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Apolipoprotein E polymorphism and dendritic shape in hippocampal interneurons

Authors
Journal
Neurobiology of Aging
0197-4580
Publisher
Elsevier
Publication Date
Volume
28
Issue
5
Identifiers
DOI: 10.1016/j.neurobiolaging.2006.03.016
Keywords
  • Alzheimer'S Disease
  • Apolipoprotein E (Apoe)
  • Dendritic Plasticity
  • Hippocampus
  • Parvalbumin
Disciplines
  • Biology
  • Mathematics
  • Medicine

Abstract

Abstract The apolipoprotein E genetic polymorphism exerts a well described influence on Alzheimer's disease (AD) risk, although the pathogenetic mechanism is still not clear. Increasing evidence points to a diminished neuroplasticity in apolipoprotein E ɛ4-allele carriers. But, alternatively or additionally, developmental differences in dendritic geometry may be associated with the polymorphism. We morphometrically examined the dendritic ramification of CA1 Parvalbumin-positive GABAergic hippocampal neurons ( n = 571) in matched pairs of aged non-demented individuals with different apolipoprotein E genotype. We chose Parvalbumin-positive interneurons since they lack potentially confounding AD-like cytoskeletal changes. To minimize the risk of transneuronal dendritic changes due to significant deafferentation we focused on non-demented individuals. In this chosen paradigm, neither the disease-associated apolipoprotein E ɛ4-allele nor the apolipoprotein E ɛ2-allele had a significant impact on dendritic shape when compared to the most common allelic variant apolipoprotein E ɛ3/3. At least with respect to the studied cell type, the data suggest that the apolipoprotein E polymorphism does not modulate the original formation of dendrites in vivo, contrary to conclusions drawn from in vitro studies on neurite outgrowth.

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