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Showing papers by "Fabrice Crivello published in 2012"


Journal ArticleDOI
Joshua C. Bis1, Charles DeCarli2, Albert V. Smith3, Fedde van der Lijn4, Fabrice Crivello5, Fabrice Crivello6, Myriam Fornage7, Stephanie Debette8, Stephanie Debette9, Joshua M. Shulman10, Joshua M. Shulman11, Helena Schmidt12, Velandai Srikanth13, Velandai Srikanth14, Maaike Schuur4, Lei Yu15, Seung Hoan Choi8, Sigurdur Sigurdsson, Benjamin F.J. Verhaaren4, Anita L. DeStefano8, Jean-Charles Lambert16, Clifford R. Jack17, Maksim Struchalin4, Jim Stankovich14, Carla A. Ibrahim-Verbaas4, Debra A. Fleischman15, Alex P. Zijdenbos18, Tom den Heijer4, Bernard Mazoyer5, Bernard Mazoyer6, Laura H. Coker19, Christian Enzinger12, Patrick Danoy20, Najaf Amin4, Konstantinos Arfanakis21, Konstantinos Arfanakis15, Mark A. van Buchem22, Renée F A G de Bruijn4, Alexa S. Beiser8, Carole Dufouil9, Juebin Huang23, Margherita Cavalieri12, Russell Thomson14, Wiro J. Niessen4, Wiro J. Niessen24, Lori B. Chibnik10, Lori B. Chibnik11, Gauti Kjartan Gislason, Albert Hofman4, Aleksandra Pikula8, Philippe Amouyel16, Kevin B. Freeman23, Thanh G. Phan13, Ben A. Oostra4, Jason L. Stein25, Sarah E. Medland11, Sarah E. Medland26, Alejandro Arias Vasquez27, Derrek P. Hibar25, Margaret J. Wright26, Barbara Franke27, Nicholas G. Martin26, Paul M. Thompson25, Mike A. Nalls28, André G. Uitterlinden4, Rhoda Au8, Alexis Elbaz9, Richard Beare13, Richard Beare29, John C. van Swieten4, Oscar L. Lopez30, Tamara B. Harris28, Vincent Chouraki16, Monique M.B. Breteler31, Monique M.B. Breteler10, Monique M.B. Breteler32, Philip L. De Jager10, Philip L. De Jager11, James T. Becker30, Meike W. Vernooij4, David S. Knopman17, Franz Fazekas12, Philip A. Wolf8, Aad van der Lugt4, Vilmundur Gudnason3, William T. Longstreth1, Matthew A. Brown20, David A. Bennett15, Cornelia M. van Duijn4, Cornelia M. van Duijn22, Thomas H. Mosley23, Reinhold Schmidt12, Christophe Tzourio6, Christophe Tzourio9, Lenore J. Launer27, M. Arfan Ikram4, Sudha Seshadri8 
TL;DR: In this article, a genome-wide association study (GWAS) of dementia-free persons (n = 9,232) identified 46 SNPs at four loci with P values of <4.0 × 10(-7).
Abstract: Aging is associated with reductions in hippocampal volume that are accelerated by Alzheimer's disease and vascular risk factors. Our genome-wide association study (GWAS) of dementia-free persons (n = 9,232) identified 46 SNPs at four loci with P values of <4.0 × 10(-7). In two additional samples (n = 2,318), associations were replicated at 12q14 within MSRB3-WIF1 (discovery and replication; rs17178006; P = 5.3 × 10(-11)) and at 12q24 near HRK-FBXW8 (rs7294919; P = 2.9 × 10(-11)). Remaining associations included one SNP at 2q24 within DPP4 (rs6741949; P = 2.9 × 10(-7)) and nine SNPs at 9p33 within ASTN2 (rs7852872; P = 1.0 × 10(-7)); along with the chromosome 12 associations, these loci were also associated with hippocampal volume (P < 0.05) in a third younger, more heterogeneous sample (n = 7,794). The SNP in ASTN2 also showed suggestive association with decline in cognition in a largely independent sample (n = 1,563). These associations implicate genes related to apoptosis (HRK), development (WIF1), oxidative stress (MSR3B), ubiquitination (FBXW8) and neuronal migration (ASTN2), as well as enzymes targeted by new diabetes medications (DPP4), indicating new genetic influences on hippocampal size and possibly the risk of cognitive decline and dementia.

238 citations


Journal ArticleDOI
TL;DR: Evidence is provided that modulation of spontaneous low-frequency fluctuations in the brain is at least partially explained by spontaneous conscious cognition while at rest, and mind wandering can be characterized by widespread modular segregation.

104 citations


Journal ArticleDOI
TL;DR: The amygdala, which develops neuropathology in the early stage of AD and is involved in the pathogenesis of depression, may be an important brain structure involved inThe association between EPA and cognitive decline and depressive symptoms.
Abstract: Objective: The long-chain -3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are potential candidates for interventions to delay Alzheimer disease (AD), but evidence from clinical studies is mixed. We aimed at determining whether plasma levels of EPA or DHA predict atrophy of medial temporal lobe (MTL) gray matter regions in older subjects. Methods: A total of 281 community dwellers from the Three-City Study, aged 65 years or older, had plasma fatty acid measurements at baseline and underwent MRI examinations at baseline and at 4 years. We studied the association between plasma EPA and DHA and MTL gray matter volume change at 4 years. Results: Higher plasma EPA, but not DHA, was associated with lower gray matter atrophy of the right hippocampal/parahippocampal area and of the right amygdala (p 0.05, familywise error corrected). Based on a mean right amygdala volume loss of 6.0 mm 3 /y (0.6%) ,a1S Dhigher plasma EPA (0.64% of total plasma fatty acids) at baseline was related to a 1.3 mm 3 smaller gray matter loss per year in the right amygdala. Higher atrophy of the right amygdala was associated with greater 4-year decline in semantic memory performances and more depressive symptoms. Conclusion: The amygdala, which develops neuropathology in the early stage of AD and is involved in the pathogenesis of depression, may be an important brain structure involved in the association between EPA and cognitive decline and depressive symptoms. Neurology ® 2012;79:642–650

92 citations


Joshua C. Bis1, Charles DeCarli2, Albert V. Smith3, Fedde van der Lijn4, Fabrice Crivello5, Fabrice Crivello6, Myriam Fornage7, Stephanie Debette8, Stephanie Debette9, Joshua M. Shulman10, Joshua M. Shulman11, Helena Schmidt12, Velandai Srikanth13, Velandai Srikanth14, Maaike Schuur4, Lei Yu15, Seung Hoan Choi8, Sigurdur Sigurdsson, Benjamin F.J. Verhaaren4, Anita L. DeStefano8, Jean-Charles Lambert16, Clifford R. Jack17, Maksim Struchalin4, Jim Stankovich14, Carla A. Ibrahim-Verbaas4, Debra A. Fleischman15, Alex P. Zijdenbos18, Tom den Heijer4, Bernard Mazoyer6, Bernard Mazoyer5, Laura H. Coker19, Christian Enzinger12, Patrick Danoy20, Najaf Amin4, Konstantinos Arfanakis21, Konstantinos Arfanakis15, Mark A. van Buchem22, Renée F A G de Bruijn4, Alexa S. Beiser8, Carole Dufouil9, Juebin Huang23, Margherita Cavalieri12, Russell Thomson14, Wiro J. Niessen4, Wiro J. Niessen24, Lori B. Chibnik10, Lori B. Chibnik11, Gauti Kjartan Gislason, Albert Hofman4, Aleksandra Pikula8, Philippe Amouyel16, Kevin B. Freeman23, Thanh G. Phan13, Ben A. Oostra4, Jason L. Stein25, Sarah E. Medland26, Sarah E. Medland11, Alejandro Arias Vasquez27, Derrek P. Hibar25, Margaret J. Wright26, Barbara Franke27, Nicholas G. Martin26, Paul M. Thompson25, Mike A. Nalls28, André G. Uitterlinden4, Rhoda Au8, Alexis Elbaz9, Richard Beare29, Richard Beare13, John C. van Swieten4, Oscar L. Lopez30, Tamara B. Harris28, Vincent Chouraki16, Monique M.B. Breteler31, Monique M.B. Breteler10, Monique M.B. Breteler32, Philip L. De Jager10, Philip L. De Jager11, James T. Becker30, Meike W. Vernooij4, David S. Knopman17, Franz Fazekas12, Philip A. Wolf8, Aad van der Lugt4, Vilmundur Gudnason3, William T. Longstreth1, Matthew A. Brown20, David A. Bennett15, Cornelia M. van Duijn22, Cornelia M. van Duijn4, Thomas H. Mosley23, Reinhold Schmidt12, Christophe Tzourio6, Christophe Tzourio9, Lenore J. Launer27, M. Arfan Ikram4, Sudha Seshadri8 
15 Apr 2012
TL;DR: These associations implicate genes related to apoptosis (HRK), development (WIF1), oxidative stress (MSR3B), ubiquitination (FBXW8) and neuronal migration (ASTN2), as well as enzymes targeted by new diabetes medications (DPP4), indicating new genetic influences on hippocampal size and possibly the risk of cognitive decline and dementia.
Abstract: Aging is associated with reductions in hippocampal volume that are accelerated by Alzheimer's disease and vascular risk factors. Our genome-wide association study (GWAS) of dementia-free persons ( n = 9,232) identified 46 SNPs at four loci with P values of −7 . In two additional samples ( n = 2,318), associations were replicated at 12q14 within MSRB3 - WIF1 (discovery and replication; rs17178006; P = 5.3 × 10 −11 ) and at 12q24 near HRK - FBXW8 (rs7294919; P = 2.9 × 10 −11 ). Remaining associations included one SNP at 2q24 within DPP4 (rs6741949; P = 2.9 × 10 −7 ) and nine SNPs at 9p33 within ASTN2 (rs7852872; P = 1.0 × 10 −7 ); along with the chromosome 12 associations, these loci were also associated with hippocampal volume ( P n = 7,794). The SNP in ASTN2 also showed suggestive association with decline in cognition in a largely independent sample ( n = 1,563). These associations implicate genes related to apoptosis ( HRK ), development ( WIF1) , oxidative stress ( MSR3B ), ubiquitination ( FBXW8 ) and neuronal migration ( ASTN2 ), as well as enzymes targeted by new diabetes medications ( DPP4 ), indicating new genetic influences on hippocampal size and possibly the risk of cognitive decline and dementia.

29 citations


Journal ArticleDOI
TL;DR: This work proposes a method based on group analysis of individual ICA components, using a multi-scale clustering (MICCA), which proved to be reproducible in a random splitting of the data sample and more robust than the classical concatenation method.
Abstract: Functional connectivity-based analysis of functional magnetic resonance imaging data (fMRI) is an emerging technique for human brain mapping. One powerful method for the investigation of functional connectivity is independent component analysis (ICA) of concatenated data. However, this research field is evolving toward processing increasingly larger database taking into account inter-individual variability. Concatenated data analysis only handles these features using some additional procedures such as bootstrap or including a model of between-subject variability during the preprocessing step of the ICA. In order to alleviate these limitations, we propose a method based on group analysis of individual ICA components, using a multi-scale clustering (MICCA). MICCA start with two steps repeated several times: 1) single subject data ICA followed by 2) clustering of all subject independent components according to a spatial similarity criterion. A final third step consists in selecting reproducible clusters across the repetitions of the two previous steps. The core of the innovation lies in the multi-scale and unsupervised clustering algorithm built as a chain of three processes: robust proto-cluster creation, aggregation of the proto-clusters, and cluster consolidation. We applied MICCA to the analysis of 310 fMRI resting state dataset. MICCA identified 28 resting state brain networks. Overall, the cluster neuroanatomical substrate included 98% of the cerebrum gray matter. MICCA results proved to be reproducible in a random splitting of the data sample and more robust than the classical concatenation method.

17 citations