NDLI: ApoE4 Decreases Spine Density and Dendritic Complexity in Cortical Neurons in vivo

Content Provider	PubMed Central
Author	Dumanis, Sonya B. Tesoriero, Joseph A. Babus, Lenard W. Nguyen, Tuong-vi Trotter, Justin H. Ladu, Mary Jo Weeber, Edwin J. Turner, R. Scott Xu, Baoji Rebeck, G. William Hoe, Hyang-sook
Abstract	The three human alleles of apolipoprotein E (APOE) differentially influence outcome after CNS injury and affect one’s risk of developing Alzheimer’s disease (AD). It remains unclear how ApoE isoforms contribute to various AD-related pathological changes (e.g. amyloid plaques, synaptic and neuron loss). Here, we systematically examined whether apoE isoforms (E2, E3, E4) exhibit differential effects on dendritic spine density and morphology in APOE targeted replacement (TR) mice which lack AD pathological changes. Using Golgi staining, we found age-dependent effects of APOE4 on spine density in the cortex. The APOE4 TR mice had significantly reduced spine density at three independent time points (4 weeks, 3 months, and 1 year, 27.7% ± 7.4%, 24.4% ± 8.6%, 55.6% ± 10.5%, respectively) compared to APOE3 TR mice and APOE2 TR mice. Additionally, in APOE4 TR mice, shorter spines were evident compared to other APOE TR mice at 1 year. APOE2 TR mice exhibited longer spines as well as significantly increased apical dendritic arborization in the cortex compared to APOE4 and APOE3 TR mice at 4 weeks. However, there were no differences in spine density across APOE genotypes in hippocampus. These findings demonstrate that apoE isoforms differentially affect dendritic complexity and spine formation, suggesting a role for APOE genotypes not only in acute and chronic brain injuries including AD, but also in normal brain functions.
Related Links	http://dx.doi.org/10.1523/jneurosci.4026-09.2009
Ending Page	15322
Page Count	6
Starting Page	15317
File Format	PDF
ISSN	02706474
e-ISSN	15292401
Journal	The Journal of neuroscience : the official journal of the Society for Neuroscience
Issue Number	48
Volume Number	29
Language	English
Publisher Date	2009-12-02
Access Restriction	Open
Subject Keyword	Neuroscience(all) Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Neuroscience

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