List of publications for the week of September 6, 2021
Physical activity and cognitive and imaging biomarkers of Alzheimer’s disease in down syndrome
(2021) Neurobiology of Aging, 107, pp. 118-127.
Fleming, V.a b , Piro-Gambetti, B.a b , Patrick, A.a c , Zammit, M.a c , Alexander, A.a c , Christian, B.T.a c , Handen, B.d , Cohen, A.d , Klunk, W.d , Laymon, C.e , Ances, B.M.f , Plante, D.T.g , Okonkwo, O.g h , Hartley, S.L.a b
a Waisman Center, University of Wisconsin-Madison, Madison, WI, United States
b School of Human Ecology, University of Wisconsin-Madison, Madison, WI, United States
c Department of Medical Physics, University of Wisconsin-Madison, Madison, WI, United States
d Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA, United States
e Department of Radiology, University of Pittsburgh, Pittsburgh, PA, United States
f Department of Neurology, Washington University at St. Louis, St. Louis, MO, United States
g Department of Psychiatry, University of Wisconsin-Madison, Madison, WI, United States
h Department of Medicine, University of Wisconsin-Madison, Madison, WI, United States
Abstract
Adults with Down syndrome (DS) are at risk for Alzheimer’s disease. Despite sharing trisomy 21, however, there is variability in the age of disease onset. This variability may mean that other factors, such as lifestyle, influence cognitive aging and disease timing. The present study assessed the association between everyday life physical activity using an actigraph accelerometer and cognitive functioning and early Alzheimer’s disease pathology via positron emission tomography amyloid-β and tau and diffusion tension imaging measures of white matter integrity in 61 non-demented adults with DS. Percent time in sedentary behavior and in moderate-to-vigorous activity were associated (negatively and positively, respectively) with cognitive functioning (r = -.472 to.572, p < 0.05). Neither sedentary behavior nor moderate-to-vigorous activity were associated with amyloid-β or tau, but both were associated with white matter integrity in the superior and inferior longitudinal fasciculus (Fractional Anisotropy: r = -.397 to -.419, p < 0.05; Mean Diffusivity: r =.400, p < 0.05). Longitudinal studies are needed to determine if physical activity promotes healthy aging in DS. © 2021 Elsevier Inc.
Author Keywords
Alzheimer’s disease; Biomarkers; Cognitive functioning; Down syndrome; Physical activity
Funding details
National Institute on AgingNIAR01 AG031110, R01 AG070028, U01 AG051406, U19 AG068054
National Institute of Child Health and Human DevelopmentNICHDU54 HD09025
Document Type: Article
Publication Stage: Final
Source: Scopus
Familial History of Autoimmune Disorders Among Patients With Pediatric Multiple Sclerosis
(2021) Neurology(R) Neuroimmunology & Neuroinflammation, 8 (5), .
Greenberg, B.M., Casper, T.C., Mar, S.S., Ness, J.M., Plumb, P., Liang, S., Goyal, M., Weinstock-Guttman, B., Rodriguez, M., Aaen, G.S., Belman, A., Barcellos, L.F., Rose, J.W., Gorman, M.P., Benson, L.A., Candee, M., Chitnis, T., Harris, Y.C., Kahn, I.L., Roalstad, S., Hart, J., Lotze, T.E., Rensel, M., Rubin, J.P., Schreiner, T.L., Tillema, J.-M., Waldman, A.T., Krupp, L., Graves, J., Drake, K., Waubant, E.
From the University of Texas Southwestern (B.M.G.), Department of Neurology, Department of Pediatrics, Dallas; Data Coordinating and Analysis Center (T.C.C., S.S.R., K.D.), University of Utah, Salt Lake City; Washington University (S.S.M.), St. Louis, MO; University of Alabama Birmingham (J.M.N.); The University of Texas Southwestern (P.P.), Department of Neurology, Dallas; Department of Radiology (S.L., M.G.), Washington University in St. Louis, MO; Jacobs Pediatric Multiple Sclerosis Center (B.W.-G.), State University of New York at Buffalo, NY; Mayo Clinic Pediatric Multiple Sclerosis Center (M.R., J.-M.T.), Mayo Clinic, Rochester, MN; Pediatric Multiple Sclerosis Center (G.S.A.), Loma Linda University Children’s Hospital, CA; Lourie Center for Pediatric Multiple Sclerosis (A.B.), Stony Brook University Hospital, NY; Epidemiology (L.F.B.), University of California, Berkeley; Department of Neurology (J.W.R.), University of Utah, Salt Lake City; Pediatric Multiple Sclerosis and Related Disorders Program (M.P.G., L.A.B.), Boston Children’s Hospital, MA; Primary Children’s Hospital (M.C.), University of Utah, Salt Lake City; Partners Pediatric Multiple Sclerosis Center (T.C.)
Abstract
BACKGROUND AND OBJECTIVE: The objective of this study was to determine whether family members of patients with pediatric multiple sclerosis (MS) have an increased prevalence of autoimmune conditions compared with controls. METHODS: Data collected during a pediatric MS case-control study of risk factors included information about various autoimmune diseases in family members. The frequency of these disorders was compared between cases and controls. RESULTS: There was an increased rate of autoimmune diseases among family members of pediatric MS cases compared with controls with first-degree history of MS excluded (OR = 2.27, 95% CI 1.71-3.01, p < 0.001). There was an increased rate of MS among second-degree relatives of pediatric MS cases compared with controls (OR = 3.47, 95% CI 1.36-8.86, p = 0.009). The OR for MS was 2.64 when restricted to maternal relatives and 6.37 when restricted to paternal relatives. DISCUSSION: The increased rates of autoimmune disorders, including thyroid disorders and MS among families of patients with pediatric MS, suggest shared genetic factors among families with children diagnosed with pediatric MS. Copyright © 2021 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology.
Document Type: Article
Publication Stage: Final
Source: Scopus
Alterations of the gut mycobiome in patients with MS
(2021) EBioMedicine, 71, art. no. 103557, .
Shah, S.a , Locca, A.b , Dorsett, Y.c , Cantoni, C.b , Ghezzi, L.b d , Lin, Q.a , Bokoliya, S.c , Panier, H.c , Suther, C.c e , Gormley, M.f , Liu, Y.f , Evans, E.b , Mikesell, R.b , Obert, K.b , Salter, A.g , Cross, A.H.b h , Tarr, P.I.i , Lovett-Racke, A.f , Piccio, L.b h j , Zhou, Y.c
a Department of Computer Science and Engineering, University of Connecticut, Storrs, CT, United States
b Department of Neurology, Washington University School of Medicine, St. Louis, MO, United States
c Department of Medicine, UConn Health, Farmington, CT, United States
d University of Milan, Dino Ferrari Centre, Milan, Italy
e Department of Food Science, University of Massachusetts, Amherst, MA, United States
f Department of Microbial Infection and Immunity, Ohio State University, Columbus, OH, United States
g Division of Biostatistics, School of Medicine, Washington University, St. Louis, MO, United States
h Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO 63110, United States
i Department of Pediatrics and Molecular Microbiology, Washington University School of Medicine, St. Louis, MO, United States
j Brain and Mind Centre, School of Medical Sciences, University of Sydney, Sydney, NSW 2050, Australia
Abstract
Background: The mycobiome is the fungal component of the gut microbiome and is implicated in several autoimmune diseases. However, its role in MS has not been studied. Methods: In this case-control observational study, we performed ITS sequencing and characterised the gut mycobiome in people with MS (pwMS) and healthy controls at baseline and after six months. Findings: The mycobiome had significantly higher alpha diversity and inter-subject variation in pwMS than controls. Saccharomyces and Aspergillus were over-represented in pwMS. Saccharomyces was positively correlated with circulating basophils and negatively correlated with regulatory B cells, while Aspergillus was positively correlated with activated CD16+ dendritic cells in pwMS. Different mycobiome profiles, defined as mycotypes, were associated with different bacterial microbiome and immune cell subsets in the blood. Initial treatment with dimethyl fumarate, a common immunomodulatory therapy which also has fungicidal activity, did not cause uniform gut mycobiome changes across all pwMS. Interpretation: There is an alteration of the gut mycobiome in pwMS, compared to healthy controls. Further study is required to assess any causal association of the mycobiome with MS and its direct or indirect interactions with bacteria and autoimmunity. Funding: This work was supported by the Washington University in St. Louis Institute of Clinical and Translational Sciences, funded, in part, by Grant Number # UL1 TR000448 from the National Institutes of Health, National Center for Advancing Translational Sciences, Clinical and Translational Sciences Award (Zhou Y, Piccio, L, Lovett-Racke A and Tarr PI); R01 NS102633-04 (Zhou Y, Piccio L); the Leon and Harriet Felman Fund for Human MS Research (Piccio L and Cross AH). Cantoni C. was supported by the National MS Society Career Transition Fellowship (TA-1805-31003) and by donations from Whitelaw Terry, Jr. / Valerie Terry Fund. Ghezzi L. was supported by the Italian Multiple Sclerosis Society research fellowship (FISM 2018/B/1) and the National Multiple Sclerosis Society Post-Doctoral Fellowship (FG- 1907-34474). Anne Cross was supported by The Manny & Rosalyn Rosenthal-Dr. John L. Trotter MS Center Chair in Neuroimmunology of the Barnes-Jewish Hospital Foundation. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. © 2021
Author Keywords
fungi; gut microbiome; immune system; multiple sclerosis; mycobiome
Funding details
National Institutes of HealthNIH
National Multiple Sclerosis SocietyFG-1907-34474, TA-1805-31003
Biogen
National Center for Advancing Translational SciencesNCATSR01 NS102633-04
Foundation for Barnes-Jewish Hospital
Associazione Italiana Sclerosi MultiplaAISMFISM 2018/B/1
University of MassachusettsUMASS
Institute of Clinical and Translational SciencesICTSUL1 TR000448
Document Type: Article
Publication Stage: Final
Source: Scopus
Static magnetic fields dampen focused ultrasound- mediated blood-brain barrier opening
(2021) Radiology, 300 (3), p. 681.
Yang, Y.a , Pacia, C.P.a , Ye, D.a , Yue, Y.a , Chien, C.-Y.a , Chen, H.a b
a Departments of Biomedical Engineering, Washington University in St Louis, 4511 Forest Park Ave, St Louis, MO 63108, United States
b Departments of Radiation Oncology, Washington University in St Louis, 4511 Forest Park Ave, St Louis, MO 63108, United States
Abstract
Background: Focused ultrasound combined with microbubbles has been used in clinical studies for blood-brain barrier (BBB) opening in conjunction with MRI. However, the impact of the static magnetic field generated by an MRI scanner on the BBB opening outcome has not been evaluated. Purpose: To determine the relationship of the static magnetic field of an MRI scanner on focused ultrasound combined with microbubble- induced BBB opening. Materials and Methods: Thirty wild-type mice were divided into four groups. Mice from different groups were sonicated with focused ultrasound in different static magnetic fields (approximately 0, 1.5, 3.0, and 4.7 T), with all other experimental parameters kept the same. Focused ultrasound sonication was performed after intravenous injection of microbubbles. Microbubble cavitation activity, the fundamental physical mechanism underlying focused ultrasound BBB opening, was monitored with passive cavitation detection. After sonication, contrast-enhanced T1-weighted MRI was performed to assess BBB opening outcome. Intravenously injected Evans blue was used as a model agent to evaluate trans-BBB delivery efficiency. Results: The microbubble cavitation dose decreased by an average of 2.1 dB at 1.5 T (P = .05), 2.9 dB at 3.0 T (P = .01), and 3.0 dB at 4.7 T (P = .01) compared with that outside the magnetic field (approximately 0 T). The static magnetic field of an MRI scanner decreased BBB opening volume in mice by 3.2-fold at 1.5 T (P <001), 4.5-fold at 3.0 T (P <.001), and 11.6-fold at 4.7 T (P <.001) compared with mice treated outside the magnetic field. It also decreased Evans blue trans-BBB delivery 1.4-fold at 1.5 T (P = .009), 1.6-fold at 3.0 T (P <.001), and 1.9-fold at 4.7 T (P <.001). Conclusion: Static magnetic fields dampened microbubble cavitation activity and decreased trans-blood-brain barrier (BBB) delivery by focused ultrasound combined with microbubble-induced BBB opening. © 2021 Radiological Society of North America Inc.. All rights reserved.
Funding details
National Institutes of HealthNIHR01EB027223, R01EB030102, R01MH116981
Document Type: Article
Publication Stage: Final
Source: Scopus
Parallel hippocampal-parietal circuits for self- And goal-oriented processing
(2021) Proceedings of the National Academy of Sciences of the United States of America, 118 (34), art. no. e2101743118, .
Zheng, A.a , Montez, D.F.a , Marek, S.b , Gilmore, A.W.c , Newbold, D.J.a , Laumann, T.O.b , Kay, B.P.a , Seider, N.A.a , Van, A.N.a , Hampton, J.M.a b , Alexopoulos, D.a , Schlaggar, B.L.d e f , Sylvester, C.M.b , Greene, D.J.g , Shimony, J.S.h , Nelson, S.M.i j , Wig, G.S.k l , Gratton, C.m n , McDermott, K.B.c h , Raichle, M.E.a h , Gordon, E.M.h , Dosenbach, N.U.F.a h o p q
a Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, United States
b Department of Psychiatry, Washington University School of Medicine, St. Louis, MO 63110, United States
c Department of Psychological and Brain Sciences, Washington University in St. Louis, St. Louis, MO 63130, United States
d Kennedy Krieger Institute, Baltimore, MD 21205, United States
e Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, United States
f Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, United States
g Department of Cognitive Science, University of California, San Diego, CA 92093, United States
h Mallinckrodt Institute of Radiology, Washington University School of Medicine, St. Louis, MO 63110, United States
i Department of Pediatrics, University of Minnesota, Minneapolis, MN 55454, United States
j Masonic Institute for the Developing Brain, University of Minnesota, Minneapolis, MN 55414, United States
k Center for Vital Longevity, School of Behavioral and Brain Sciences, University of Texas at Dallas, Dallas, TX 75235, United States
l Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas, TX 75390, United States
m Department of Psychology, Northwestern University, Evanston, IL 60208, United States
n Department of Neurology, Northwestern University, Evanston, IL 60208, United States
o Department of Biomedical Engineering, Washington University in St. Louis, St. Louis, MO 63130, United States
p Department of Pediatrics, Washington University School of Medicine, St. Louis, MO 63110, United States
q Program in Occupational Therapy, Washington University School of Medicine, St. Louis, MO 63110, United States
Abstract
The hippocampus is critically important for a diverse range of cognitive processes, such as episodic memory, prospective memory, affective processing, and spatial navigation. Using individual-specific precision functional mapping of resting-state functional MRI data, we found the anterior hippocampus (head and body) to be preferentially functionally connected to the default mode network (DMN), as expected. The hippocampal tail, however, was strongly preferentially functionally connected to the parietal memory network (PMN), which supports goal-oriented cognition and stimulus recognition. This anterior–posterior dichotomy of resting-state functional connectivity was well-matched by differences in task deactivations and anatomical segmentations of the hippocampus. Task deactivations were localized to the hippocampal head and body (DMN), relatively sparing the tail (PMN). The functional dichotomization of the hippocampus into anterior DMN-connected and posterior PMN-connected parcels suggests parallel but distinct circuits between the hippocampus and medial parietal cortex for self- versus goal-oriented processing. © 2021 National Academy of Sciences. All rights reserved.
Author Keywords
Brain networks; Functional connectivity; Hippocampus; Individual variability; Resting state
Funding details
HD087011, MH109983, MH121518, MH122389, NS110332, P30AG13854
National Institutes of HealthNIHMH096773, MH118370, MH121276, MH122066, MH123091, MH124567, NS088590, NS115672
Washington University in St. LouisWUSTL
McDonnell Center for Systems Neuroscience
Jacobs Foundation
Document Type: Article
Publication Stage: Final
Source: Scopus
Enhanced Multiplexing of Immunofluorescence Microscopy Using a Long-Stokes-Shift Fluorophore
(2021) Current Protocols, 1 (8), art. no. e214, .
Reitz, S.J., Sauerbeck, A.D., Kummer, T.T.
Department of Neurology, Washington University School of Medicine, St. Louis, MO, United States
Abstract
Immunofluorescence labeling and microscopy offer a highly specific means to visualize proteins or other molecular species in a sample by labeling target antigens with fluorescent probes. These fluorescent probes can then be visualized using a fluorescence microscope, allowing their relative spatial relationships to be determined. Due to spectral overlap of common fluorophores, however, it can be challenging to analyze more than three antigens in a single sample with standard imaging approaches. This article describes multiplexed labeling and imaging of four target antigens through the use of a long-Stokes-shift fluorophore—a fluorophore with an unusually large gap between its excitation and emission maxima—in tandem with three conventional fluorophores. This combination allows for multiplexed imaging of four antigens in a single sample with excellent spectral discrimination suitable for sensitive analyses using standard imaging hardware. Particular advantages of this approach are its flexibility in terms of target antigens and the lack of any specialized procedures, reagents, or equipment beyond the commercially available labeling reagent coupled to the long-Stokes-shift fluorophore. © 2021 Wiley Periodicals LLC. Basic Protocol 1: Four-probe immunofluorescence labeling. Basic Protocol 2: Four-probe immunofluorescence imaging. © 2021 Wiley Periodicals LLC
Author Keywords
fluorophore; immunofluorescence microscopy; immunolabeling; microglia; multiplex imaging; neuroscience; Stokes shift
Funding details
CDI‐CORE‐2015‐505
National Institutes of HealthNIHI01BX005204, OD021629, S10 OD025029
Foundation for Barnes-Jewish Hospital3770
University of WashingtonUW
Document Type: Article
Publication Stage: Final
Source: Scopus
Plasma amyloid β levels are driven by genetic variants near APOE, BACE1, APP, PSEN2: A genome-wide association study in over 12,000 non-demented participants
(2021) Alzheimer’s and Dementia, .
Damotte, V.a , van der Lee, S.J.b c , Chouraki, V.a d , Grenier-Boley, B.a , Simino, J.e , Adams, H.f , Tosto, G.g h , White, C.i j , Terzikhan, N.c k , Cruchaga, C.l , Knol, M.J.c , Li, S.m n , Schraen, S.o , Grove, M.L.p , Satizabal, C.d n , Amin, N.c , Berr, C.q , Younkin, S.r , Gottesman, R.F.s t , Buée, L.a u , Beiser, A.d m n , Knopman, D.S.v , Uitterlinden, A.w , DeCarli, C.x , Bressler, J.p , DeStefano, A.d m n , Dartigues, J.-F.y , Yang, Q.m n , Boerwinkle, E.p z , Tzourio, C.y , Fornage, M.p aa , Ikram, M.A.f , Amouyel, P.a , de Jager, P.i j ab , Reitz, C.g h ac ad , Mosley, T.H.ae , Lambert, J.-C.a , Seshadri, S.d n af , van Duijn, C.M.c ag , Alzheimer’s Disease Neuroimaging Initiativeah
a Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, Lille, France
b Alzheimer Center Amsterdam, Department of Neurology, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, Netherlands
c Department of Epidemiology, Erasmus Medical Center, Rotterdam, Netherlands
d Department of Neurology, Boston University School of Medicine, Boston, MA, United States
e Gertrude C. Ford MIND Center, Department of Data Science, John D. Bower School of Population Health, University of Mississippi Medical Center, Jackson, MS, United States
f Departments of Epidemiology, Neurology, and Radiology and Nuclear Medicine, Erasmus Medical Center, Rotterdam, Netherlands
g Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, Columbia University, New York, NY, United States
h Gertrude H. Sergievsky Center, Columbia University, New York, NY, United States
i Program in Translational NeuroPsychiatric Genomics, Institute for the Neurosciences, Departments of Neurology and Psychiatry, Brigham and Women’s Hospital, Boston, MA, United States
j Program in Medical and Population Genetics, Broad Institute, Cambridge, MA, United States
k Department of Respiratory Medicine, Ghent University Hospital, Ghent, Belgium
l Department of Psychiatry, Washington University in St. Louis, Saint Louis, MO, United States
m Department of Biostatistics, Boston University School of Public Health, Boston, MA, United States
n The Framingham Heart Study, Framingham, MA, United States
o Université Lille, CHU-Lille, Inserm, UF de Neurobiologie, CBPG, Lille, France
p Human Genetics Center, Department of Epidemiology, Human Genetics, and Environmental Sciences, School of Public Health, The University of Texas Health Science Center at Houston, Houston, TX, United States
q INSERM U1061, University of Montpellier, Montpellier, France
r Department of Neuroscience, Mayo Clinic, Jacksonville, FL, United States
s Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, United States
t Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, United States
u Institut National de la Santé et de la Recherche Medicale (INSERM, Université de Lille, Lille, France
v Department of Neurology, Mayo Clinic College of Medicine, Rochester, MN, United States
w Department of Internal Medicine, Erasmus Medical Center, Rotterdam, Netherlands
x Department of Neurology, University of California at Davis, Davis, CA, United States
y Bordeaux Population Health Research Center, INSERM, UMR1219, Bordeaux University, Bordeaux, France
z Human Genome Sequencing Center, Baylor College of Medicine, Houston, TX, United States
aa Brown Foundation Institute of Molecular Medicine, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX, United States
ab Center for Translational & Systems Neuroimmunology, Department of Neurology, Columbia University Medical Center, New York, New York, NY, United States
ac Department of Neurology, Columbia University, New York, NY, United States
ad Department of Epidemiology, Columbia University, New York, NY, United States
ae Department of Medicine, Gertrude C. Ford MIND Center, University of Mississippi Medical Center, Jackson, MS, United States
af Glenn Biggs Institute for Alzheimer’s and Neurodegenerative Diseases, UT Health San Antonio, San Antonio, TX, United States
ag Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom
Abstract
Introduction: There is increasing interest in plasma amyloid beta (Aβ) as an endophenotype of Alzheimer’s disease (AD). Identifying the genetic determinants of plasma Aβ levels may elucidate important biological processes that determine plasma Aβ measures. Methods: We included 12,369 non-demented participants from eight population-based studies. Imputed genetic data and measured plasma Aβ1-40, Aβ1-42 levels and Aβ1-42/Aβ1-40 ratio were used to perform genome-wide association studies, and gene-based and pathway analyses. Significant variants and genes were followed up for their association with brain positron emission tomography Aβ deposition and AD risk. Results: Single-variant analysis identified associations with apolipoprotein E (APOE) for Aβ1-42 and Aβ1-42/Aβ1-40 ratio, and BACE1 for Aβ1-40. Gene-based analysis of Aβ1-40 additionally identified associations for APP, PSEN2, CCK, and ZNF397. There was suggestive evidence for interaction between a BACE1 variant and APOE ε4 on brain Aβ deposition. Discussion: Identification of variants near/in known major Aβ-processing genes strengthens the relevance of plasma-Aβ levels as an endophenotype of AD. © 2021 The Authors. Alzheimer’s & Dementia published by Wiley Periodicals LLC on behalf of Alzheimer’s Association
Author Keywords
Alzheimer’s disease; APOE; APP; BACE1; endophenotype; genetic epidemiology; genome‑wide association study; plasma amyloid beta levels; plasma biomarkers; preclinical biomarkers; PSEN2
Funding details
115975
018947, LSHG‐CT‐2006‐01947
733051021
602633, QLG2‐CT‐2002‐01254
PO1AG007232, R01AG037212, RF1AG054023
National Institutes of HealthNIHAG034189, AG042483, AG045334, HHSN268200625226C, HL096814, HL096899, HL096902, HL096917, U01 AG024904, U01 HL096812, UL1TR001873
U.S. Department of DefenseDODW81XWH‐12‐2‐0012
National Institute of Mental HealthNIMH
National Institute on Drug AbuseNIDA
National Institute on AgingNIAAG008122, AG033040, AG033193, AG054076, R01AG049607, U01‐AG049505
National Heart, Lung, and Blood InstituteNHLBIHHSN268201100010C, N01‐HC‐25195, R01HL086694, R01HL087641, R01HL59367
National Human Genome Research InstituteNHGRIU01HG004402
National Cancer InstituteNCI
National Institute on Deafness and Other Communication DisordersNIDCDR01HL70825, UL1RR025005
National Institute of Neurological Disorders and StrokeNINDSR01‐NS017950, R01‐NS087541
National Institute of Biomedical Imaging and BioengineeringNIBIB
Alzheimer’s AssociationAA
Alzheimer’s Drug Discovery FoundationADDF
Biogen
National Center for Advancing Translational SciencesNCATS
AbbVie
Alzheimer’s Disease Neuroimaging InitiativeADNI
BioClinica
European CommissionEC
Agence Nationale de la RechercheANR
Institut National de la Santé et de la Recherche MédicaleInserm
ZonMw
Erasmus Universiteit RotterdamEUR
Ministerie van Volksgezondheid, Welzijn en SportVWS
Erasmus Medisch CentrumErasmus MC
Ministerie van Onderwijs, Cultuur en WetenschapOCW
Nederlandse Organisatie voor Wetenschappelijk OnderzoekNWO
Labex
Seventh Framework ProgrammeFP7FP7/2007‐2013, HEALTH‐F4‐2007‐201413
Agence Française de Sécurité Sanitaire des Produits de SantéAFSSAPS
Horizon 2020667375
Hersenstichting
Internationale Stichting Alzheimer OnderzoekISAO
European Regional Development FundERDF
Institute Pasteur De Lille
Centre for Medical Systems BiologyCMSB
Document Type: Article
Publication Stage: Article in Press
Source: Scopus