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Lesion-induced hippocampal plasticity in transgenic Alzheimer's disease mouse models: influences of age, genotype, and estrogen.
J Alzheimers Dis. 2009; 18(2):429-45.JA

Abstract

We have studied entorhinal cortex lesion-induced sprouting in the hippocampus in young, adult, and aged control and transgenic Alzheimer's disease model mice. The entorhinal cortex was unilaterally, partially lesioned, and four weeks later the subsequent axonal sprouting in dentate gyrus was analyzed. Our data demonstrate that young and adult, control and amyloid-beta protein precursor (AbetaPP)/presenilin 1 (PS1) mice display a significantly increased density of staining for synaptophysin in dentate gyrus, indicative of axonal sprouting. However, whereas young and adult mice demonstrate sprouting, aged mice (control and AbetaPP/PS1) do not show a significant upregulation of synaptophysin staining following the lesions. In contrast, aged mice overexpressing PS1 show an increased regenerative response compared to age-matched control mice and mice overexpressing AbetaPP which do not show sprouting. Further, the data demonstrate that a significant Abeta load in the dentate gyrus does not prevent axonal sprouting. Lastly, only aged mice show significant shrinkage of the molecular layer of dentate gyrus following entorhinal cortex lesions. Further, adult ovariectomized females (control and AbetaPP/PS1) are significantly reduced in their plasticity following lesions. Taken together, the data indicate that amyloid-beta deposits do not negatively impact plasticity in the brain and that overexpression of AbetaPP is not beneficial, but that normal estrogen levels are beneficial for plasticity.

Authors+Show Affiliations

Department of Cell Biology, University of Alabama at Birmingham, Birmingham, AL 35294, USA. ikadisha@uab.eduNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

19584452

Citation

Kadish, Inga, and Thomas van Groen. "Lesion-induced Hippocampal Plasticity in Transgenic Alzheimer's Disease Mouse Models: Influences of Age, Genotype, and Estrogen." Journal of Alzheimer's Disease : JAD, vol. 18, no. 2, 2009, pp. 429-45.
Kadish I, van Groen T. Lesion-induced hippocampal plasticity in transgenic Alzheimer's disease mouse models: influences of age, genotype, and estrogen. J Alzheimers Dis. 2009;18(2):429-45.
Kadish, I., & van Groen, T. (2009). Lesion-induced hippocampal plasticity in transgenic Alzheimer's disease mouse models: influences of age, genotype, and estrogen. Journal of Alzheimer's Disease : JAD, 18(2), 429-45. https://doi.org/10.3233/JAD-2009-1157
Kadish I, van Groen T. Lesion-induced Hippocampal Plasticity in Transgenic Alzheimer's Disease Mouse Models: Influences of Age, Genotype, and Estrogen. J Alzheimers Dis. 2009;18(2):429-45. PubMed PMID: 19584452.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Lesion-induced hippocampal plasticity in transgenic Alzheimer's disease mouse models: influences of age, genotype, and estrogen. AU - Kadish,Inga, AU - van Groen,Thomas, PY - 2009/7/9/entrez PY - 2009/7/9/pubmed PY - 2009/12/18/medline SP - 429 EP - 45 JF - Journal of Alzheimer's disease : JAD JO - J Alzheimers Dis VL - 18 IS - 2 N2 - We have studied entorhinal cortex lesion-induced sprouting in the hippocampus in young, adult, and aged control and transgenic Alzheimer's disease model mice. The entorhinal cortex was unilaterally, partially lesioned, and four weeks later the subsequent axonal sprouting in dentate gyrus was analyzed. Our data demonstrate that young and adult, control and amyloid-beta protein precursor (AbetaPP)/presenilin 1 (PS1) mice display a significantly increased density of staining for synaptophysin in dentate gyrus, indicative of axonal sprouting. However, whereas young and adult mice demonstrate sprouting, aged mice (control and AbetaPP/PS1) do not show a significant upregulation of synaptophysin staining following the lesions. In contrast, aged mice overexpressing PS1 show an increased regenerative response compared to age-matched control mice and mice overexpressing AbetaPP which do not show sprouting. Further, the data demonstrate that a significant Abeta load in the dentate gyrus does not prevent axonal sprouting. Lastly, only aged mice show significant shrinkage of the molecular layer of dentate gyrus following entorhinal cortex lesions. Further, adult ovariectomized females (control and AbetaPP/PS1) are significantly reduced in their plasticity following lesions. Taken together, the data indicate that amyloid-beta deposits do not negatively impact plasticity in the brain and that overexpression of AbetaPP is not beneficial, but that normal estrogen levels are beneficial for plasticity. SN - 1875-8908 UR - https://www.unboundmedicine.com/medline/citation/19584452/Lesion_induced_hippocampal_plasticity_in_transgenic_Alzheimer's_disease_mouse_models:_influences_of_age_genotype_and_estrogen_ L2 - https://content.iospress.com/openurl?genre=article&issn=1387-2877&volume=18&issue=2&spage=429 DB - PRIME DP - Unbound Medicine ER -