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Impact of sub-chronic aluminium-maltolate exposure on catabolism of amyloid precursor protein in rats

Rui Feng Liang1, Wei Qing Li, Hong Wang

  • 1Department of Occupational Health, School of Public Health, Shanxi Medical University, Taiyuan 030001, Shanxi, China.

Biomedical and Environmental Sciences : BES
|July 3, 2013
PubMed
Abstract

Insights

Sub-chronic exposure to Aluminium-maltolate (Al(mal)3) in rats increased amyloid precursor protein (APP) and secretase expressions. This suggests Al(mal)3 may elevate amyloid-beta 1-42 generation, contributing to neurotoxicity.

Area of Science:

  • Neuroscience
  • Toxicology
  • Biochemistry

Background:

  • Amyloid precursor protein (APP) catabolism is crucial in neurodegenerative diseases.
  • Aluminium-maltolate (Al(mal)3) is a compound with potential neurotoxic effects.
  • Understanding Al(mal)3's impact on APP processing is vital for neuroprotection strategies.

Purpose of the Study:

  • To investigate the effect of sub-chronic Aluminium-maltolate (Al(mal)3) exposure on amyloid precursor protein (APP) catabolism in rats.
  • To determine the dose-dependent relationship between Al(mal)3 exposure and changes in APP processing pathways.
  • To explore potential mechanisms of Al(mal)3-induced neurotoxicity related to amyloid-beta (Aβ) generation.

Main Methods:

  • Forty Sprague-Dawley rats were divided into control and Al(mal)3-treated groups (0.27, 0.54, 1.08 mg/kg BW) for two months.
  • Intraperitoneal injections of saline, maltolate, or Al(mal)3 were administered daily.
  • Neural behavior was assessed via open field tests (OFT); APP, BACE1, PS1 expressions, and Aβ levels were quantified using ELISA and RT-PCR.

Main Results:

  • Al(mal)3 exposure dose-dependently increased the expression of APP, BACE1, and PS1 proteins and their mRNAs.
  • BACE1 enzyme activity was significantly elevated in rats exposed to higher Al(mal)3 doses.
  • Aβ1-40 levels decreased, while Aβ1-42 levels increased with escalating Al(mal)3 doses.

Conclusions:

  • Al(mal)3 exposure appears to promote the generation of amyloid-beta 1-42.
  • This is likely mediated by enhanced expression of APP and its secretases (β- and γ-secretase).
  • These findings suggest a potential mechanism for Al(mal)3-induced neurotoxicity.
Keywords:
Aluminium-maltolateAmyloid precursor proteinRatβ-amyloid protein

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