VEGFR2 alteration in Alzheimer's disease.

Sci Rep

Division of Brain Diseases, Center for Biomedical Sciences, Korea National Institute of Health, 187 Osongsaengmyeong2-ro, Osong-eup, Heungdeok-gu, Cheongju-si, Chungcheongbuk-do, 28159, Korea.

Published: December 2017

AI Article Synopsis

  • Alzheimer's disease (AD) is linked to cognitive decline in the elderly and may involve angiogenesis factors like VEGF and its receptors.
  • Plasma VEGF levels are higher in AD patients, while soluble VEGF receptors (sVEGFR1 and sVEGFR2) are lower compared to healthy controls.
  • Changes in the expression of VEGF and its receptors could indicate potential risks for developing Alzheimer's disease.

Article Abstract

Alzheimer's disease (AD) is a common disorder of progressive cognitive decline among elderly subjects. Angiogenesis-related factors including vascular endothelial growth factor (VEGF) might be involved in the pathogenesis of AD. Soluble form of the VEGF receptor is likely to be an intrinsic negative counterpart of VEGF. We measured the plasma levels of VEGF and its two soluble receptors (sVEGFR1 and sVEGFR2) in 120 control subjects, 75 patients with mild cognitive impairment, and 76 patients with AD using ELISA. Plasma levels of VEGF in patients with AD were higher than those in healthy control subjects. However, plasma levels of sVEGFR1 and sVEGFR2 were lower in patients with AD than in healthy control subjects. Levels of VEGFR2 mRNA were significantly decreased in human umbilical vein endothelial cells after amyloid-beta treatment. Further, protein levels of VEGFR2 were also decreased in the brains of AD model mice. In addition, we show that the expression of sVEGFR2 and VEGFR2 was also decreased by the transfection with the Notch intracellular domain. These results indicate that the alterations of VEGF and its two receptors levels might be associated with those at risk for Alzheimer's disease.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5735090PMC
http://dx.doi.org/10.1038/s41598-017-18042-1DOI Listing

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