volume 28, issue 4, P951-960 2012
DOI: 10.3233/jad-2011-111517
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Abstract: Abstract. The senescence accelerated mouse-prone 8 (SAMP8) mouse model of Alzheimer's disease has a natural mutation leading to age-related increases in the amyloid-␤ protein precursor (A␤PP) and amyloid-␤ (A␤) in the brain, memory impairment, and deficits in A␤ removal from the brain. Previous studies show that centrally administered antisense oligonucleotide directed against A␤PP can decrease A␤PP expression and A␤ production in the brains of aged SAMP8 mice, and improve memory. The same antisense crosses t…

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