Abstract
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).
Highlights
Accumulation of A-beta peptides and hyperphosphorylated Tau has been observed in immunohistochemical (IHC) studies of kaolin-induced hydrocephalus in the aged rat
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 hyperphosphorylated Tau (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)
A-beta 42 and 40 ELISA shows a significant increase over the course of hydrocephalus at 6 and 10 weeks postinduction when compared to the controls, e.g., A-beta 40: 9.7 ± 1.3 and 9.5 ± 0.5 (6,10 wk) vs. 3.2 ± 1.2; p < 0.01 (ANOVA)
Summary
Accumulation of A-beta peptides and hyperphosphorylated Tau (hpTAU) has been observed in immunohistochemical (IHC) studies of kaolin-induced hydrocephalus in the aged rat. 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)
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