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Cortical atrophy in presymptomatic Alzheimer's disease presenilin 1 mutation carriers

Background Sporadic late-onset Alzheimer's disease (AD) dementia has been associated with a ‘signature’ of cortical atrophy in paralimbic and heteromodal association regions measured with MRI. Objective To investigate whether a similar pattern of cortical atrophy is present in presymptomatic preseni... Full description

Journal Title: Journal of Neurology Neurosurgery & Psychiatry, 2013-05, Vol.84 (5), p.556-561
Main Author: Quiroz, Yakeel T
Other Authors: Stern, Chantal E , Reiman, Eric M , Brickhouse, Michael , Ruiz, Adriana , Sperling, Reisa A , Lopera, Francisco , Dickerson, Bradford C
Format: Electronic Article Electronic Article
Language: English
Subjects:
MRI
Publisher: England: BMJ Publishing Group Ltd
ID: ISSN: 0022-3050
Link: https://www.ncbi.nlm.nih.gov/pubmed/23134660
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title: Cortical atrophy in presymptomatic Alzheimer's disease presenilin 1 mutation carriers
format: Article
creator:
  • Quiroz, Yakeel T
  • Stern, Chantal E
  • Reiman, Eric M
  • Brickhouse, Michael
  • Ruiz, Adriana
  • Sperling, Reisa A
  • Lopera, Francisco
  • Dickerson, Bradford C
subjects:
  • Adult
  • Alzheimer Disease - genetics
  • Alzheimer Disease - pathology
  • Alzheimer's Disease
  • Analysis
  • Article
  • Atrophy
  • Cerebral Cortex - pathology
  • Diagnosis
  • DNA - genetics
  • Female
  • genetics
  • Heterozygote
  • Humans
  • Magnetic Resonance Imaging
  • Male
  • Memory - physiology
  • Mental Recall - physiology
  • MRI
  • Mutation - genetics
  • Neuropsychological Tests
  • Presenilin-1 - genetics
  • Recognition, Psychology - physiology
  • Socioeconomic Factors
  • Temporal lobes
  • Verbal Behavior - physiology
ispartof: Journal of Neurology, Neurosurgery & Psychiatry, 2013-05, Vol.84 (5), p.556-561
description: Background Sporadic late-onset Alzheimer's disease (AD) dementia has been associated with a ‘signature’ of cortical atrophy in paralimbic and heteromodal association regions measured with MRI. Objective To investigate whether a similar pattern of cortical atrophy is present in presymptomatic presenilin 1 E280A mutation carriers an average of 6 years before clinical symptom onset. Methods 40 cognitively normal volunteers from a Colombian population with familial AD were included; 18 were positive for the AD-associated presenilin 1 mutation (carriers, mean age=38) whereas 22 were non-carriers. T1-weighted volumetric MRI images were acquired and cortical thickness was measured. A priori regions of interest from our previous work were used to obtain thickness from AD-signature regions. Results Compared to non-carriers, presymptomatic presenilin 1 mutation carriers exhibited thinner cortex within the AD-signature summary measure (p
language: eng
source:
identifier: ISSN: 0022-3050
fulltext: no_fulltext
issn:
  • 0022-3050
  • 1468-330X
url: Link


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titleCortical atrophy in presymptomatic Alzheimer's disease presenilin 1 mutation carriers
creatorQuiroz, Yakeel T ; Stern, Chantal E ; Reiman, Eric M ; Brickhouse, Michael ; Ruiz, Adriana ; Sperling, Reisa A ; Lopera, Francisco ; Dickerson, Bradford C
creatorcontribQuiroz, Yakeel T ; Stern, Chantal E ; Reiman, Eric M ; Brickhouse, Michael ; Ruiz, Adriana ; Sperling, Reisa A ; Lopera, Francisco ; Dickerson, Bradford C
descriptionBackground Sporadic late-onset Alzheimer's disease (AD) dementia has been associated with a ‘signature’ of cortical atrophy in paralimbic and heteromodal association regions measured with MRI. Objective To investigate whether a similar pattern of cortical atrophy is present in presymptomatic presenilin 1 E280A mutation carriers an average of 6 years before clinical symptom onset. Methods 40 cognitively normal volunteers from a Colombian population with familial AD were included; 18 were positive for the AD-associated presenilin 1 mutation (carriers, mean age=38) whereas 22 were non-carriers. T1-weighted volumetric MRI images were acquired and cortical thickness was measured. A priori regions of interest from our previous work were used to obtain thickness from AD-signature regions. Results Compared to non-carriers, presymptomatic presenilin 1 mutation carriers exhibited thinner cortex within the AD-signature summary measure (p<0.008). Analyses of individual regions demonstrated thinner angular gyrus, precuneus and superior parietal lobule in carriers compared to non-carriers, with trend-level effects in the medial temporal lobe. Conclusion Results demonstrate that cognitively normal individuals genetically determined to develop AD have a thinner cerebral cortex than non-carriers in regions known to be affected by typical late-onset sporadic AD. These findings provide further support for the hypothesis that cortical atrophy is present in preclinical AD more than 5 years prior to symptom onset. Further research is needed to determine whether this method could be used to characterise the age-dependent trajectory of cortical atrophy in presymptomatic stages of AD.
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subjectAdult ; Alzheimer Disease - genetics ; Alzheimer Disease - pathology ; Alzheimer's Disease ; Analysis ; Article ; Atrophy ; Cerebral Cortex - pathology ; Diagnosis ; DNA - genetics ; Female ; genetics ; Heterozygote ; Humans ; Magnetic Resonance Imaging ; Male ; Memory - physiology ; Mental Recall - physiology ; MRI ; Mutation - genetics ; Neuropsychological Tests ; Presenilin-1 - genetics ; Recognition, Psychology - physiology ; Socioeconomic Factors ; Temporal lobes ; Verbal Behavior - physiology
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descriptionBackground Sporadic late-onset Alzheimer's disease (AD) dementia has been associated with a ‘signature’ of cortical atrophy in paralimbic and heteromodal association regions measured with MRI. Objective To investigate whether a similar pattern of cortical atrophy is present in presymptomatic presenilin 1 E280A mutation carriers an average of 6 years before clinical symptom onset. Methods 40 cognitively normal volunteers from a Colombian population with familial AD were included; 18 were positive for the AD-associated presenilin 1 mutation (carriers, mean age=38) whereas 22 were non-carriers. T1-weighted volumetric MRI images were acquired and cortical thickness was measured. A priori regions of interest from our previous work were used to obtain thickness from AD-signature regions. Results Compared to non-carriers, presymptomatic presenilin 1 mutation carriers exhibited thinner cortex within the AD-signature summary measure (p<0.008). Analyses of individual regions demonstrated thinner angular gyrus, precuneus and superior parietal lobule in carriers compared to non-carriers, with trend-level effects in the medial temporal lobe. Conclusion Results demonstrate that cognitively normal individuals genetically determined to develop AD have a thinner cerebral cortex than non-carriers in regions known to be affected by typical late-onset sporadic AD. These findings provide further support for the hypothesis that cortical atrophy is present in preclinical AD more than 5 years prior to symptom onset. Further research is needed to determine whether this method could be used to characterise the age-dependent trajectory of cortical atrophy in presymptomatic stages of AD.
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titleCortical atrophy in presymptomatic Alzheimer's disease presenilin 1 mutation carriers
authorQuiroz, Yakeel T ; Stern, Chantal E ; Reiman, Eric M ; Brickhouse, Michael ; Ruiz, Adriana ; Sperling, Reisa A ; Lopera, Francisco ; Dickerson, Bradford C
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abstractBackground Sporadic late-onset Alzheimer's disease (AD) dementia has been associated with a ‘signature’ of cortical atrophy in paralimbic and heteromodal association regions measured with MRI. Objective To investigate whether a similar pattern of cortical atrophy is present in presymptomatic presenilin 1 E280A mutation carriers an average of 6 years before clinical symptom onset. Methods 40 cognitively normal volunteers from a Colombian population with familial AD were included; 18 were positive for the AD-associated presenilin 1 mutation (carriers, mean age=38) whereas 22 were non-carriers. T1-weighted volumetric MRI images were acquired and cortical thickness was measured. A priori regions of interest from our previous work were used to obtain thickness from AD-signature regions. Results Compared to non-carriers, presymptomatic presenilin 1 mutation carriers exhibited thinner cortex within the AD-signature summary measure (p<0.008). Analyses of individual regions demonstrated thinner angular gyrus, precuneus and superior parietal lobule in carriers compared to non-carriers, with trend-level effects in the medial temporal lobe. Conclusion Results demonstrate that cognitively normal individuals genetically determined to develop AD have a thinner cerebral cortex than non-carriers in regions known to be affected by typical late-onset sporadic AD. These findings provide further support for the hypothesis that cortical atrophy is present in preclinical AD more than 5 years prior to symptom onset. Further research is needed to determine whether this method could be used to characterise the age-dependent trajectory of cortical atrophy in presymptomatic stages of AD.
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