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Review Article
128 (
4
); 545-556
doi:
10.25259/IJMR_20081284_545

Molecular toxicity of aluminium in relation to neurodegeneration

Department of Biochemistry & Nutrition, Central Food Technological Research Institute, CSIR, Mysore, India
Molecular Biophysics Unit, Indian Institute of Science, Bangalore, India
Department of Physiology/Neuroscience, Medical University of South Carolina, Charleston, USA

Reprint requests: Dr K.S.J. Rao, Department of Biochemistry and Nutrition, Central Food Technological Research Institute Mysore 570 020, India e-mail: kjr5n@yahoo.co.in

Licence
This open access article is licensed under Creative Commons Attribution 4.0 International (CC BY 4.0). http://creativecommons.org/licenses/by/4.0

Abstract

Exposure to high levels of aluminium (Al) leads to neurofibrillary degeneration and that Al concentration is increased in degenerating neurons in Alzheimer’s disease (AD). Nevertheless, the role of Al in AD remains controversial and there is little proof directly interlinking Al to AD. The major problem in understanding Al toxicity is the complex Al speciation chemistry in biological systems. A new dimension is provided to show that Al-maltolate treated aged rabbits can be used as a suitable animal model for understanding the pathology in AD. The intracisternal injection of Al-maltolate into aged New Zealand white rabbits results in pathology that mimics several of the neuropathological, biochemical and behavioural changes as observed in AD. The neurodegenerative effects include the formation of intraneuronal neurofilamentous aggregates that are tau positive, oxidative stress and apoptosis. The present review discusses the role of Al and use of Al-treated aged rabbit as a suitable animal model to understand AD pathogenesis.

Keywords

Aluminium
animal model
Alzheimer's disease
neuropathology

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