| Alzheimer’s disease(AD) is a neurodegenerative diseases, in which, senile plaques(SPs) and neurofibrillary tangles(NFTs) in the brain are the remarkable pathological features. More and more studies have shown that Aβ deposition not only in brain but also in retina of AD patients or transgenic AD model mice. AD retina shows similar neuropathological changes compared to AD brain. Because retina can be inspected by retinal imaging, such as Aβ deposition and vascular examination, it is assumed that retina detection might be AD biomarker. Retina is considered an extension of the central nervous system(CNS). As well as an embryological link to the CNS, both retinal and CNS tissues share many properties such as having similar vascularization patterns, blood flow auto-regulation, as well as blood–tissue barrier functions. This combination of properties has made the retina a valuable tool for the in vivo visualization of changes in AD, study of their pathogenesis, and monitoring disease progression and response to potential AD therapies. In this study, three transgenic AD model mice were used as the animal model to study the effects of sodium selenate on AD and explore the molecular mechanisms behind the phenomena.The thickness of each layer and the number of retinal ganglion cells(RGCs) were calculated in retinal sections of 6 months, 10 months and 12 months AD model mice and those with selenate treatment. Selenate administration increases thickness of retina and number of RGCs. Then, expression levels of Aβ, synaptophysin and 15 k Da selenoprotein(sep15) were detected by immunofluorescence, Western-Blot and ELISA. Endoplasmic reticulum stress marker, Bi P, pro-apoptotic protein CHOP, BAX, BCL-2, caspase12 in the retina were also detected to further clarify the molecular mechanisms.In summaries, the thickness of retina in 3×TgAD model mice decreased compared to WT mice, but sodium selenate protects retina neurodegeneration through inhibition of apoptotic pathway induced by ER stress. |
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