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Intraneuronal A beta Accumulation, Amyloid Plaques, and Synapse Pathology in Alzheimer's Disease

Capetillo-Zarate, Estibaliz; Gracia, Luis; Tampellini, Davide LU and Gouras, Gunnar LU (2012) In Neurodegenerative Diseases 10(1-4). p.56-59
Abstract
Background: beta-Amyloid (A beta) plaques are a pathological hallmark of Alzheimer's disease (AD) and multiple lines of evidence have linked A beta with AD. However, synapse loss is known as the best pathological correlate of cognitive impairment in AD, and intraneuronal A beta accumulation has been shown to precede plaque pathology. The progression of A beta accumulation to synapse loss and plaque formation remains incomplete. The objective is to investigate the progression of intraneuronal A beta accumulation in the brain. Methods: To visualize and analyze the development of A beta pathology we perform immunohistochemistry and immunofluorescence microscopy using antibodies against different A beta conformations, synaptic proteins and... (More)
Background: beta-Amyloid (A beta) plaques are a pathological hallmark of Alzheimer's disease (AD) and multiple lines of evidence have linked A beta with AD. However, synapse loss is known as the best pathological correlate of cognitive impairment in AD, and intraneuronal A beta accumulation has been shown to precede plaque pathology. The progression of A beta accumulation to synapse loss and plaque formation remains incomplete. The objective is to investigate the progression of intraneuronal A beta accumulation in the brain. Methods: To visualize and analyze the development of A beta pathology we perform immunohistochemistry and immunofluorescence microscopy using antibodies against different A beta conformations, synaptic proteins and structural neuronal proteins in brain tissue of AD transgenic mouse models. Results: Our results show the intraneuronal onset of A beta 42 accumulation in AD mouse brains with aging. We observe an inverse correlation of A beta 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 A beta 42 accumulation and aggregation begin within AD-vulnerable neurons in the brain. Progressive intraneuronal A beta 42 aggregation disrupts the normal cytoarchitecture of neurites. Copyright (C) 2012 S. Karger AG, Basel (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Amyloid, Neuropathology, Alzheimer's disease, Synapse
in
Neurodegenerative Diseases
volume
10
issue
1-4
pages
56 - 59
publisher
Karger
external identifiers
  • wos:000303660600011
  • scopus:84860216294
ISSN
1660-2862
DOI
10.1159/000334762
language
English
LU publication?
yes
id
9126f5c6-295c-48cf-94a0-8989f7460f1d (old id 2826890)
date added to LUP
2012-07-03 10:27:10
date last changed
2017-01-01 03:54:57
@article{9126f5c6-295c-48cf-94a0-8989f7460f1d,
  abstract     = {Background: beta-Amyloid (A beta) plaques are a pathological hallmark of Alzheimer's disease (AD) and multiple lines of evidence have linked A beta with AD. However, synapse loss is known as the best pathological correlate of cognitive impairment in AD, and intraneuronal A beta accumulation has been shown to precede plaque pathology. The progression of A beta accumulation to synapse loss and plaque formation remains incomplete. The objective is to investigate the progression of intraneuronal A beta accumulation in the brain. Methods: To visualize and analyze the development of A beta pathology we perform immunohistochemistry and immunofluorescence microscopy using antibodies against different A beta conformations, synaptic proteins and structural neuronal proteins in brain tissue of AD transgenic mouse models. Results: Our results show the intraneuronal onset of A beta 42 accumulation in AD mouse brains with aging. We observe an inverse correlation of A beta 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 A beta 42 accumulation and aggregation begin within AD-vulnerable neurons in the brain. Progressive intraneuronal A beta 42 aggregation disrupts the normal cytoarchitecture of neurites. Copyright (C) 2012 S. Karger AG, Basel},
  author       = {Capetillo-Zarate, Estibaliz and Gracia, Luis and Tampellini, Davide and Gouras, Gunnar},
  issn         = {1660-2862},
  keyword      = {Amyloid,Neuropathology,Alzheimer's disease,Synapse},
  language     = {eng},
  number       = {1-4},
  pages        = {56--59},
  publisher    = {Karger},
  series       = {Neurodegenerative Diseases},
  title        = {Intraneuronal A beta Accumulation, Amyloid Plaques, and Synapse Pathology in Alzheimer's Disease},
  url          = {http://dx.doi.org/10.1159/000334762},
  volume       = {10},
  year         = {2012},
}