Fig. 1

a The effects of zinc, copper, and cobalt deficiencies in AD. In AD brain, the paucity of zinc limits the accessibility of metalloproteinase, and causes β-amyloid to aggregate. The built-up β-amyloid that forms plaques traps copper and abate its level, subsequently expediting the possibility of oxidative stress. Similarly, the AD brain has augmented levels of cobalt, which potentially downregulates PIN-1 expression and decreases the level of cyclin D. Downregulated PIN-1 expression instigates cognitive dysfunction by accelerating phosphorylated tau protein and β-amyloid accumulation. b The therapeutic effect of molybdenum and iodine. Dietary iodine may counteract oxidative stress in AD by mitigating hydrogen peroxidation formation and enhancing the output of glutathione peroxidase. Similarly, molybdenum may impair neuroinflammation through the inhibition of astrocyte and microglia formation, and result in hindering both oxidative stress and β-amyloid