Metalloneurotoxins are among numerous environmental factors strongly affecting cellular toxicity and endangering human health. Habitual and often-involuntary exposure of humans to such toxins emerging from dietary sources, aquatic environments, industrial and atmospheric sources influence normal cellular physiology, which in combination with the underlying human genetic disposition influence unknown to-date pathways linked to neurodegenerative events. Over the last decades, aluminum (Al) has been linked to numerous human pathological disorders, emphatically associated with the onset of neurological diseases [1,2,3], including Alzheimer’s disease. The present study targets the chemical reactivity of well-characterized Al(III) forms in a neuronal and glial cellular environment, thereby lending credence to the association of Al(III) with Alzheimer Disease etiopathology [3-5]. The selected molecular targets interacting with Al(III) are Ν-methyl D-aspartic acid (NMDA) and Voltage-Dependent Calcium Channels (VDCC), both of them key structures on neurocellular membranes, playing an important role in memory processes. The experimental effort attempts to assess the neurotoxic potential of Al(III) interacting with the above cellular receptors, thereby contributing to neurodegeneration in Alzheimer Disease.
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