor-interacting serine/threonine-protein kinase 1, PSAP prosaposin, Sall1 spalt like transcription factor 1, Wnt wingless-type MMTV integration site family, STAT3 signal transducer and activator of transcription 3, HIF-1a hypoxia-inducible factor 1-alpha