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Transgenic Research

, Volume 28, Issue 5–6, pp 499–508 | Cite as

Serum amyloid A1 is involved in amyloid plaque aggregation and memory decline in amyloid beta abundant condition

  • Soyoung Jang
  • Woo Young Jang
  • Minjee Choi
  • Jinhee Lee
  • Wookbong Kwon
  • Junkoo Yi
  • Si Jun Park
  • Duhak Yoon
  • Sanggyu Lee
  • Myoung Ok Kim
  • Zae Young RyooEmail author
Original Paper

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder, characterized by cognitive impairment, progressive neurodegeneration, and amyloid-β (Aβ) lesion. In the neuronal death and disease progression, inflammation is known to play an important role. Our previous study on acute-phase protein serum amyloid A1 (SAA1) overexpressed mice showed that the liver-derived SAA1 accumulated in the brain by crossing the brain blood barrier (BBB) and trigger the depressive-like behavior on mouse. Since SAA1 involved in immune responses in other diseases, we focused on the possibility that SAA1 may exacerbate the neuronal inflammation related to Alzheimer’s disease. A APP/SAA overexpressed double transgenic mouse was generated using amyloid precursor protein overexpressed (APP)-c105 mice and SAA1 overexpressed mice to examine the function of SAA1 in Aβ abundant condition. Comparisons between APP and APP/SAA1 transgenic mice showed that SAA1 exacerbated amyloid aggregation and glial activation; which lead to the memory decline. Behavior tests also supported this result. Overall, overexpression of SAA1 intensified the neuronal inflammation in amyloid abundant condition and causes the greater memory decline compared to APP mice, which only expresses Aβ 1–42.

Keywords

Serum amyloid A1 Alzheimer’s disease Amyloid beta Double transgenic Glia 

Notes

Acknowledgments

This work was supported by the National Research Foundation of Korea (NRF) Grant funded by the Korea Government (MSIP) (No. 2016R1A2B4014686) and (No. 2017R1A2B4007888)

Supplementary material

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Supplementary material 1 (JPEG 62 kb)
11248_2019_166_MOESM2_ESM.docx (11 kb)
Supplementary material 2 (DOCX 10 kb)

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Copyright information

© Springer Nature Switzerland AG 2019

Authors and Affiliations

  • Soyoung Jang
    • 1
  • Woo Young Jang
    • 4
    • 5
  • Minjee Choi
    • 1
    • 7
  • Jinhee Lee
    • 1
  • Wookbong Kwon
    • 1
  • Junkoo Yi
    • 3
  • Si Jun Park
    • 1
  • Duhak Yoon
    • 6
  • Sanggyu Lee
    • 1
  • Myoung Ok Kim
    • 2
  • Zae Young Ryoo
    • 1
    Email author
  1. 1.School of Life Science and Biotechnology, KNU Creative BioResearch Group (BK21 Plus Project)Kyungpook National UniversityDaeguRepublic of Korea
  2. 2.School of Animal Biotechnology (BT) ScienceKyungpook National UniversityDaeguRepublic of Korea
  3. 3.Gyeongsangbukdo Livestock Institute ResearchYeongju-cityRepublic of Korea
  4. 4.Laboratory Animal Resources Division, Toxicological Evaluation and Research DepartmentNational Institute of Food and Drug Safety EvaluationCheongju-siRepublic of Korea
  5. 5.Osong Health Technology Administration ComplexCheongju-siRepublic of Korea
  6. 6.Department of Animal ScienceKyungpook National UniversityDaeguRepublic of Korea
  7. 7.Core Protein Resources CenterDGISTDaeguRepublic of Korea

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