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:
https://lup.lub.lu.se/record/2826890
- author
- Capetillo-Zarate, Estibaliz
; Gracia, Luis
; Tampellini, Davide
LU
and Gouras, Gunnar
LU
- organization
- publishing date
- 2012
- 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
- pmid:22269167
- 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
- 2016-04-01 10:48:28
- date last changed
- 2022-04-04 21:29:11
@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}},
keywords = {{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}},
doi = {{10.1159/000334762}},
volume = {{10}},
year = {{2012}},
}