| First Author | Jang S | Year | 2019 |
| Journal | Transgenic Res | Volume | 28 |
| Issue | 5-6 | Pages | 499-508 |
| PubMed ID | 31407125 | Mgi Jnum | J:292296 |
| Mgi Id | MGI:6447769 | Doi | 10.1007/s11248-019-00166-x |
| Citation | Jang S, et al. (2019) Serum amyloid A1 is involved in amyloid plaque aggregation and memory decline in amyloid beta abundant condition. Transgenic Res 28(5-6):499-508 |
| abstractText | Alzheimer's disease (AD) is a neurodegenerative disorder, characterized by cognitive impairment, progressive neurodegeneration, and amyloid-beta (Abeta) 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 Abeta 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 Abeta 1-42. |
