Memory Function in a Mouse Genetic Model of Alzheimer's Disease

Abstract

The E4 allele of the apolipoprotein E (ApoE) gene has been identified as a major risk factor for the development of late onset Alzheimer's disease (AD). However, the mechanisms by which this gene affects AD are not fully understood. Studies of ApoE knock-out (ApoE KO) mice have revealed an exacerbation of two major pathologies that are diagnostic of AD: neurofibrillary tangles and senile plaques. However, evidence as to whether these mice have cognitive deficits is not yet conclusive. This ambiguity may arise partly from confounds associated with reliance on limited memory models, primarily, the Morris water maze task. An 8-arm radial maze task was therefore used to measure spatial memory in the ApoE KO mice, compared to controls over time. Furthermore, the effectiveness of a combination antioxidant therapy (CAT), designed to slow down the progression of AD based on concepts of oxidative stress and inflammatory processes underlying the pathology, was tested on memory ability. A significant strain difference was observed with the ApoE KO mice performing better than controls in terms of reference memory and corrects entries. No significant strain difference was observed for performance in terms of working memory errors. No significant effect of the CAT supplementation was observed.

Toll-interacting protein deficiency promotes neurodegeneration via impeding autophagy completion in high-fat diet-fed ApoE−/− mouse model

“…Utilizing the well-recognized Alzheimer's disease model of ApoE deficient mice (Avdesh et al, 2011; Richardson and Burns, 2002), we examined the effect of Tollip deficiency on neurons and found that the densities of neurons in Cerebral cortex (Fig. 1, upper panel: A–B), Hippocampus (Fig.…”

“…ApoE deficient mice offer a unique model to study the pathogenesis of Alzheimer's disease (Avdesh et al, 2011). Under the regimen of high fat diet (HFD) feeding, ApoE deficient mice develop Alzheimer's disease-like symptoms, potentially due to elevated oxidative modifications of proteins, lipids and DNAs resembling AD patients (Galloway et al, 2008; To et al, 2011).…”

Attenuation of Spatial Memory Impairment in a Tau Mouse Model of Alzheimer's Disease with Riluzole

“…This coincides with findings of impaired working memory functioning in mouse and rat models of AD (Cotel et al, 2012;Mustroph et al, 2012). However, knocking out the APOE gene, using APOE KO mice, improves reference memory compared to controls, without affecting working memory (Avdesh et al, 2011).…”

Effects of apoE Deficiency and Occlusal Disharmony on Amyloid-Beta Production and Spatial Memory in Rats

“…However, other groups have not detected cholinergic and behavioral deficits in apoE-deficient mice [47-50]. Another study showed that apoE-deficient mice perform better than controls in terms of reference memory and correct entries into the eight-arm maze [51]. Although inconsistent results regarding spatial memory in apoE-deficient mice have been reported, the reason may depend on the method of knockout, age, gender, or the stress system [52]…”