Skip to main content

Main menu

  • HOME
  • CONTENT
    • Early Release
    • Featured
    • Current Issue
    • Issue Archive
    • Collections
    • Podcast
  • ALERTS
  • FOR AUTHORS
    • Information for Authors
    • Fees
    • Journal Clubs
    • eLetters
    • Submit
    • Special Collections
  • EDITORIAL BOARD
    • Editorial Board
    • ECR Advisory Board
    • Journal Staff
  • ABOUT
    • Overview
    • Advertise
    • For the Media
    • Rights and Permissions
    • Privacy Policy
    • Feedback
    • Accessibility
  • SUBSCRIBE

User menu

  • Log out
  • Log in
  • My Cart

Search

  • Advanced search
Journal of Neuroscience
  • Log out
  • Log in
  • My Cart
Journal of Neuroscience

Advanced Search

Submit a Manuscript
  • HOME
  • CONTENT
    • Early Release
    • Featured
    • Current Issue
    • Issue Archive
    • Collections
    • Podcast
  • ALERTS
  • FOR AUTHORS
    • Information for Authors
    • Fees
    • Journal Clubs
    • eLetters
    • Submit
    • Special Collections
  • EDITORIAL BOARD
    • Editorial Board
    • ECR Advisory Board
    • Journal Staff
  • ABOUT
    • Overview
    • Advertise
    • For the Media
    • Rights and Permissions
    • Privacy Policy
    • Feedback
    • Accessibility
  • SUBSCRIBE
PreviousNext
Neurobiology of Disease

Treatment with an Amyloid-β Antibody Ameliorates Plaque Load, Learning Deficits, and Hippocampal Long-Term Potentiation in a Mouse Model of Alzheimer's Disease

Richard E. Hartman, Yukitoshi Izumi, Kelly R. Bales, Steven M. Paul, David F. Wozniak and David M. Holtzman
Journal of Neuroscience 29 June 2005, 25 (26) 6213-6220; https://doi.org/10.1523/JNEUROSCI.0664-05.2005
Richard E. Hartman
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Yukitoshi Izumi
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Kelly R. Bales
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Steven M. Paul
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
David F. Wozniak
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
David M. Holtzman
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • Article
  • Figures & Data
  • Info & Metrics
  • eLetters
  • PDF
Loading

Article Figures & Data

Figures

  • Tables
  •   Figure 1.
    • Download figure
    • Open in new tab
    • Download powerpoint
    Figure 1.

    PDAPP mice on a C57BL/6 background exhibit profound spatial learning deficits from an early age. Performance was assessed by distance to find the visible platform (cued) versus the hidden platform (spatial positions 1-5) in the water maze. Each point represents the average of four daily trials. Significant main effects of genotype are indicated by *, and a significant genotype-by-day interaction is indicated by **. Error bars represent SEM.

  •   Figure 2.
    • Download figure
    • Open in new tab
    • Download powerpoint
    Figure 2.

    Old mice of each genotype perform worse than young or middle-aged mice in the spatial version of the water maze. Each point represents the average of four daily trials. Significant main effects of age are indicated by *. Error bars represent SEM.

  •   Figure 3.
    • Download figure
    • Open in new tab
    • Download powerpoint
    Figure 3.

    PDAPP mice developed more severe age-dependent spatial learning deficits than wild-type mice. Average swim distance across all five platform positions was assessed. Each bar represents the average performance across all platform positions. Significant main effects of genotype are indicated by **, and a significant genotype-by-age interaction is indicated by **. Error bars represent SEM.

  •   Figure 4.
    • Download figure
    • Open in new tab
    • Download powerpoint
    Figure 4.

    Both Aβ (A) and thioflavine-S+ Aβ (B) load increased with age in PDAPP mice. Significant main effects of age are indicated by *. Error bars represent SEM.

  •   Figure 5.
    • Download figure
    • Open in new tab
    • Download powerpoint
    Figure 5.

    Treatment with 10D5 improved the spatial learning performance of aged PDAPP mice. Each point represents the average of four daily trials. Significant main effects of age are indicated by *. Error bars represent SEM.

  •   Figure 6.
    • Download figure
    • Open in new tab
    • Download powerpoint
    Figure 6.

    Treatment with 10D5 reduced Aβ (A) and thioflavine-S+ Aβ (B) load and increased Aβ40 (C) and Aβ42 (D) levels in the plasma of aged PDAPP mice. Significant main effects of age are indicated by *. Error bars represent SEM.

  •   Figure 7.
    • Download figure
    • Open in new tab
    • Download powerpoint
    Figure 7.

    Treatment with 10 D5 improved hippocampal LTP in aged PDAPP mice. A, Six series of tetanic bursts consisting of six trains of six pulses were delivered at time 0 (arrows). At 60 min after tetani, PDAPP plus saline mice exhibited impaired LTP compared with PDAPP plus 10D5 and WT mice. B, The bars represent levels of LTP 60 min after the induction of tetani. Traces depict EPSPs before (dotted traces) and 60 min after (solid traces) tetanic bursts. Error bars represent SEM.

Tables

  • Figures
    • View popup
    Table 1.

    ELISA hippocampal Aβ levels (pg/μg protein; means ± SE)

    Assay Young Old p
    PDAPP carbonate-soluble Aβ40 0.29 ± 0.03 2.95 ± 0.67 0.0002
    PDAPP carbonate-insoluble Aβ40 1.21 ± 0.15 67.23 ± 15.56 0.00008
    PDAPP carbonate-soluble Aβ42 0.38 ± 0.05 14.97 ± 3.17 0.00003
    PDAPP carbonate-insoluble Aβ42 4.81 ± 0.65 667.89 ± 143.61 0.00003
    WT carbonate-soluble Aβ40 0.07 ± 0.01 0.09 ± 0.01 NS
    WT carbonate-insoluble Aβ40 0.11 ± 0.02 0.13 ± 0.02 NS
    WT carbonate-soluble Aβ42 0.03 ± 0.003 0.04 ± 0.004 NS
    WT carbonate-insoluble Aβ42 0.12 ± 0.01 0.16 ± 0.01 NS
    • View popup
    Table 2.

    ELISA Aβ levels (means ± SE)

    Assay PDAPP plus saline PDAPP plus 10D5 p
    Plasma Aβ40a 60.5 ± 7 143.2 ± 17.6 0.0001
    Plasma Aβ42a 21.9 ± 5.5 544 ± 253.9 0.04
    Carbonate-soluble hippocampal Aβ40b 10.27 ± 7.22 8.88 ± 1.71 NS
    Carbonate-insoluble hippocampal Aβ40b 276.59 ± 122.23 190.13 ± 41.15 NS
    Carbonate-soluble hippocampal Aβ42b 37.82 ± 8.35 34.98 ± 5.38 NS
    Carbonate-insoluble hippocampal Aβ42b 1,275.15 ± 743.33 939.25 ± 232.44 NS
    • ↵ a Picograms of protein per milliliter.

    • ↵ b Picograms of protein per microliter.

Back to top

In this issue

The Journal of Neuroscience: 25 (26)
Journal of Neuroscience
Vol. 25, Issue 26
29 Jun 2005
  • Table of Contents
  • About the Cover
  • Index by author
Email

Thank you for sharing this Journal of Neuroscience article.

NOTE: We request your email address only to inform the recipient that it was you who recommended this article, and that it is not junk mail. We do not retain these email addresses.

Enter multiple addresses on separate lines or separate them with commas.
Treatment with an Amyloid-β Antibody Ameliorates Plaque Load, Learning Deficits, and Hippocampal Long-Term Potentiation in a Mouse Model of Alzheimer's Disease
(Your Name) has forwarded a page to you from Journal of Neuroscience
(Your Name) thought you would be interested in this article in Journal of Neuroscience.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Print
View Full Page PDF
Citation Tools
Treatment with an Amyloid-β Antibody Ameliorates Plaque Load, Learning Deficits, and Hippocampal Long-Term Potentiation in a Mouse Model of Alzheimer's Disease
Richard E. Hartman, Yukitoshi Izumi, Kelly R. Bales, Steven M. Paul, David F. Wozniak, David M. Holtzman
Journal of Neuroscience 29 June 2005, 25 (26) 6213-6220; DOI: 10.1523/JNEUROSCI.0664-05.2005

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Respond to this article
Request Permissions
Share
Treatment with an Amyloid-β Antibody Ameliorates Plaque Load, Learning Deficits, and Hippocampal Long-Term Potentiation in a Mouse Model of Alzheimer's Disease
Richard E. Hartman, Yukitoshi Izumi, Kelly R. Bales, Steven M. Paul, David F. Wozniak, David M. Holtzman
Journal of Neuroscience 29 June 2005, 25 (26) 6213-6220; DOI: 10.1523/JNEUROSCI.0664-05.2005
Twitter logo Facebook logo Mendeley logo
  • Tweet Widget
  • Facebook Like
  • Google Plus One

Jump to section

  • Article
    • Abstract
    • Introduction
    • Materials and Methods
    • Results
    • Discussion
    • Footnotes
    • References
  • Figures & Data
  • Info & Metrics
  • eLetters
  • PDF

Responses to this article

Respond to this article

Jump to comment:

No eLetters have been published for this article.

Related Articles

Cited By...

More in this TOC Section

  • Disruption of grin2A, an epilepsy-associated gene, produces altered spontaneous swim behavior in zebrafish
  • Unveiling cortical criticality changes along the prodromal to the overt continuum of alpha-synucleinopathy
  • Atypical Retinal Ganglion Cell Function in a Mouse Model of Fragile X Syndrome
Show more Neurobiology of Disease
  • Home
  • Alerts
  • Follow SFN on BlueSky
  • Visit Society for Neuroscience on Facebook
  • Follow Society for Neuroscience on Twitter
  • Follow Society for Neuroscience on LinkedIn
  • Visit Society for Neuroscience on Youtube
  • Follow our RSS feeds

Content

  • Early Release
  • Current Issue
  • Issue Archive
  • Collections

Information

  • For Authors
  • For Advertisers
  • For the Media
  • For Subscribers

About

  • About the Journal
  • Editorial Board
  • Privacy Notice
  • Contact
  • Accessibility
(JNeurosci logo)
(SfN logo)

Copyright © 2025 by the Society for Neuroscience.
JNeurosci Online ISSN: 1529-2401

The ideas and opinions expressed in JNeurosci do not necessarily reflect those of SfN or the JNeurosci Editorial Board. Publication of an advertisement or other product mention in JNeurosci should not be construed as an endorsement of the manufacturer’s claims. SfN does not assume any responsibility for any injury and/or damage to persons or property arising from or related to any use of any material contained in JNeurosci.