Filamentous inclusions of tau protein are hallmarks of tauopathies including Alzheimer’s disease. Here a rat model for tauopathies was developed using pore-forming halitoxin Poly-APS. Tau protein was delivered through the membrane into the neurons where it is metabolized. Rats were injected with recombinant human Tau441 only (controls), Tau+Poly-APS (double) and Tau+PolyAPS+Okadaic Acid (triple). Cognitive and neurodegenerative changes were examined with Morrris water maze behavioral test and immunohistochemistry, respectively. Acquisition of the spatial reference memory was unaffected by administration of Tau or Tau+Poly-APS. However, enhanced phosphorylation of exogenously delivered tau with the triple infusion impaired learning. Hippocampal tau was visualized using antibodies against Tau441 and phosphorylated Tau-S404. The higher intensity of Tau441 immunostaining in double and triple groups suggests that exogenous tau is sequestered from the infusion solution into the cells. With respect to phospho-tau izoform we observed different cellular compartmentalization of P-Tau-S404 in double and triple treated rats. In double treated rats P-TauS401 was distributed both in the cell bodies and neuronal fi bers, while in triple group presence of OA caused redistribution of phospho-tau staining from neuronal processes to the perikaryon. This is similar to age-dependent tau redistribution between cellular compartments and could be a result of hyperphosphorylation.
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