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Volume 12 Supplement 1

Abstracts from Hydrocephalus 2015

  • Poster presentation
  • Open Access

Amyloid deposition and ApoE4 carriers in idiopathic normal pressure hydrocephalus

  • 1Email author,
  • 1,
  • 1,
  • 1,
  • 1,
  • 1 and
  • 1
Fluids and Barriers of the CNS201512 (Suppl 1) :P5

https://doi.org/10.1186/2045-8118-12-S1-P5

  • Published:

Keywords

  • General Population
  • Hydrocephalus
  • Bonferroni Correction
  • Specific Effect
  • Alzheimer Disease

Introduction

It is known that idiopathic normal pressure hydrocephalus (iNPH) can co-morbid with Alzheimer disease (AD). Previous studies, probing amyloid (Aβ) deposition by cortical biopsy during a ventriculo-peritoneal shunt, have shown that Aβ deposition was found in 40~45 % of iNPH patients. However, the reason for this high prevalence is not well understood. Therefore, the objective of this study was to investigate whether the prevalence of the Aβ deposition in iNPH is explainable by a simple overlap of the AD pathology in general population, or is modified by some specific effects of iNPH.

Methods

In this study, 11C-Pittsburgh compound B (11C-PiB) PET and Apolipoprotein E genotype were examined in age- matched 70 Cognitively Normal Elderly (CNE), 19 Alzheimer disease (AD) and 31 probable iNPH patients, to investigate the risk of co-morbidity of AD in iNPH patients. The chi-square analysis was used for the statistical analysis. The Bonferroni correction was used for the multiple comparisons.

Results

Amyloid deposition was shown in 19.0% of CNE, 81.3% of AD, and 52.0% of iNPH, while ApoE4 carriers were found in 19.0% of CNE, 73.7% of AD, and 29.0 of iNPH. The rate of amyloid deposition of iNPH was significantly higher than CNE (p < 0.005) and lower than AD (p < 0.005). On the other hand, the probability of the apoE4 carriers in iNPH was significantly lower than AD (p < 0.005), but did not show any significant difference from CNE (p = 0.56).

Conclusions

In iNPH, the rate of amyloid deposition is higher than CNE, while there were no differences in the probability of the ApoE4 carriers. These results suggest that iNPH patients may have some mechanisms to facilitate the amyloid deposition.

Authors’ Affiliations

(1)
National center for geriatrics and gerontology, Japan

Copyright

© Bundo et al. 2015

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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