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Serum Amyloid A1 Involves Amyloid Plaque Aggregation and Aggravates Memory Deficits in Amyloid Beta Abundant Condition
disease is a characterized by cognitive impairment, progressive neurodegeneration and formation of amyloid-β (Aβ)-containing plaques and neurofibrillary tangles. In progress of disease, inflammation plays major role to lead the neuronal death. Previously Serum amyloid A (SAA1), one of the acute-phase proteins, was examined and found that this liver derived protein pass through the brain blood barrier (BBB). By making double transgenic mice through the crossing over APP c105 mice, produce amyloid beta1-42 in brain as a pathogen, and SAA1 overexpression mice confirm the SAA exacerbate inflammation that triggered by amyloid beta accumulation in brain. Followed behavior test also shows double transgenic mice have more damage in memory than the APP mouse that only designed to express the amyloid beta 1-42.
