Unbound MEDLINE

APP/PS1 transgenic mice treated with aluminum: an update of Alzheimer's disease model.

Abstract

There is still no animal model available that can mimic all the cognitive, behavioral, biochemical, and histopathological abnormalities observed in patients with Alzheimer's disease (AD). We undertook to consider the interaction between genetic factors, including amyloid precursor protein (APP) and presenilin-1 (PS1), and environmental factors, such as Aluminum (Al) in determining susceptibility outcomes when studying the pathogenesis of AD. In this article, we provide an AD model in APP/PS1 transgenic mice triggered by Al. The animal model was established via intracerebral ventricular microinjection of aluminum chloride once a day for 5 days in APP/PS1 transgenic mice. Twenty wild type (WT) mice and 20 APP/PS1 transgenic (TG) mice were separately divided into 2 groups (control and Al group), and a stainless steel injector with stopper was used for microinjection into the left-lateral cerebral ventricle of each mouse. The Morris water maze task was used to evaluate behavioral function of learning and memory ability on the 20th day after the last injection. This AD model's brain was analyzed by: (1) amyloid beta immunohistochemical staining; (2) Tunnel staining; (3) apoptotic rates; (4) caspase-3 gene expression. Here, decrease of cognitive ability and neural cells loss were shown in APP/PS1 transgenic mice exposed to Al, which were more extensive than those in APP/PS1 TG alone and WT mice exposed to Al alone. These findings indicate that there is a close relationship between over-expression of APP and PS1 genes and Al overload. It is also suggested that APP/PS1 TG mice exposed to Al have potential value for improving AD models.

Links

  • Aggregator Full Text
  • Authors

    Zhang QL, Jia L, Jiao X, Guo WL, Ji JW, Yang HL, Niu Q

    Source

    International journal of immunopathology and pharmacology 25:1 pg 49-58

    MeSH

    Aluminum
    Alzheimer Disease
    Amyloid beta-Protein Precursor
    Animals
    Apoptosis
    Caspase 3
    Disease Models, Animal
    In Situ Nick-End Labeling
    Male
    Mice
    Mice, Inbred C57BL
    Mice, Transgenic
    Necrosis
    Presenilin-1

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    22507317