Abstract：
:Genetic abnormalities in amyloid precursor protein (APP) are associated with Down's syndrome and familial Alzheimer's disease where hallmark plaques contain A beta peptides derived from APP. Both APP and its derivatives are implicated in neurodegenerative processes and may play important physiological and pathophysiological roles in synaptic function. Here, we show that young APP23 transgenic mice overexpressing human APP with the Swedish double mutation display altered novelty seeking behavior before the age of plaque onset. Using short interfering RNA (siRNA) targeted against APP, we investigate the direct contribution of APP and its derivatives to this behavioral deficit. After validating siRNAs targeting human APP in vitro, siRNAs were infused directly into the brain of APP23 mice for 2 weeks. Behavioral analysis shows that infusion of siRNA targeted against APP completely reverses increased exploratory activity in APP23 mice. Collectively, these data suggest that excessive APP and/or its derivatives, causes a hyperactive phenotype in APP23 mice when placed in a novel environment, which is fully reversible and not linked to plaque deposits.
journal_name
Brain Resjournal_title
Brain researchauthors
Senechal Y,Prut L,Kelly PH,Staufenbiel M,Natt F,Hoyer D,Wiessner C,Dev KKdoi
10.1016/j.brainres.2008.09.024subject
Has Abstractpub_date
2008-12-03 00:00:00pages
124-33eissn
0006-8993issn
1872-6240pii
S0006-8993(08)02267-1journal_volume
1243pub_type
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