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N-Acetyl Cysteine Supplement Minimize Tau Expression and Neuronal Loss in Animal Model of Alzheimer’s Disease

1
Department of Anatomy, Kasturba Medical College, Mangalore 576104, India
2
Manipal Academy of Higher Education, Mangalore 576104, India
3
Department of Anatomy, Faculty of Medicine, Kuwait University, Kuwait City 13110, Kuwait
*
Author to whom correspondence should be addressed.
Brain Sci. 2018, 8(10), 185; https://doi.org/10.3390/brainsci8100185
Received: 9 September 2018 / Revised: 1 October 2018 / Accepted: 6 October 2018 / Published: 11 October 2018
(This article belongs to the Special Issue Dementia and Cognitive Ageing)
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Abstract

Alzheimer’s disease (AD) is characterized by the accumulation of neurofibrillary tangles (NFT), deposition of beta amyloid plaques, and consequent neuronal loss in the brain tissue. Oxidative stress to the neurons is often attributed to AD, but its link to NFT and β-amyloid protein (BAP) still remains unclear. In an animal model of AD, we boosted the oxidative defense by N-Acetyl cysteine (NAC), a precursor of glutathione, a powerful antioxidant and free radical scavenger, to understand the link between oxidative stress and NFT. In mimicking AD, intracerebroventricular (ICV) colchicine, a microtubule disrupting agent also known to cause oxidative stress was administered to the rats. The animal groups consisted of an age-matched control, sham operated, AD, and NAC treated in AD models of rats. Cognitive function was evaluated in a passive avoidance test; neuronal degeneration was quantified using Nissl staining. NFT in the form of abnormal tau expression in different regions of the brain were evaluated through immunohistochemistry using rabbit anti-tau antibody. ICV has resulted in significant cognitive and neuronal loss in medial prefrontal cortex (MFC) and all the regions of the hippocampus. It has also resulted in increased accumulation of intraneuronal tau in the hippocampus and MFC. NAC treatment in AD model rats has reversed the cognitive loss and neuronal degeneration. The intraneuronal tau expression also minimized with NAC treatment in AD model rats. Thus, our findings suggest that an antioxidant supplement during the progression of AD is likely to prevent neuronal degeneration by minimizing the neurofibrillary degeneration in the form of tau accumulation. View Full-Text
Keywords: hippocampus; medial prefrontal cortex; N-Acetyl cysteine; neurofibrillary tangles; oxidative stress; tau protein hippocampus; medial prefrontal cortex; N-Acetyl cysteine; neurofibrillary tangles; oxidative stress; tau protein
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
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Joy, T.; Rao, M.S.; Madhyastha, S. N-Acetyl Cysteine Supplement Minimize Tau Expression and Neuronal Loss in Animal Model of Alzheimer’s Disease. Brain Sci. 2018, 8, 185.

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