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Abnormal structural brain connectome in individuals with preclinical Alzheimer's disease

Pereira, Joana B. LU ; Van Westen, Danielle LU ; Stomrud, Erik LU ; Strandberg, Tor Olof; Volpe, Giovanni; Westman, Eric and Hansson, Oskar LU (2018) In Cerebral Cortex 28(10). p.3638-3649
Abstract

Alzheimer's disease has a long preclinical phase during which amyloid pathology and neurodegeneration accumulate in the brain without producing overt cognitive deficits. It is currently unclear whether these early disease stages are associated with a progressive disruption in the communication between brain regions that subsequently leads to cognitive decline and dementia. In this study we assessed the organization of structural networks in cognitively normal (CN) individuals harboring amyloid pathology (A+N-), neurodegeneration (A-N+), or both (A+N+) from the prospective and longitudinal Swedish BioFINDER study. We combined graph theory with diffusion tensor imaging to investigate integration, segregation, and centrality measures in... (More)

Alzheimer's disease has a long preclinical phase during which amyloid pathology and neurodegeneration accumulate in the brain without producing overt cognitive deficits. It is currently unclear whether these early disease stages are associated with a progressive disruption in the communication between brain regions that subsequently leads to cognitive decline and dementia. In this study we assessed the organization of structural networks in cognitively normal (CN) individuals harboring amyloid pathology (A+N-), neurodegeneration (A-N+), or both (A+N+) from the prospective and longitudinal Swedish BioFINDER study. We combined graph theory with diffusion tensor imaging to investigate integration, segregation, and centrality measures in the brain connectome in the previous groups. At baseline, our findings revealed a disrupted network topology characterized by longer paths, lower efficiency, increased clustering and modularity in CN A-N+ and CN A+N+, but not in CN A+N-. After 2 years, CN A+N+ showed significant abnormalities in all global network measures, whereas CN A-N+ only showed abnormalities in the global efficiency. Network connectivity and organization were associated with memory in CN A+N+ individuals. Altogether, our findings suggest that amyloid pathology is not sufficient to disrupt structural network topology, whereas neurodegeneration is.

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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
amyloid, diffusion tensor imaging, graph theory, neurodegeneration, structural connectivity
in
Cerebral Cortex
volume
28
issue
10
pages
12 pages
publisher
Oxford University Press
external identifiers
  • scopus:85046635478
ISSN
1047-3211
DOI
10.1093/cercor/bhx236
language
English
LU publication?
yes
id
444c37c4-0915-4011-b70b-3b0286294f89
date added to LUP
2019-05-28 22:49:39
date last changed
2019-09-17 04:55:28
@article{444c37c4-0915-4011-b70b-3b0286294f89,
  abstract     = {<p>Alzheimer's disease has a long preclinical phase during which amyloid pathology and neurodegeneration accumulate in the brain without producing overt cognitive deficits. It is currently unclear whether these early disease stages are associated with a progressive disruption in the communication between brain regions that subsequently leads to cognitive decline and dementia. In this study we assessed the organization of structural networks in cognitively normal (CN) individuals harboring amyloid pathology (A+N-), neurodegeneration (A-N+), or both (A+N+) from the prospective and longitudinal Swedish BioFINDER study. We combined graph theory with diffusion tensor imaging to investigate integration, segregation, and centrality measures in the brain connectome in the previous groups. At baseline, our findings revealed a disrupted network topology characterized by longer paths, lower efficiency, increased clustering and modularity in CN A-N+ and CN A+N+, but not in CN A+N-. After 2 years, CN A+N+ showed significant abnormalities in all global network measures, whereas CN A-N+ only showed abnormalities in the global efficiency. Network connectivity and organization were associated with memory in CN A+N+ individuals. Altogether, our findings suggest that amyloid pathology is not sufficient to disrupt structural network topology, whereas neurodegeneration is.</p>},
  author       = {Pereira, Joana B. and Van Westen, Danielle and Stomrud, Erik and Strandberg, Tor Olof and Volpe, Giovanni and Westman, Eric and Hansson, Oskar},
  issn         = {1047-3211},
  keyword      = {amyloid,diffusion tensor imaging,graph theory,neurodegeneration,structural connectivity},
  language     = {eng},
  month        = {10},
  number       = {10},
  pages        = {3638--3649},
  publisher    = {Oxford University Press},
  series       = {Cerebral Cortex},
  title        = {Abnormal structural brain connectome in individuals with preclinical Alzheimer's disease},
  url          = {http://dx.doi.org/10.1093/cercor/bhx236},
  volume       = {28},
  year         = {2018},
}