作者: Anna Lord , Hillevi Englund , Linda Söderberg , Stina Tucker , Fredrik Clausen
DOI: 10.1111/J.1742-4658.2008.06836.X
关键词:
摘要: Oligomeric assemblies of amyloid-beta (Abeta) are suggested to be central in the pathogenesis Alzheimer's disease because levels soluble Abeta correlate much better with extent cognitive dysfunctions than do senile plaque counts. Moreover, such species have been shown neurotoxic, interfere learned behavior and inhibit maintenance hippocampal long-term potentiation. The tg-ArcSwe model (i.e. transgenic mice Arctic Swedish Alzheimer mutations) expresses elevated protofibrils brain, making a highly suitable for investigating pathogenic role these assemblies. In present study, we estimated protofibril brain cerebrospinal fluid mice, also assessed their respect functions. Protofibril levels, specifically measured sandwich ELISA, were found young compared several models lacking mutation. aged considerable deposition, approximately 50% higher younger whereas total exponentially increased. Young showed deficits spatial learning, individual performances Morris water maze correlated inversely protofibrils, but not levels. We conclude that accumulate an age-dependent manner although far lesser Abeta. Our findings suggest increased could result learning impairment.