Aluminum chloride does not facilitate deposition of human synthetic amyloid β1-42 peptide in the rat ventricular system of a short-term infusion model

Yasushi Nakagawa, Toshiro Kawashima, Tomomi Yamada, Mutsuo Harano, Akira Monji, Takefumi Yuzuriha, Toru Iwaki

Research output: Contribution to journalArticlepeer-review

2 Citations (Scopus)

Abstract

Recent data have demonstrated that a 39-43 amino acid peptide called β-amyloid peptide (Aβ), which predominantly contains 42 residues (Aβ1-42), has a strong tendency to form insoluble aggregates and that the toxic effects of Aβ are based on its aggregation. In a previous study, we reported that infusion of 100 μg of human synthetic Aβ1-42 (sAβ1-42), which is a main component of diffuse plaques, into the lateral ventricle of the rat brain of a short-term infusion model resulted in almost complete disappearance of sAβ1-42 aggregates from the ventricles by 28 days. In addition, aluminum is considered a potential etiological factor in Alzheimer's disease (AD). Neurotoxicity from excess brain exposure to aluminum has been documented from both clinical observations and animal experiments, although a direct relationship between aluminum and AD has yet to be clearly established. We therefore investigated the effects of sAβ1-42 aggregates with aluminum chloride (AlCl3) in the ventricular system of the rat brain of a short-term infusion model. At either 2 or 7 days following infusion, sAβ1-42 formed aggregates with AlCl3 that spread throughout the entire ventricular system. However, sAβ1-42 aggregates with AlCl 3 had almost disappeared from the ventricles by 28 days, resulting in similarities with respect to the time-course and the neuropathological changes observed in sAβ1-42 aggregation without AlCl3. We herein report for the first time that considerable amounts of sAβ1-42 aggregates with AlCl3 almost disappear from the rat ventricular system by 28 days post-infusion.

Original languageEnglish
Pages (from-to)195-200
Number of pages6
JournalNeuropathology
Volume25
Issue number3
DOIs
Publication statusPublished - Sep 2005

All Science Journal Classification (ASJC) codes

  • Pathology and Forensic Medicine
  • Clinical Neurology

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