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Deficits in working memory and motor performance in the APP/PS1ki mouse model for Alzheimer's disease.
Neurobiol Aging 2008; 29(6):891-901NA

Abstract

The APP/PS1ki mouse model for Alzheimer's disease (AD) exhibits robust brain and spinal cord axonal degeneration and hippocampal CA1 neuron loss starting at 6 months of age. It expresses human mutant APP751 with the Swedish and London mutations together with two FAD-linked knocked-in mutations (PS1 M233T and PS1 L235P) in the murine PS1 gene. The present report covers a phenotypical analysis of this model using either behavioral tests for working memory and motor performance, as well as an analysis of weight development and body shape. At the age of 6 months, a dramatic, age-dependent change in all of these properties and characteristics was observed, accompanied by a significantly reduced ability to perform working memory and motor tasks. The APP/PS1ki mice were smaller and showed development of a thoracolumbar kyphosis, together with an incremental loss of body weight. While 2-month-old APP/PS1ki mice were inconspicuous in all of these tasks and properties, there is a massive age-related impairment in all tested behavioral paradigms. We have previously reported robust axonal degeneration in brain and spinal cord, as well as abundant hippocampal CA1 neuron loss starting at 6 months of age in the APP/PS1ki mouse model, which coincides with the onset of motor and memory deficits described in the present report.

Authors+Show Affiliations

Department of Psychiatry, University of Goettingen, von-Siebold-Str. 5, D-37075 Goettingen, Germany. owirths@uni-goettingen.deNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17215062

Citation

Wirths, Oliver, et al. "Deficits in Working Memory and Motor Performance in the APP/PS1ki Mouse Model for Alzheimer's Disease." Neurobiology of Aging, vol. 29, no. 6, 2008, pp. 891-901.
Wirths O, Breyhan H, Schäfer S, et al. Deficits in working memory and motor performance in the APP/PS1ki mouse model for Alzheimer's disease. Neurobiol Aging. 2008;29(6):891-901.
Wirths, O., Breyhan, H., Schäfer, S., Roth, C., & Bayer, T. A. (2008). Deficits in working memory and motor performance in the APP/PS1ki mouse model for Alzheimer's disease. Neurobiology of Aging, 29(6), pp. 891-901.
Wirths O, et al. Deficits in Working Memory and Motor Performance in the APP/PS1ki Mouse Model for Alzheimer's Disease. Neurobiol Aging. 2008;29(6):891-901. PubMed PMID: 17215062.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Deficits in working memory and motor performance in the APP/PS1ki mouse model for Alzheimer's disease. AU - Wirths,Oliver, AU - Breyhan,Henning, AU - Schäfer,Stephanie, AU - Roth,Christian, AU - Bayer,Thomas A, Y1 - 2007/01/09/ PY - 2006/09/28/received PY - 2006/11/23/revised PY - 2006/12/11/accepted PY - 2007/1/12/pubmed PY - 2008/6/21/medline PY - 2007/1/12/entrez SP - 891 EP - 901 JF - Neurobiology of aging JO - Neurobiol. Aging VL - 29 IS - 6 N2 - The APP/PS1ki mouse model for Alzheimer's disease (AD) exhibits robust brain and spinal cord axonal degeneration and hippocampal CA1 neuron loss starting at 6 months of age. It expresses human mutant APP751 with the Swedish and London mutations together with two FAD-linked knocked-in mutations (PS1 M233T and PS1 L235P) in the murine PS1 gene. The present report covers a phenotypical analysis of this model using either behavioral tests for working memory and motor performance, as well as an analysis of weight development and body shape. At the age of 6 months, a dramatic, age-dependent change in all of these properties and characteristics was observed, accompanied by a significantly reduced ability to perform working memory and motor tasks. The APP/PS1ki mice were smaller and showed development of a thoracolumbar kyphosis, together with an incremental loss of body weight. While 2-month-old APP/PS1ki mice were inconspicuous in all of these tasks and properties, there is a massive age-related impairment in all tested behavioral paradigms. We have previously reported robust axonal degeneration in brain and spinal cord, as well as abundant hippocampal CA1 neuron loss starting at 6 months of age in the APP/PS1ki mouse model, which coincides with the onset of motor and memory deficits described in the present report. SN - 1558-1497 UR - https://www.unboundmedicine.com/medline/citation/17215062/Deficits_in_working_memory_and_motor_performance_in_the_APP/PS1ki_mouse_model_for_Alzheimer's_disease_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0197-4580(06)00465-9 DB - PRIME DP - Unbound Medicine ER -