Our hypotheses are that (a) astrocytes and oligodendrocytes are principal targets and dysfunctional players in the pathogenesis of GGT; (b) GGT, like other neurodegenerative diseases with hyper-phosphorylated tau deposition, is a more generalized disease with hyper-phosphorylation of a large number of proteins in addition to tau; and (c) inoculation in wild-type (WT) mice of abnormal mutant tau from human GGT brain homogenates has the capacity to recruit murine tau to generate seeding and spreading largely dependent on the characteristics of host tau. The gene discussed is GGT1; the disease is neurodegenerative disease.