RT Journal Article SR Electronic T1 α-1-Antichymotrypsin Promotes β-Sheet Amyloid Plaque Deposition in a Transgenic Mouse Model of Alzheimer's Disease JF The Journal of Neuroscience JO J. Neurosci. FD Society for Neuroscience SP 1444 OP 1451 DO 10.1523/JNEUROSCI.21-05-01444.2001 VO 21 IS 5 A1 Lars N. G. Nilsson A1 Kelly R. Bales A1 Giovanni DiCarlo A1 Marcia N. Gordon A1 Dave Morgan A1 Steven M. Paul A1 Huntington Potter YR 2001 UL http://www.jneurosci.org/content/21/5/1444.abstract AB α1-Antichymotrypsin (ACT), an acute-phase inflammatory protein, is an integral component of the amyloid deposits in Alzheimer's disease (AD) and has been shown to catalyze amyloid β-peptide polymerization in vitro. We have investigated the impact of ACT on amyloid deposition in vivo by generating transgenic GFAP-ACT-expressing mice and crossing them with the PDGF-hAPP/V717F mice, which deposit amyloid in an age-dependent manner. The number of amyloid deposits measured by Congo Red birefringence was increased in the double ACT/amyloid precursor protein (APP) transgenic mice compared with transgenic mice that only expressed APP, particularly in the hippocampus where ACT expression was highest, and the increase was preceded by elevated total amyloid β-peptide levels at an early age. Our data demonstrate that ACT promotes amyloid deposition and provide a specific mechanism by which inflammation and the subsequent upregulation of astrocytic ACT expression in AD brain contributes to AD pathogenesis.