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Vol. 10, No. 1-4, 2012
Issue release date: April 2012
Section title: Paper
Neurodegenerative Dis 2012;10:56–59
(DOI:10.1159/000334762)

Intraneuronal Aβ Accumulation, Amyloid Plaques, and Synapse Pathology in Alzheimer’s Disease

Capetillo-Zarate E. · Gracia L. · Tampellini D. · Gouras G.K.
aDepartment of Neurology and Neuroscience, and bThe HRH Prince Alwaleed Bin Talal Bin Abdulaziz Alsaud Institute for Computational Biomedicine, Weill Cornell Medical College, New York, N.Y., USA; cWallenberg Neuroscience Center, Department of Experimental Medical Science, Lund University, Lund, Sweden

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Article / Publication Details

First-Page Preview
Abstract of Paper

Received: 7/1/2011 4:01:58 PM
Accepted: 10/28/2011
Published online: 1/21/2012

Number of Print Pages: 4
Number of Figures: 1
Number of Tables: 0

ISSN: 1660-2854 (Print)
eISSN: 1660-2862 (Online)

For additional information: http://www.karger.com/NDD

Abstract

Background: β-Amyloid (Aβ) plaques are a pathological hallmark of Alzheimer’s disease (AD) and multiple lines of evidence have linked Aβ with AD. However, synapse loss is known as the best pathological correlate of cognitive impairment in AD, and intraneuronal Aβ accumulation has been shown to precede plaque pathology. The progression of Aβ accumulation to synapse loss and plaque formation remains incomplete. The objective is to investigate the progression of intraneuronal Aβ accumulation in the brain. Methods: To visualize and analyze the development of Aβ pathology we perform immunohistochemistry and immunofluorescence microscopy using antibodies against different Aβ conformations, synaptic proteins and structural neuronal proteins in brain tissue of AD transgenic mouse models. Results: Our results show the intraneuronal onset of Aβ42 accumulation in AD mouse brains with aging. We observe an inverse correlation of Aβ and amyloid fibrils with structural proteins within neurites. Images reveal aggregated amyloid within selective pyramidal neurons, neurites and synapses in AD transgenic mice as plaques arise. Conclusion: The data support that Aβ42 accumulation and aggregation begin within AD-vulnerable neurons in the brain. Progressive intraneuronal Aβ42 aggregation disrupts the normal cytoarchitecture of neurites.


  

Author Contacts

Estibaliz Capetillo-Zarate, PhD
Department of Neurology and Neuroscience, Weill Cornell Medical College
1300 York Avenue, A569E
New York, NY 10065 (USA)
Tel. +1 212 746 4570, E-Mail cae2006@med.cornell.edu

  

Article Information

Received: July 1, 2011
Accepted after revision: October 28, 2011
Published online: January 21, 2012
Number of Print Pages : 4
Number of Figures : 1, Number of Tables : 0, Number of References : 35

  

Publication Details

Neurodegenerative Diseases

Vol. 10, No. 1-4, Year 2012 (Cover Date: April 2012)

Journal Editor: Nitsch R.M. (Zürich), Hock C. (Zürich)
ISSN: 1660-2854 (Print), eISSN: 1660-2862 (Online)

For additional information: http://www.karger.com/NDD


Article / Publication Details

First-Page Preview
Abstract of Paper

Received: 7/1/2011 4:01:58 PM
Accepted: 10/28/2011
Published online: 1/21/2012

Number of Print Pages: 4
Number of Figures: 1
Number of Tables: 0

ISSN: 1660-2854 (Print)
eISSN: 1660-2862 (Online)

For additional information: http://www.karger.com/NDD


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