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17 .   Neuroprotective effects of chelator agents toward aluminium and Aβ amyloid peptide interactions in hippocampal cells

Authors: Christiane Nday, Benjamin Drever, Αthanasios Salifoglou

Volume 16, Issue 2;
Pages: 77-79;
ISSN:1453-1399, Agroprint;
ISSN (online):2068 9551



Abstract:

Alzheimers disease (AD), as the most common type of dementia, is a neurodegenerative disease characterized by progressive cognitive deterioration, together with declining activities of daily living, neuropsychiatric symptoms or behavioral changes and progressive loss of memory. Aβ is generated from the Amyloid Precursor Protein (APP), a molecule implicated in neurotrophic actions and brain repair from nerve injuries, thus maintaining healthy brain tissues and regulating neural synaptic activity, plasticity and memory. Aluminum, as a metallotoxin, has also been found to play a role in the precipitation and cytotoxicity of APP-originating amyloid Aβ peptide in Alzheimers disease. In an effort to comprehend the role of that metal ion in disease, we investigated the potential biological activity of well-characterized Al(III) forms in neuronal and glial cellular environment. The investigation of the potential biological activity of well-characterized Al(III) forms in cellular environment constitutes a challenge, because of the neurotoxic potential of the metal interacting with the cellular peptide and the epidemiological evidence linking aluminum and Beta amyloid to Alzheimer Disease.

Keywords: Aluminum, Aβ(1-40) amyloid peptide, chelator agents, neurodegeneration, Alzheimer, neurons, glial cells

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