Literature DB >> 11773429

Learning and memory in transgenic mice modeling Alzheimer's disease.

K H Ashe1.   

Abstract

Recent advances in behavioral analyses of transgenic mouse models of Alzheimer's disease (AD) are discussed, and their impact on our understanding of the molecular basis of cognitive impairment in AD is considered. Studies of the relationship between memory and A Beta in transgenic mice expressing the amyloid precursor protein (APP) and its variants suggest that aging promotes the formation of soluble A Beta assemblies mediating negative effects on memory. A significant component of memory loss in APP transgenic mice is apparently caused by soluble A Beta assemblies, but whether and how much of the dementia within individuals afflicted with AD is caused by these A Beta species is unclear. Future studies in composite transgenic mice developing amyloid plaques, neurofibrillary tangles, and other AD pathology may allow for the determination of the relative contribution of A Beta and non-A Beta components to dementia.

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Year:  2001        PMID: 11773429     DOI: 10.1101/lm.43701

Source DB:  PubMed          Journal:  Learn Mem        ISSN: 1072-0502            Impact factor:   2.460


  72 in total

Review 1.  Synaptic plasticity in animal models of early Alzheimer's disease.

Authors:  Michael J Rowan; Igor Klyubin; William K Cullen; Roger Anwyl
Journal:  Philos Trans R Soc Lond B Biol Sci       Date:  2003-04-29       Impact factor: 6.237

Review 2.  Vaccines for Alzheimer's disease: how close are we?

Authors:  Christopher Janus
Journal:  CNS Drugs       Date:  2003       Impact factor: 5.749

3.  Preserved fronto-striatal plasticity and enhanced procedural learning in a transgenic mouse model of Alzheimer's disease overexpressing mutant hAPPswe.

Authors:  Silvia Middei; Raffaella Geracitano; Antonio Caprioli; Nicola Mercuri; Martine Ammassari-Teule
Journal:  Learn Mem       Date:  2004 Jul-Aug       Impact factor: 2.460

Review 4.  APP transgenic mice for modelling behavioural and psychological symptoms of dementia (BPSD).

Authors:  R Lalonde; K Fukuchi; C Strazielle
Journal:  Neurosci Biobehav Rev       Date:  2012-02-21       Impact factor: 8.989

5.  BACE1 gene deletion prevents neuron loss and memory deficits in 5XFAD APP/PS1 transgenic mice.

Authors:  Masuo Ohno; Sarah L Cole; Marina Yasvoina; Jie Zhao; Martin Citron; Robert Berry; John F Disterhoft; Robert Vassar
Journal:  Neurobiol Dis       Date:  2006-12-20       Impact factor: 5.996

6.  Danish dementia mice suggest that loss of function and not the amyloid cascade causes synaptic plasticity and memory deficits.

Authors:  Robert Tamayev; Shuji Matsuda; Mauro Fà; Ottavio Arancio; Luciano D'Adamio
Journal:  Proc Natl Acad Sci U S A       Date:  2010-11-22       Impact factor: 11.205

7.  Long-lasting impairment in hippocampal neurogenesis associated with amyloid deposition in a knock-in mouse model of familial Alzheimer's disease.

Authors:  Chen Zhang; Elizabeth McNeil; Lindsay Dressler; Robert Siman
Journal:  Exp Neurol       Date:  2006-10-27       Impact factor: 5.330

8.  Highly stabilized curcumin nanoparticles tested in an in vitro blood-brain barrier model and in Alzheimer's disease Tg2576 mice.

Authors:  Kwok Kin Cheng; Chin Fung Yeung; Shuk Wai Ho; Shing Fung Chow; Albert H L Chow; Larry Baum
Journal:  AAPS J       Date:  2012-12-11       Impact factor: 4.009

9.  Partial reduction of BACE1 improves synaptic plasticity, recent and remote memories in Alzheimer's disease transgenic mice.

Authors:  Ryoichi Kimura; Latha Devi; Masuo Ohno
Journal:  J Neurochem       Date:  2010-01-20       Impact factor: 5.372

Review 10.  Amyloid-Beta and Phosphorylated Tau Accumulations Cause Abnormalities at Synapses of Alzheimer's disease Neurons.

Authors:  Ravi Rajmohan; P Hemachandra Reddy
Journal:  J Alzheimers Dis       Date:  2017       Impact factor: 4.472

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