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A longitudinal study of behavioral deficits in an AβPP transgenic mouse model of Alzheimer's disease.
J Alzheimers Dis. 2011; 25(2):231-43.JA

Abstract

Elucidating the age-dependent alterations in transgenic (Tg) mice overexpressing amyloid-β protein precursor (AβPP) is important for understanding the pathogenesis of Alzheimer's disease (AD) and designing experimental therapies. Cross-studies have previously characterized some time-dependent behavioral and pathological alterations in AβPP Tg mice, however, a more comprehensive longitudinal study is needed to fully examine the progressive nature of behavioral deficits in these mice. In order to better understand the age- and gender-dependent progression of behavioral alterations, we performed a longitudinal study wherein Tg mice overexpressing human AβPP751 with the London (V717I) and Swedish (K670M/N671L) mutations under the regulatory control of the neuron specific murine (m)Thy-1 promoter (mThy1-hAβPP751) were behaviorally analyzed at 3 months and then re-tested at 6 and 9 months of age. The results show that there was an age-associated impairment in learning in the water maze task and habituation in the hole-board task. Motor coordination of the mThy1-hAβPP751 Tg mice was well-preserved throughout the investigated life span however, gender-specific deficits were observed in spontaneous activity and thigmotaxis. Neuropathologically, mThy1-hAβPP751 Tg mice displayed a progressive increase in the number of Aβ plaques and mean plaque size in the cortex and hippocampus from 3 to 6 and from 6 to 9 months of age. Taken together, these results indicate that the mThy1-hAβPP751 Tg mice model AD from the early onset of the disease through to later stages, allowing them to be utilized at numerous points during the timeline for drug test designs.

Authors+Show Affiliations

JSW LIFESCIENCES, Grambach, Austria.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

21403389

Citation

Havas, Daniel, et al. "A Longitudinal Study of Behavioral Deficits in an AβPP Transgenic Mouse Model of Alzheimer's Disease." Journal of Alzheimer's Disease : JAD, vol. 25, no. 2, 2011, pp. 231-43.
Havas D, Hutter-Paier B, Ubhi K, et al. A longitudinal study of behavioral deficits in an AβPP transgenic mouse model of Alzheimer's disease. J Alzheimers Dis. 2011;25(2):231-43.
Havas, D., Hutter-Paier, B., Ubhi, K., Rockenstein, E., Crailsheim, K., Masliah, E., & Windisch, M. (2011). A longitudinal study of behavioral deficits in an AβPP transgenic mouse model of Alzheimer's disease. Journal of Alzheimer's Disease : JAD, 25(2), 231-43. https://doi.org/10.3233/JAD-2011-101866
Havas D, et al. A Longitudinal Study of Behavioral Deficits in an AβPP Transgenic Mouse Model of Alzheimer's Disease. J Alzheimers Dis. 2011;25(2):231-43. PubMed PMID: 21403389.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - A longitudinal study of behavioral deficits in an AβPP transgenic mouse model of Alzheimer's disease. AU - Havas,Daniel, AU - Hutter-Paier,Birgit, AU - Ubhi,Kiren, AU - Rockenstein,Edward, AU - Crailsheim,Karl, AU - Masliah,Eliezer, AU - Windisch,Manfred, PY - 2011/3/16/entrez PY - 2011/3/16/pubmed PY - 2011/11/5/medline SP - 231 EP - 43 JF - Journal of Alzheimer's disease : JAD JO - J. Alzheimers Dis. VL - 25 IS - 2 N2 - Elucidating the age-dependent alterations in transgenic (Tg) mice overexpressing amyloid-β protein precursor (AβPP) is important for understanding the pathogenesis of Alzheimer's disease (AD) and designing experimental therapies. Cross-studies have previously characterized some time-dependent behavioral and pathological alterations in AβPP Tg mice, however, a more comprehensive longitudinal study is needed to fully examine the progressive nature of behavioral deficits in these mice. In order to better understand the age- and gender-dependent progression of behavioral alterations, we performed a longitudinal study wherein Tg mice overexpressing human AβPP751 with the London (V717I) and Swedish (K670M/N671L) mutations under the regulatory control of the neuron specific murine (m)Thy-1 promoter (mThy1-hAβPP751) were behaviorally analyzed at 3 months and then re-tested at 6 and 9 months of age. The results show that there was an age-associated impairment in learning in the water maze task and habituation in the hole-board task. Motor coordination of the mThy1-hAβPP751 Tg mice was well-preserved throughout the investigated life span however, gender-specific deficits were observed in spontaneous activity and thigmotaxis. Neuropathologically, mThy1-hAβPP751 Tg mice displayed a progressive increase in the number of Aβ plaques and mean plaque size in the cortex and hippocampus from 3 to 6 and from 6 to 9 months of age. Taken together, these results indicate that the mThy1-hAβPP751 Tg mice model AD from the early onset of the disease through to later stages, allowing them to be utilized at numerous points during the timeline for drug test designs. SN - 1875-8908 UR - https://www.unboundmedicine.com/medline/citation/21403389/A_longitudinal_study_of_behavioral_deficits_in_an_AβPP_transgenic_mouse_model_of_Alzheimer's_disease_ L2 - https://content.iospress.com/openurl?genre=article&id=doi:10.3233/JAD-2011-101866 DB - PRIME DP - Unbound Medicine ER -