Resting-state fMRI changes in Alzheimer's disease and mild cognitive impairment

Binnewijzend, Maja; Schoonheim, Menno M.; Sanz-Arigita, Ernesto; Wink, Alle Meije; Flier, Wiesje M. van der; Tolboom, Nelleke; Adriaanse, Sofie; Damoiseaux, Jessica S.; Scheltens, Philip; Berckel, Bart N.M. van; Barkhof, Frederik

doi:10.1016/j.neurobiolaging.2011.07.003

Cited by 343 publications

(297 citation statements)

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“…The “canonical” pattern of the DMN is the precuneus, superior lateral parietal lobes, and the ACC. When analyses are limited to the DMN regions, this is where the changes are found (Binnewijzend et al., 2012; Filippini et al., 2009). Analyses of AD‐related functional brain network differences associated with the DMN but not part of the DMN report changes in superior parietal and occipital regions (Agosta et al., 2012; Lee et al., 2016).…”

Section: Discussionmentioning

confidence: 99%

“…Resting‐state functional MRI (RS‐fMRI) detects functional connections in the brain as synchronized activity between brain regions in the absence of a task (Binnewijzend et al., 2012). Brain regions linked to AD pathology in studies using MEG and structural MRI (de Haan, Mott, et al., 2012; de Haan, van der Flier, et al., 2012; Tijms et al., 2013) show high connectivity in RS‐fMRI; they are hub regions .…”

Section: Introductionmentioning

confidence: 99%

“…The high vulnerability of hubs for AD is also found in RS‐fMRI studies (Buckner et al., 2009; Qi et al., 2010). The default mode network (DMN) and other resting‐state networks, that is, regions with synchronized fMRI activity, have been studied as markers for AD progression (Binnewijzend et al., 2012; Filippini et al., 2009; Sheline et al., 2010). Functional brain connectivity changes in healthy adults are related to amyloid depositions (Hedden et al., 2009; Sperling et al., 2009), and carriers of the APOE‐ε4 allele show increased co‐activation with the DMN in young adults (Bookheimer et al., 2000; Filippini et al., 2009), indicating that functional connectivity is sensitive to AD‐related alterations of the brain.…”

Section: Introductionmentioning

confidence: 99%

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Functional brain network centrality is related to APOE genotype in cognitively normal elderly

et al. 2018

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IntroductionAmyloid plaque deposition in the brain is an early pathological change in Alzheimer's disease (AD), causing disrupted synaptic connections. Brain network disruptions in AD have been demonstrated with eigenvector centrality (EC), a measure that identifies central regions within networks. Carrying an apolipoprotein (APOE)‐ε4 allele is a genetic risk for AD, associated with increased amyloid deposition. We studied whether APOE‐ε4 carriership is associated with EC disruptions in cognitively normal individuals.MethodsA total of 261 healthy middle‐aged to older adults (mean age 56.6 years) were divided into high‐risk (APOE‐ε4 carriers) and low‐risk (noncarriers) groups. EC was computed from resting‐state functional MRI data. Clusters of between‐group differences were assessed with a permutation‐based method. Correlations between cluster mean EC with brain volume, CSF biomarkers, and psychological test scores were assessed.ResultsDecreased EC in the visual cortex was associated with APOE‐ε4 carriership, a genetic risk factor for AD. EC differences were correlated with age, CSF amyloid levels, and scores on the trail‐making and 15‐object recognition tests.ConclusionOur findings suggest that the APOE‐ε4 genotype affects brain connectivity in regions previously found to be abnormal in AD as a sign of very early disease‐related pathology. These differences were too subtle in healthy elderly to use EC for single‐subject prediction of APOE genotype.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Functional brain network centrality is related to APOE genotype in cognitively normal elderly

et al. 2018

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“…The DMN is typically found deactivated during cognitive tasks requiring externally focused attention and activated during internally focused mental tasks, such as episodic memory retrieval, mental state attribution, and visual imagery (Buckner, Andrews-Hanna, & Schacter, 2008;Mason et al, 2007;Raichle et al, 2001;Shulman et al, 1997). In addition to the regional atrophy and neuronal hypometabolism affecting DMN nodes, disruptions in functional connectivity of the DMN in AD dementia have been widely replicated (Agosta et al, 2012;Binnewijzend et al, 2012;Greicius, Srivastava, Reiss, & Menon, 2004), and have been linked to core memory and visuospatial deficits Supekar, Menon, Rubin, Musen, & Greicius, 2008;Zhang et al, 2010). Intriguingly, connectivity disruption and impaired task-related down regulation of the DMN may already emerge during the presymptomatic phase of AD as modeled cross-sectionally on the basis of imaging evidence of cortical amyloid pathology Sperling et al, 2009) or an apolipoprotein E4 (APOE4) positive genotype, which is a major genetic risk factor for late onset AD (Damoiseaux et al, 2012;Machulda et al, 2011;Persson et al, 2008).…”

Section: Functional Connectivity Changes In the Course Of Admentioning

confidence: 99%

Measuring Cortical Connectivity in Alzheimer’s Disease as a Brain Neural Network Pathology: Toward Clinical Applications

Teipel

Grothe

Zhou

et al. 2016

J Int Neuropsychol Soc

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Objectives: The objective was to review the literature on diffusion tensor imaging as well as resting-state functional magnetic resonance imaging and electroencephalography (EEG) to unveil neuroanatomical and neurophysiological substrates of Alzheimer's disease (AD) as a brain neural network pathology affecting structural and functional cortical connectivity underlying human cognition. Methods: We reviewed papers registered in PubMed and other scientific repositories on the use of these techniques in amnesic mild cognitive impairment (MCI) and clinically mild AD dementia patients compared to cognitively intact elderly individuals (Controls). Results: Hundreds of peer-reviewed (cross-sectional and longitudinal) papers have shown in patients with MCI and mild AD compared to Controls (1) impairment of callosal (splenium), thalamic, and anterior-posterior white matter bundles; (2) reduced correlation of resting state blood oxygen level-dependent activity across several intrinsic brain circuits including default mode and attention-related networks; and (3) abnormal power and functional coupling of resting state cortical EEG rhythms. Clinical applications of these measures are still limited. Conclusions: Structural and functional (in vivo) cortical connectivity measures represent a reliable marker of cerebral reserve capacity and should be used to predict and monitor the evolution of AD and its relative impact on cognitive domains in pre-clinical, prodromal, and dementia stages of AD. (JINS, 2016, 22, 138-163)

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“…The DMN is of special interest because: 1) age-related decreases in DMN functional connectivity have been the most consistent finding in rs-fMRI studies of the elderly population (for a review, see Ferreira & Busatto 128 ); 2) patients with AD and MCI exhibit increased age-related changes in the DMN 129-131 ; 3) hypoperfusion and hypometabolism (assessed by SPECT and PET) in the precuneus and posterior cingulate cortex --a major DMN hub --are frequently found in AD 132,133 ; 4) functional connectivity within the DMN has been shown to correlate with behavioral performance in healthy older adults 128 and in patients with AD 129,130 ; and 5) baseline functional connectivity within the DMN has been associated with conversion from MCI to AD. 134 A study of middle-aged subjects with type 2 diabetes focused on the functional connectivity of the posterior cingulate cortex found decreased connectivity in the bilateral middle temporal gyrus, the left medial and right inferior frontal gyri, and the left thalamus in the diabetes group as compared with controls.…”

Section: Cardiovascular Risk Factors and Cognitive Declinementioning

confidence: 99%

The link between cardiovascular risk, Alzheimer's disease, and mild cognitive impairment: support from recent functional neuroimaging studies

Ferreira

Tamashiro-Duran

Squarzoni

et al. 2014

Rev. Bras. Psiquiatr.

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Objective: To review functional neuroimaging studies about the relationship between cardiovascular risk factors (CVRFs), Alzheimer's disease (AD), and mild cognitive impairment (MCI). Methods: We performed a comprehensive literature search to identify articles in the neuroimaging field addressing CVRF in AD and MCI. We included studies that used positron emission tomography (PET), single photon emission computerized tomography (SPECT), or functional magnetic resonance imaging (fMRI). Results: CVRFs have been considered risk factors for cognitive decline, MCI, and AD. Patterns of AD-like changes in brain function have been found in association with several CVRFs (both regarding individual risk factors and also composite CVRF measures). In vivo assessment of AD-related pathology with amyloid imaging techniques provided further evidence linking CVRFs and AD, but there is still limited information resulting from this new technology. Conclusion: There is a large body of evidence from functional neuroimaging studies supporting the hypothesis that CVRFs may play a causal role in the pathophysiology of AD. A major limitation of most studies is their cross-sectional design; future longitudinal studies using multiple imaging modalities are expected to better document changes in CVRF-related brain function patterns and provide a clearer picture of the complex relationship between aging, CVRFs, and AD.

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Resting-state fMRI changes in Alzheimer's disease and mild cognitive impairment

Cited by 343 publications

References 50 publications

Functional brain network centrality is related to APOE genotype in cognitively normal elderly

Functional brain network centrality is related to APOE genotype in cognitively normal elderly

Measuring Cortical Connectivity in Alzheimer’s Disease as a Brain Neural Network Pathology: Toward Clinical Applications

The link between cardiovascular risk, Alzheimer's disease, and mild cognitive impairment: support from recent functional neuroimaging studies

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