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Molecules 2017, 22(11), 2007; doi:10.3390/molecules22112007

Studies for Improving a Rat Model of Alzheimer’s Disease: Icv Administration of Well-Characterized β-Amyloid 1-42 Oligomers Induce Dysfunction in Spatial Memory

1
Department of Medical Chemistry, University of Szeged, Dome square 8, Szeged H-6720, Hungary
2
LipidArt Research and Development Ltd., Temesvári krt. 62, Szeged H-6726, Hungary
3
Department of Applied and Environmental Chemistry, University of Szeged, Rerrich Béla square 1, Szeged H-6720, Hungary
*
Author to whom correspondence should be addressed.
Received: 9 October 2017 / Revised: 7 November 2017 / Accepted: 13 November 2017 / Published: 18 November 2017
(This article belongs to the Special Issue 25th Anniversary of the Amyloid Hypothesis and Alzheimer Disease)
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Abstract

During the past 15 years, several genetically altered mouse models of human Alzheimer’s disease (AD) have been developed. These costly models have greatly facilitated the evaluation of novel therapeutic approaches. Injecting synthetic β-amyloid (Aβ) 1-42 species into different parts of the brain of non-transgenic rodents frequently provided unreliable results, owing to a lack of a genuine characterization of the administered Aβ aggregates. Previously, we have published a new rat AD-model in which protofibrillar-fibrillar Aβ1-42 was administered into rat entorhinal cortex (Sipos 2007). In order to develop a more reliable model, we have injected well-characterized toxic soluble Aβ1-42 species (oligomers, protofibrils and fibrils) intracerebroventricularly (icv) into rat brain. Studies of the distribution of fluorescent-labeled Aβ1-42 in the brain showed that soluble Aβ-species diffused into all parts of the rat brain. After seven days, the Aβ-treated animals showed a significant decrease of spatial memory in Morris water maze test and impairment of synaptic plasticity (LTP) measured in acute hippocampal slices. The results of histological studies (decreased number of viable neurons, increased tau levels and decreased number of dendritic spines) also supported that icv administration of well-characterized toxic soluble Aβ species into rat brain provides a reliable rat AD-model. View Full-Text
Keywords: amyloid beta; AD rat model; icv administration; hippocampus; spatial memory; Morris water maze; long-term potentiation; Golgi staining amyloid beta; AD rat model; icv administration; hippocampus; spatial memory; Morris water maze; long-term potentiation; Golgi staining
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MDPI and ACS Style

Kasza, Á.; Penke, B.; Frank, Z.; Bozsó, Z.; Szegedi, V.; Hunya, Á.; Németh, K.; Kozma, G.; Fülöp, L. Studies for Improving a Rat Model of Alzheimer’s Disease: Icv Administration of Well-Characterized β-Amyloid 1-42 Oligomers Induce Dysfunction in Spatial Memory. Molecules 2017, 22, 2007.

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