Fig. 2.
TYROBP influences AD pathology in standard AD-related mouse models of cerebral amyloidosis or tauopathy. In APP/PSEN1 mice, absence of TYROBP decreased microglial recruitment around Aβ deposits. APP/PSEN1 mice overexpressing TYROBP showed decreased Aβ load. In MAPTP301S (PS19) mice, both absence and overexpression of TYROBP increased the stoichiometry of phosphorylation of TAU. While observations of these TAU phenotypic effects are usually associated with worsening clinical phenotype, absence of Tyrobp decreased the expression of C1q, the initiating protein in the classical complement cascade, and improved learning behavior and synaptic function in both amyloidosis and tauopathy mouse models. Abbreviations: TYROBP, tyrosine kinase binding protein; C1q, Complement component 1q; WT, Wildtype; KO, Knockout; DHPG, Dihydroxyphenylglycine