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      EGCG Nanoparticles Attenuate Aluminum Chloride Induced Neurobehavioral Deficits, Beta Amyloid and Tau Pathology in a Rat Model of Alzheimer’s Disease

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          Abstract

          Rational: Alzheimer’s disease (AD) is a neurodegenerative pathology characterized by the presence of neuritic plaques and neurofibrillary tangles. Aluminum has been reported to play an important role in the etiology and pathogenesis of this disease. Hence, the present study aimed to evaluate the neuroprotective role of epigallocatechin-gallate (EGCG) loaded nanoparticles (nanoEGCG) against aluminum chloride (AlCl 3) induced neurobehavioral and pathological changes in AD induced rats.

          Method: 100 mg/kg body weight AlCl 3 was administered orally for 60 days, which was followed by 10 mg/kg body weight free EGCG and nanoEGCG treatment for 30 days. Morris water maze, open field and novel object recognition tests were employed for neurobehavioral assessment of the rats. This was followed by histopathological assessment of the cortex and the hippocampus in the rat brain. For further validation biochemical, immunohistochemistry and western blot assays were carried out.

          Result: Aluminum exposure reduced the exploratory and locomotor activities in open field and significantly reduced the memory and learning curve of rats in Morris water maze and novel object recognition tests. These neurobehavioral impairments were significantly attenuated in nanoEGCG treated rats. Histopathological assessment of the cortex and hippocampus of AlCl 3 induced rat brains showed the presence of both neuritic plaques and neurofibrillary tangles. In nanoEGCG treated rats this pathology was absent. Significant increase in biochemical, immunohistochemical and protein levels was noted in AlCl 3 induced rats. While these levels were greatly reduced in nanoEGCG treated rats.

          Conclusion: In conclusion, this study strengthens the hypothesis that EGCG nanoparticles can reverse memory loss, neuritic plaque and neurofibrillary tangles formation.

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          Most cited references45

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          Analysis of nitrate, nitrite, and [15N]nitrate in biological fluids.

          L Green, D A Wagner, J. Glogowski … (1982)
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            EGCG redirects amyloidogenic polypeptides into unstructured, off-pathway oligomers.

            Dagmar E. Ehrnhoefer, Jan Bieschke, Annett Boeddrich … (2008)
            The accumulation of beta-sheet-rich amyloid fibrils or aggregates is a complex, multistep process that is associated with cellular toxicity in a number of human protein misfolding disorders, including Parkinson's and Alzheimer's diseases. It involves the formation of various transient and intransient, on- and off-pathway aggregate species, whose structure, size and cellular toxicity are largely unclear. Here we demonstrate redirection of amyloid fibril formation through the action of a small molecule, resulting in off-pathway, highly stable oligomers. The polyphenol (-)-epigallocatechin gallate efficiently inhibits the fibrillogenesis of both alpha-synuclein and amyloid-beta by directly binding to the natively unfolded polypeptides and preventing their conversion into toxic, on-pathway aggregation intermediates. Instead of beta-sheet-rich amyloid, the formation of unstructured, nontoxic alpha-synuclein and amyloid-beta oligomers of a new type is promoted, suggesting a generic effect on aggregation pathways in neurodegenerative diseases.
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              Aluminium as a risk factor in Alzheimer's disease, with emphasis on drinking water.

              Trond Flaten (2001)
              Aluminium (Al) is clearly a powerful neurotoxicant. Considerable evidence exists that Al may play a role in the aetiology or pathogenesis of Alzheimer's disease (AD), but whether the link is causal is still open to debate. This paper reviews the epidemiological evidence linking Al and AD. Nine out of 13 published epidemiological studies of Al in drinking water and AD have shown statistically significant positive relations. Given the difficulty in producing high-quality data for the occurrence of AD and also for Al exposure, with the resulting unavoidable misclassification errors biasing any true association towards the null value, these studies are remarkably consistent. A major problem in their interpretation is that drinking water, even at high Al concentrations, only contributes a fraction of the total dietary intake of Al. In particular, regular consumers of antacids ingest gram amounts of Al daily, thousands of times the amounts taken in through drinking water, and epidemiological studies of antacid exposure and AD have been largely negative. However, Al is very poorly absorbed in the gastrointestinal tract, and the possibility that some Al fractions present in drinking water may be particularly bioavailable cannot be dismissed at present. The combined evidence linking Al and AD warrants substantial research efforts. Such efforts should focus on clarification of the cellular and molecular mechanisms in Al toxicity and of the basic metabolism and kinetics of Al in the human body, and on further epidemiological studies including diverse routes of Al exposure and also variables that are known or suspected to influence the individuals' susceptibility to AD, such as apolipoprotein E allele status and family history of AD.
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                Author and article information

                Contributors
                Journal
                Journal ID (nlm-ta): Front Aging Neurosci
                Journal ID (iso-abbrev): Front Aging Neurosci
                Journal ID (publisher-id): Front. Aging Neurosci.
                Title: Frontiers in Aging Neuroscience
                Publisher: Frontiers Media S.A.
                ISSN (Electronic): 1663-4365
                Publication date (Electronic): 13 August 2018
                Publication date Collection: 2018
                Volume: 10
                Electronic Location Identifier: 244
                Affiliations
                [1] 1Department of Integrative Biology, School of Biosciences and Technology, Vellore Institute of Technology , Vellore, India
                [2] 2Department of Biotechnology, School of Biosciences and Technology, Vellore Institute of Technology , Vellore, India
                [3] 3University Institute of Biotechnology, Chandigarh University , Mohali, India
                Author notes

                Edited by: Antonio Camins, University of Barcelona, Spain

                Reviewed by: Miren Ettcheto, Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Spain; Elena Sanchez López, University of Barcelona, Spain

                *Correspondence: Zaved Ahmed Khan khan.zaved@ 123456gmail.com
                Article
                DOI: 10.3389/fnagi.2018.00244
                PMC ID: 6099078
                PubMed ID: 30150930
                SO-VID: 319604aa-a8f9-4e53-9d0c-b53ee554afcf
                Copyright © Copyright © 2018 Singh, Bhardwaj, Ravi, Ramesh, Mandal and Khan.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                Date received : 14 March 2018
                Date accepted : 24 July 2018
                Page count
                Figures: 8, Tables: 3, Equations: 0, References: 58, Pages: 13, Words: 8942
                Categories
                Subject: Neuroscience
                Subject: Original Research

                ScienceOpen disciplines: Neurosciences
                Keywords: alzheimer disease,aluminum chloride,egcg,nanoparticles,neurobehavioral impairments,neuritic plaques,neurofibrillary tangles
                Data availability:
                ScienceOpen disciplines: Neurosciences
                Keywords: alzheimer disease, aluminum chloride, egcg, nanoparticles, neurobehavioral impairments, neuritic plaques, neurofibrillary tangles

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