Evidence of TAU pathology in kaolin-induced hydrocephalus model of the aged rat

Background Accumulation of A-beta peptides and hyperphosphorylated Tau (hpTAU) has been observed in immunohistochemical (IHC) studies of kaolin-induced hydrocephalus in the aged rat. Defective clearance via CSF and altered transport via blood brain barrier receptor expressions was suggested to be causal [1]. The present study reports further evidence to the significance of A-beta and TAU pathology as disease mechanisms in hydrocephalus using quantitative A-beta and hpTAU ELISA in addition to IHC studies of the lipid oxygenase 12/15 enzyme (LOX12/15), a marker of the cytokine-induced inflammation in Alzheimer disease (AD).