Literature DB >> 15810905

Behavioral phenotypes of amyloid-based genetically modified mouse models of Alzheimer's disease.

D T Kobayashi1, K S Chen.   

Abstract

Alzheimer's disease (AD) is the most common neurodegenerative affliction of the elderly, presenting with progressive memory loss and dementia and terminating with death. There have been significant advances in understanding the biology and subsequent diagnosis of AD; however, the furious pace of research has not yet translated into a disease-modifying treatment. While scientific inquiry in AD is largely centered on identifying biological players and pathological mechanisms, the day-to-day realities of AD patients and their caregivers revolve around their steady and heartbreaking cognitive decline. In the past decade, AD research has been fundamentally transformed by the development of genetically modified animal models of amyloid-driven neurodegeneration. These important in vivo models not only replicate some of the hallmark pathology of the disease, such as plaque-like amyloid accumulations and astrocytic inflammation, but also some of the cognitive impairments relevant to AD. In this article, we will provide a detailed review of the behavioral and cognitive deficits present in several transgenic mouse models of AD and discuss their functional changes in response to experimental treatments.

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Year:  2005        PMID: 15810905     DOI: 10.1111/j.1601-183X.2005.00124.x

Source DB:  PubMed          Journal:  Genes Brain Behav        ISSN: 1601-183X            Impact factor:   3.449


  61 in total

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Journal:  Brain       Date:  2011-01       Impact factor: 13.501

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Journal:  Neurobiol Dis       Date:  2006-12-20       Impact factor: 5.996

4.  Memory deficits and neurochemical changes induced by C-reactive protein in rats: implication in Alzheimer's disease.

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Journal:  Psychopharmacology (Berl)       Date:  2009-03-05       Impact factor: 4.530

5.  Transsynaptic progression of amyloid-β-induced neuronal dysfunction within the entorhinal-hippocampal network.

Authors:  Julie A Harris; Nino Devidze; Laure Verret; Kaitlyn Ho; Brian Halabisky; Myo T Thwin; Daniel Kim; Patricia Hamto; Iris Lo; Gui-Qiu Yu; Jorge J Palop; Eliezer Masliah; Lennart Mucke
Journal:  Neuron       Date:  2010-11-04       Impact factor: 17.173

6.  Cystatin C-cathepsin B axis regulates amyloid beta levels and associated neuronal deficits in an animal model of Alzheimer's disease.

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Journal:  Neuron       Date:  2008-10-23       Impact factor: 17.173

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Authors:  Barbara Biscaro; Olle Lindvall; Christoph Hock; Christine T Ekdahl; Roger M Nitsch
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8.  Partial reduction of BACE1 improves synaptic plasticity, recent and remote memories in Alzheimer's disease transgenic mice.

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Journal:  J Neurochem       Date:  2010-01-20       Impact factor: 5.372

9.  Spatial learning impairments in PLB1Triple knock-in Alzheimer mice are task-specific and age-dependent.

Authors:  D Ryan; D Koss; E Porcu; H Woodcock; L Robinson; B Platt; G Riedel
Journal:  Cell Mol Life Sci       Date:  2013-03-28       Impact factor: 9.261

10.  Many neuronal and behavioral impairments in transgenic mouse models of Alzheimer's disease are independent of caspase cleavage of the amyloid precursor protein.

Authors:  Julie A Harris; Nino Devidze; Brian Halabisky; Iris Lo; Myo T Thwin; Gui-Qiu Yu; Dale E Bredesen; Eliezer Masliah; Lennart Mucke
Journal:  J Neurosci       Date:  2010-01-06       Impact factor: 6.167

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