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Fig. 2 | Molecular Brain

Fig. 2

From: Zinc transporters in Alzheimer’s disease

Fig. 2

Schematic depiction of the major altered expression of zinc transporters in the neurons of developing AD. Exchangeable zinc ions across the blood-brain barrier/blood-CSF barrier by binding with His or Cys to form Zn (His)2 or Zn (Cys)(His), and then the complex is transferred into or out of the glial cells and neurons through zinc-binding proteins (ZIPs, ZnTs and DMT1). However, in AD patients, the expression levels of some major zinc transporters are altered, and this exacerbates Aβ deposition and toxicity. As shown in the figure, the highly upregulated ZnT1 pumps more zinc from presynaptic neurons and glial cells, which aggravates the deposition of Aβ proteins, and with the lower available zinc ions in the neuronal cytoplasm, upregulation of ZIP1 expression is induced to import zinc from the extracellular milieu to sustain the normal zinc homeostasis. However, this leads to a vicious cycle. In addition, the decreased expression level of ZnT3 leads to insufficient release of zinc into the cleft, and thus the inhibitory function of zinc on NMDAR will be impaired; as a result, more Ca2+ enters the postsynaptic cells, leading to apoptosis and cognitive disorders

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