Resting state fMRI in Alzheimer's disease: beyond the default mode network

Agosta, Federica; Pievani, Michela; Geroldi, Cristina; Copetti, Massimiliano; Frisoni, Giovanni B.; Filippi, Massimo

doi:10.1016/j.neurobiolaging.2011.06.007

Cited by 495 publications

(415 citation statements)

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“…Those did not include the visual cortex as the statistical analyses were limited to changes inside the DMN. Analyses of connectivity with the rest of the brain (Agosta et al., 2012) show differential connectivity with the DMN with the same visual regions we report, between AD and controls as well as MCI vs. controls, especially on the boundary between precuneus and visual cortex.…”

Section: Discussionsupporting

confidence: 64%

“…Recent studies that focus less on the DMN alone report a shift of functionally central and highly connected regions from posterior to frontal regions in AD patients (Agosta et al., 2012; Binnewijzend et al., 2014; Sanz‐Arigita et al., 2010; Sheline et al., 2010). The decreased centralities of posterior regions in the APOE4+ risk group found in this study are in line with this shift, although we did not find locally increased centralities in frontal areas in healthy subjects.…”

Section: Discussionmentioning

confidence: 99%

“…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). These findings are consistent with those in resting and visual fMRI studies that report affected visual functioning accompanied by differences in the visual cortices (Alegret et al., 2010; Lehmann et al., 2013; Wang et al., 2015; Zhang et al., 2010) and the idea that deviations from the typical pathology, such as the involvement of functionally specific brain regions, drive the variation in neurodegenerative variation in AD.…”

Section: Discussionmentioning

confidence: 99%

“…The efficiency of fast ECM (Wink et al., 2012) and its sensitivity to disease conditions (Binnewijzend et al., 2014), and the fact that it produces single‐subject, whole‐brain patterns, make it an attractive alternative to current RS‐fMRI analyses of AD‐related brain network differences, for example, independent component analyses. As such, whole‐brain network analyses are an interesting and novel approach to multiple‐network decompositions for neurological disorders that perturb the global brain network functionally and structurally (Agosta et al., 2012; Seeley, Crawford, Zhou, Miller, & Greicius, 2009; Tijms et al., 2014). …”

Section: Discussionmentioning

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: Discussionsupporting

confidence: 64%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

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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Effect ofTMEM106BPolymorphism on Functional Network Connectivity in AsymptomaticGRNMutation Carriers

et al. 2014

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rontotemporal dementia (FTD) is a neurodegenerative disorder in which behavioral abnormalities, language impairment, and executive function deficits represent the most typical clinical features. 1,2 One of the most common causes of inherited FTD is the loss-of-function mutations within the granulin (GRN) gene (OMIM 138945). 3,4 More than 60 different pathogenetic mutations have been identified so far (http://www.molgen.ua.ac.be/FTDmutations). GRN mutations lead to FTD with TDP-43 inclusions 5 and have a wide clinical phenotype. Age at disease onset is highly heterogeneous, 6 and presenting symptoms frequently resemble either behavioral variant FTD or the agrammatic variant of primary progressive aphasia. Neuroimaging studies have demonstrated that patients carrying GRN mutations have an asymmetric gray matter loss in the frontal, posterior temporal, and parietal cortices. 7,8 Notwithstanding, little is known about the preclinical stages of the disease, such as the early and specific brain regional damage of GRN disease and the factors antedating and modulating disease onset. Studies of those who will develop the disease at some point are essential to understanding the pattern and timing of brain damage and symptom onset. Recent works by our group, carried out in a genetically coalescent cohort of families with the GRN Thr272fs mutation, 9,10 have demonstrated early abnormalities of functional network connectivity even in presymptomatic stages of disease, 11 without gray matter loss 11 but with significant alterations in white matter bundles. In light of this, resting-state functional magnetic resonance imaging (fMRI) represents the most promising IMPORTANCE Granulin (GRN) mutations represent one of the most frequent genetic causes of inherited frontotemporal dementia. The study of asymptomatic carriers of GRN Thr272fs mutation (aGRN+) provides a unique opportunity to study the natural history of the disease and the role of modulating factors on disease onset. It has been demonstrated that the TMEM106B polymorphism is associated with GRN-related frontotemporal dementia and affects age at onset in GRN mutation carriers. OBJECTIVE To ascertain whether TMEM106B genetic status modulates GRN disease by evaluating resting-state functional connectivity in aGRN+ individuals according to TMEM106 genetic variation. DESIGN, SETTING, AND PARTICIPANTS Academic tertiary referral center for neurodegenerative disorders in 17 asymptomatic carriers of aGRN+ and 14 healthy controls. MAIN OUTCOMES AND MEASURES Changes in resting-state functional connectivity, focusing on the default mode network, ventral and dorsal salience networks, executive network, frontoparietal networks, and attentive network and the effect of TMEM106B genotypes in aGRN+ participants and healthy controls (statistical nonparametric mapping). RESULTS aGRN+ participants showed decreased brain connectivity within the left frontoparietal network and increased connectivity in the executive network compared with healthy controls. The TMEM106B at-risk polymorphism (T/T...

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Resting state fMRI in Alzheimer's disease: beyond the default mode network

Cited by 495 publications

References 60 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

Effect ofTMEM106BPolymorphism on Functional Network Connectivity in AsymptomaticGRNMutation Carriers

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