Association of brain amyloid-β with cerebral perfusion and structure in Alzheimer’s disease and mild cognitive impairment
Patients with Alzheimer’s disease show reduced cerebral blood flow, but it is unclear how this relates to β-amyloid pathology. By comparing patients with Alzheimer’s dementia, mild cognitive impairment, and controls, Mattsson et al. show that high β-amyloid load is associated with increased atrophy...
Saved in:
| Published in | Brain (London, England : 1878) Vol. 137; no. 5; pp. 1550 - 1561 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Oxford
Oxford University Press
01.05.2014
|
| Subjects | |
| Online Access | Get full text |
Cover
Loading…
| Abstract | Patients with Alzheimer’s disease show reduced cerebral blood flow, but it is unclear how this relates to β-amyloid pathology. By comparing patients with Alzheimer’s dementia, mild cognitive impairment, and controls, Mattsson et al. show that high β-amyloid load is associated with increased atrophy and reduced perfusion, independent of diagnosis.
Patients with Alzheimer’s disease have reduced cerebral blood flow measured by arterial spin labelling magnetic resonance imaging, but it is unclear how this is related to amyloid-β pathology. Using 182 subjects from the Alzheimer’s Disease Neuroimaging Initiative we tested associations of amyloid-β with regional cerebral blood flow in healthy controls (n = 51), early (n = 66) and late (n = 41) mild cognitive impairment, and Alzheimer’s disease with dementia (n = 24). Based on the theory that Alzheimer’s disease starts with amyloid-β accumulation and progresses with symptoms and secondary pathologies in different trajectories, we tested if cerebral blood flow differed between amyloid-β-negative controls and -positive subjects in different diagnostic groups, and if amyloid-β had different associations with cerebral blood flow and grey matter volume. Global amyloid-β load was measured by florbetapir positron emission tomography, and regional blood flow and volume were measured in eight a priori defined regions of interest. Cerebral blood flow was reduced in patients with dementia in most brain regions. Higher amyloid-β load was related to lower cerebral blood flow in several regions, independent of diagnostic group. When comparing amyloid-β-positive subjects with -negative controls, we found reductions of cerebral blood flow in several diagnostic groups, including in precuneus, entorhinal cortex and hippocampus (dementia), inferior parietal cortex (late mild cognitive impairment and dementia), and inferior temporal cortex (early and late mild cognitive impairment and dementia). The associations of amyloid-β with cerebral blood flow and volume differed across the disease spectrum, with high amyloid-β being associated with greater cerebral blood flow reduction in controls and greater volume reduction in late mild cognitive impairment and dementia. In addition to disease stage, amyloid-β pathology affects cerebral blood flow across the span from controls to dementia patients. Amyloid-β pathology has different associations with cerebral blood flow and volume, and may cause more loss of blood flow in early stages, whereas volume loss dominates in late disease stages. |
|---|---|
| AbstractList | Patients with Alzheimer's disease have reduced cerebral blood flow measured by arterial spin labelling magnetic resonance imaging, but it is unclear how this is related to amyloid-beta pathology. Using 182 subjects from the Alzheimer's Disease Neuroimaging Initiative we tested associations of amyloid-beta with regional cerebral blood flow in healthy controls (n = 51), early (n = 66) and late (n = 41) mild cognitive impairment, and Alzheimer's disease with dementia (n = 24). Based on the theory that Alzheimer's disease starts with amyloid-beta accumulation and progresses with symptoms and secondary pathologies in different trajectories, we tested if cerebral blood flow differed between amyloid-beta-negative controls and -positive subjects in different diagnostic groups, and if amyloid-beta had different associations with cerebral blood flow and grey matter volume. Global amyloid-beta load was measured by florbetapir positron emission tomography, and regional blood flow and volume were measured in eight a priori defined regions of interest. Cerebral blood flow was reduced in patients with dementia in most brain regions. Higher amyloid-beta load was related to lower cerebral blood flow in several regions, independent of diagnostic group. When comparing amyloid-beta-positive subjects with -negative controls, we found reductions of cerebral blood flow in several diagnostic groups, including in precuneus, entorhinal cortex and hippocampus (dementia), inferior parietal cortex (late mild cognitive impairment and dementia), and inferior temporal cortex (early and late mild cognitive impairment and dementia). The associations of amyloid-beta with cerebral blood flow and volume differed across the disease spectrum, with high amyloid-beta being associated with greater cerebral blood flow reduction in controls and greater volume reduction in late mild cognitive impairment and dementia. In addition to disease stage, amyloid-beta pathology affects cerebral blood flow across the span from controls to dementia patients. Amyloid-beta pathology has different associations with cerebral blood flow and volume, and may cause more loss of blood flow in early stages, whereas volume loss dominates in late disease stages. Patients with Alzheimer's disease show reduced cerebral blood flow, but it is unclear how this relates to beta -amyloid pathology. By comparing patients with Alzheimer's dementia, mild cognitive impairment, and controls, Mattsson et al. show that high beta -amyloid load is associated with increased atrophy and reduced perfusion, independent of diagnosis.Patients with Alzheimer's disease have reduced cerebral blood flow measured by arterial spin labelling magnetic resonance imaging, but it is unclear how this is related to amyloid- beta pathology. Using 182 subjects from the Alzheimer's Disease Neuroimaging Initiative we tested associations of amyloid- beta with regional cerebral blood flow in healthy controls (n = 51), early (n = 66) and late (n = 41) mild cognitive impairment, and Alzheimer's disease with dementia (n = 24). Based on the theory that Alzheimer's disease starts with amyloid- beta accumulation and progresses with symptoms and secondary pathologies in different trajectories, we tested if cerebral blood flow differed between amyloid- beta -negative controls and -positive subjects in different diagnostic groups, and if amyloid- beta had different associations with cerebral blood flow and grey matter volume. Global amyloid- beta load was measured by florbetapir positron emission tomography, and regional blood flow and volume were measured in eight a priori defined regions of interest. Cerebral blood flow was reduced in patients with dementia in most brain regions. Higher amyloid- beta load was related to lower cerebral blood flow in several regions, independent of diagnostic group. When comparing amyloid- beta -positive subjects with -negative controls, we found reductions of cerebral blood flow in several diagnostic groups, including in precuneus, entorhinal cortex and hippocampus (dementia), inferior parietal cortex (late mild cognitive impairment and dementia), and inferior temporal cortex (early and late mild cognitive impairment and dementia). The associations of amyloid- beta with cerebral blood flow and volume differed across the disease spectrum, with high amyloid- beta being associated with greater cerebral blood flow reduction in controls and greater volume reduction in late mild cognitive impairment and dementia. In addition to disease stage, amyloid- beta pathology affects cerebral blood flow across the span from controls to dementia patients. Amyloid- beta pathology has different associations with cerebral blood flow and volume, and may cause more loss of blood flow in early stages, whereas volume loss dominates in late disease stages. Patients with Alzheimer’s disease show reduced cerebral blood flow, but it is unclear how this relates to β-amyloid pathology. By comparing patients with Alzheimer’s dementia, mild cognitive impairment, and controls, Mattsson et al . show that high β-amyloid load is associated with increased atrophy and reduced perfusion, independent of diagnosis. Patients with Alzheimer’s disease have reduced cerebral blood flow measured by arterial spin labelling magnetic resonance imaging, but it is unclear how this is related to amyloid-β pathology. Using 182 subjects from the Alzheimer’s Disease Neuroimaging Initiative we tested associations of amyloid-β with regional cerebral blood flow in healthy controls ( n = 51), early ( n = 66) and late ( n = 41) mild cognitive impairment, and Alzheimer’s disease with dementia ( n = 24). Based on the theory that Alzheimer’s disease starts with amyloid-β accumulation and progresses with symptoms and secondary pathologies in different trajectories, we tested if cerebral blood flow differed between amyloid-β-negative controls and -positive subjects in different diagnostic groups, and if amyloid-β had different associations with cerebral blood flow and grey matter volume. Global amyloid-β load was measured by florbetapir positron emission tomography, and regional blood flow and volume were measured in eight a priori defined regions of interest. Cerebral blood flow was reduced in patients with dementia in most brain regions. Higher amyloid-β load was related to lower cerebral blood flow in several regions, independent of diagnostic group. When comparing amyloid-β-positive subjects with -negative controls, we found reductions of cerebral blood flow in several diagnostic groups, including in precuneus, entorhinal cortex and hippocampus (dementia), inferior parietal cortex (late mild cognitive impairment and dementia), and inferior temporal cortex (early and late mild cognitive impairment and dementia). The associations of amyloid-β with cerebral blood flow and volume differed across the disease spectrum, with high amyloid-β being associated with greater cerebral blood flow reduction in controls and greater volume reduction in late mild cognitive impairment and dementia. In addition to disease stage, amyloid-β pathology affects cerebral blood flow across the span from controls to dementia patients. Amyloid-β pathology has different associations with cerebral blood flow and volume, and may cause more loss of blood flow in early stages, whereas volume loss dominates in late disease stages. Patients with Alzheimer's disease have reduced cerebral blood flow measured by arterial spin labelling magnetic resonance imaging, but it is unclear how this is related to amyloid-β pathology. Using 182 subjects from the Alzheimer's Disease Neuroimaging Initiative we tested associations of amyloid-β with regional cerebral blood flow in healthy controls (n = 51), early (n = 66) and late (n = 41) mild cognitive impairment, and Alzheimer's disease with dementia (n = 24). Based on the theory that Alzheimer's disease starts with amyloid-β accumulation and progresses with symptoms and secondary pathologies in different trajectories, we tested if cerebral blood flow differed between amyloid-β-negative controls and -positive subjects in different diagnostic groups, and if amyloid-β had different associations with cerebral blood flow and grey matter volume. Global amyloid-β load was measured by florbetapir positron emission tomography, and regional blood flow and volume were measured in eight a priori defined regions of interest. Cerebral blood flow was reduced in patients with dementia in most brain regions. Higher amyloid-β load was related to lower cerebral blood flow in several regions, independent of diagnostic group. When comparing amyloid-β-positive subjects with -negative controls, we found reductions of cerebral blood flow in several diagnostic groups, including in precuneus, entorhinal cortex and hippocampus (dementia), inferior parietal cortex (late mild cognitive impairment and dementia), and inferior temporal cortex (early and late mild cognitive impairment and dementia). The associations of amyloid-β with cerebral blood flow and volume differed across the disease spectrum, with high amyloid-β being associated with greater cerebral blood flow reduction in controls and greater volume reduction in late mild cognitive impairment and dementia. In addition to disease stage, amyloid-β pathology affects cerebral blood flow across the span from controls to dementia patients. Amyloid-β pathology has different associations with cerebral blood flow and volume, and may cause more loss of blood flow in early stages, whereas volume loss dominates in late disease stages. Patients with Alzheimer’s disease show reduced cerebral blood flow, but it is unclear how this relates to β-amyloid pathology. By comparing patients with Alzheimer’s dementia, mild cognitive impairment, and controls, Mattsson et al. show that high β-amyloid load is associated with increased atrophy and reduced perfusion, independent of diagnosis. Patients with Alzheimer’s disease have reduced cerebral blood flow measured by arterial spin labelling magnetic resonance imaging, but it is unclear how this is related to amyloid-β pathology. Using 182 subjects from the Alzheimer’s Disease Neuroimaging Initiative we tested associations of amyloid-β with regional cerebral blood flow in healthy controls (n = 51), early (n = 66) and late (n = 41) mild cognitive impairment, and Alzheimer’s disease with dementia (n = 24). Based on the theory that Alzheimer’s disease starts with amyloid-β accumulation and progresses with symptoms and secondary pathologies in different trajectories, we tested if cerebral blood flow differed between amyloid-β-negative controls and -positive subjects in different diagnostic groups, and if amyloid-β had different associations with cerebral blood flow and grey matter volume. Global amyloid-β load was measured by florbetapir positron emission tomography, and regional blood flow and volume were measured in eight a priori defined regions of interest. Cerebral blood flow was reduced in patients with dementia in most brain regions. Higher amyloid-β load was related to lower cerebral blood flow in several regions, independent of diagnostic group. When comparing amyloid-β-positive subjects with -negative controls, we found reductions of cerebral blood flow in several diagnostic groups, including in precuneus, entorhinal cortex and hippocampus (dementia), inferior parietal cortex (late mild cognitive impairment and dementia), and inferior temporal cortex (early and late mild cognitive impairment and dementia). The associations of amyloid-β with cerebral blood flow and volume differed across the disease spectrum, with high amyloid-β being associated with greater cerebral blood flow reduction in controls and greater volume reduction in late mild cognitive impairment and dementia. In addition to disease stage, amyloid-β pathology affects cerebral blood flow across the span from controls to dementia patients. Amyloid-β pathology has different associations with cerebral blood flow and volume, and may cause more loss of blood flow in early stages, whereas volume loss dominates in late disease stages. Patients with Alzheimer's disease have reduced cerebral blood flow measured by arterial spin labelling magnetic resonance imaging, but it is unclear how this is related to amyloid-β pathology. Using 182 subjects from the Alzheimer's Disease Neuroimaging Initiative we tested associations of amyloid-β with regional cerebral blood flow in healthy controls (n = 51), early (n = 66) and late (n = 41) mild cognitive impairment, and Alzheimer's disease with dementia (n = 24). Based on the theory that Alzheimer's disease starts with amyloid-β accumulation and progresses with symptoms and secondary pathologies in different trajectories, we tested if cerebral blood flow differed between amyloid-β-negative controls and -positive subjects in different diagnostic groups, and if amyloid-β had different associations with cerebral blood flow and grey matter volume. Global amyloid-β load was measured by florbetapir positron emission tomography, and regional blood flow and volume were measured in eight a priori defined regions of interest. Cerebral blood flow was reduced in patients with dementia in most brain regions. Higher amyloid-β load was related to lower cerebral blood flow in several regions, independent of diagnostic group. When comparing amyloid-β-positive subjects with -negative controls, we found reductions of cerebral blood flow in several diagnostic groups, including in precuneus, entorhinal cortex and hippocampus (dementia), inferior parietal cortex (late mild cognitive impairment and dementia), and inferior temporal cortex (early and late mild cognitive impairment and dementia). The associations of amyloid-β with cerebral blood flow and volume differed across the disease spectrum, with high amyloid-β being associated with greater cerebral blood flow reduction in controls and greater volume reduction in late mild cognitive impairment and dementia. In addition to disease stage, amyloid-β pathology affects cerebral blood flow across the span from controls to dementia patients. Amyloid-β pathology has different associations with cerebral blood flow and volume, and may cause more loss of blood flow in early stages, whereas volume loss dominates in late disease stages.Patients with Alzheimer's disease have reduced cerebral blood flow measured by arterial spin labelling magnetic resonance imaging, but it is unclear how this is related to amyloid-β pathology. Using 182 subjects from the Alzheimer's Disease Neuroimaging Initiative we tested associations of amyloid-β with regional cerebral blood flow in healthy controls (n = 51), early (n = 66) and late (n = 41) mild cognitive impairment, and Alzheimer's disease with dementia (n = 24). Based on the theory that Alzheimer's disease starts with amyloid-β accumulation and progresses with symptoms and secondary pathologies in different trajectories, we tested if cerebral blood flow differed between amyloid-β-negative controls and -positive subjects in different diagnostic groups, and if amyloid-β had different associations with cerebral blood flow and grey matter volume. Global amyloid-β load was measured by florbetapir positron emission tomography, and regional blood flow and volume were measured in eight a priori defined regions of interest. Cerebral blood flow was reduced in patients with dementia in most brain regions. Higher amyloid-β load was related to lower cerebral blood flow in several regions, independent of diagnostic group. When comparing amyloid-β-positive subjects with -negative controls, we found reductions of cerebral blood flow in several diagnostic groups, including in precuneus, entorhinal cortex and hippocampus (dementia), inferior parietal cortex (late mild cognitive impairment and dementia), and inferior temporal cortex (early and late mild cognitive impairment and dementia). The associations of amyloid-β with cerebral blood flow and volume differed across the disease spectrum, with high amyloid-β being associated with greater cerebral blood flow reduction in controls and greater volume reduction in late mild cognitive impairment and dementia. In addition to disease stage, amyloid-β pathology affects cerebral blood flow across the span from controls to dementia patients. Amyloid-β pathology has different associations with cerebral blood flow and volume, and may cause more loss of blood flow in early stages, whereas volume loss dominates in late disease stages. |
| Author | Insel, Philip S. Jagust, William Jack, Clifford R Donohue, Michael Schuff, Norbert Beckett, Laurel A. Mattsson, Niklas Simonson, Alix Weiner, Michael W. Tosun, Duygu |
| AuthorAffiliation | 7 Helen Wills Neuroscience Institute and School of Public Health, University of California, Berkeley, CA, USA 2 Clinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden 5 Division of Biostatistics, Department of Public Health Sciences, School of Medicine, University of California, Davis, USA 6 Division of Biostatistics and Bioinformatics, Department of Family and Preventive Medicine, University of California, San Diego, La Jolla, CA, USA 4 Department of Radiology, Mayo Clinic, Rochester, MN, USA 1 Department of Veterans Affairs Medical Centre, Centre for Imaging of Neurodegenerative Diseases, San Francisco, CA, USA 3 Department of Radiology and Biomedical Imaging, University of California, San Francisco, CA, USA |
| AuthorAffiliation_xml | – name: 3 Department of Radiology and Biomedical Imaging, University of California, San Francisco, CA, USA – name: 7 Helen Wills Neuroscience Institute and School of Public Health, University of California, Berkeley, CA, USA – name: 4 Department of Radiology, Mayo Clinic, Rochester, MN, USA – name: 2 Clinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden – name: 1 Department of Veterans Affairs Medical Centre, Centre for Imaging of Neurodegenerative Diseases, San Francisco, CA, USA – name: 5 Division of Biostatistics, Department of Public Health Sciences, School of Medicine, University of California, Davis, USA – name: 6 Division of Biostatistics and Bioinformatics, Department of Family and Preventive Medicine, University of California, San Diego, La Jolla, CA, USA |
| Author_xml | – sequence: 1 givenname: Niklas surname: Mattsson fullname: Mattsson, Niklas email: niklas.mattsson@neuro.gu.se organization: Department of Veterans Affairs Medical Centre, Centre for Imaging of Neurodegenerative Diseases, San Francisco, CA, USA – sequence: 2 givenname: Duygu surname: Tosun fullname: Tosun, Duygu organization: Department of Veterans Affairs Medical Centre, Centre for Imaging of Neurodegenerative Diseases, San Francisco, CA, USA – sequence: 3 givenname: Philip S. surname: Insel fullname: Insel, Philip S. organization: Department of Veterans Affairs Medical Centre, Centre for Imaging of Neurodegenerative Diseases, San Francisco, CA, USA – sequence: 4 givenname: Alix surname: Simonson fullname: Simonson, Alix organization: Department of Veterans Affairs Medical Centre, Centre for Imaging of Neurodegenerative Diseases, San Francisco, CA, USA – sequence: 5 givenname: Clifford R surname: Jack fullname: Jack, Clifford R organization: Department of Radiology, Mayo Clinic, Rochester, MN, USA – sequence: 6 givenname: Laurel A. surname: Beckett fullname: Beckett, Laurel A. organization: Division of Biostatistics, Department of Public Health Sciences, School of Medicine, University of California, Davis, USA – sequence: 7 givenname: Michael surname: Donohue fullname: Donohue, Michael organization: Division of Biostatistics and Bioinformatics, Department of Family and Preventive Medicine, University of California, San Diego, La Jolla, CA, USA – sequence: 8 givenname: William surname: Jagust fullname: Jagust, William organization: Helen Wills Neuroscience Institute and School of Public Health, University of California, Berkeley, CA, USA – sequence: 9 givenname: Norbert surname: Schuff fullname: Schuff, Norbert organization: Department of Veterans Affairs Medical Centre, Centre for Imaging of Neurodegenerative Diseases, San Francisco, CA, USA – sequence: 10 givenname: Michael W. surname: Weiner fullname: Weiner, Michael W. organization: Department of Veterans Affairs Medical Centre, Centre for Imaging of Neurodegenerative Diseases, San Francisco, CA, USA |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=28440742$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/24625697$$D View this record in MEDLINE/PubMed https://gup.ub.gu.se/publication/199611$$DView record from Swedish Publication Index |
| BookMark | eNqNks2KFDEUhYOMOD2jO9eSjejCcpLK_0ZoBv9gwI2uQyqV6o5UJW1SNc2IC1_D1_BBfAifxHRXjzqC4iqQ-53Duck5AUchBgfAfYyeYqTIWZOMD2dmOyFKboEFphxVNWb8CCwQQrySiqFjcJLze4QwJTW_A45rymvGlViAT8uco_Vm9DHA2MG9GzTDVR99W337Crd-XEPrkiuTHm5c6qa8Y01oYR7TZMcpOVg0y_7j2vnBpe-fv2TY-uxMdnts8H0LbVwFP_rLwg4b49PgwngX3O5Mn929w3kK3r14_vb8VXXx5uXr8-VFZRkWYyWZ7UjXMaQawoRirTGSN5IY0XKBpULYWinqshHtak4lJpLgprZUqsY2TUtOQTX75q3bTI3eJD-YdKWj8Xo1bXS5Wk06O42V4hgX_tnMF3hwrS1Ry_I3ZDcnwa_1Kl5qopQSWBSDxweDFD9MLo968Nm6vjfBxSlrzAiVjBKC_gPFShIl2C7Wg99j_cxz_ZsFeHgATLam75IJ1udfnKQUCVoXrp45m2LOyXXa-nFfgbKN7zVGelctvS-DnqtVRE_-EF37_gV_NOOxPPA_yR-xpeRA |
| CitedBy_id | crossref_primary_10_1038_s41582_021_00565_x crossref_primary_10_1038_s41398_024_03220_3 crossref_primary_10_1016_j_nbas_2022_100035 crossref_primary_10_1016_j_nicl_2016_03_002 crossref_primary_10_1177_0271678X17732449 crossref_primary_10_3389_fnagi_2017_00181 crossref_primary_10_1177_0271678X231178993 crossref_primary_10_3233_JAD_200473 crossref_primary_10_1002_trc2_12285 crossref_primary_10_3233_JAD_220910 crossref_primary_10_1002_alz_14233 crossref_primary_10_1016_j_brainres_2024_149312 crossref_primary_10_1177_13872877251321118 crossref_primary_10_1016_j_neurobiolaging_2024_03_007 crossref_primary_10_1016_j_neurobiolaging_2025_03_007 crossref_primary_10_1093_brain_awx112 crossref_primary_10_1038_s41593_024_01753_w crossref_primary_10_1093_brain_awu367 crossref_primary_10_3233_BPL_180075 crossref_primary_10_1038_s41419_023_06316_8 crossref_primary_10_1002_jmri_26810 crossref_primary_10_1016_j_neurobiolaging_2014_12_036 crossref_primary_10_1016_j_mcn_2018_06_005 crossref_primary_10_1038_s41467_023_37840_y crossref_primary_10_3389_fcvm_2022_831730 crossref_primary_10_3389_fnins_2019_00037 crossref_primary_10_1002_jnr_23777 crossref_primary_10_1016_j_arr_2021_101450 crossref_primary_10_1016_j_jalz_2015_05_002 crossref_primary_10_1016_j_neurobiolaging_2019_10_023 crossref_primary_10_1681_ASN_0000000000000185 crossref_primary_10_1007_s10741_015_9488_5 crossref_primary_10_3233_JAD_200490 crossref_primary_10_1162_imag_a_00506 crossref_primary_10_1016_j_dadm_2015_09_002 crossref_primary_10_1016_j_arr_2020_101108 crossref_primary_10_1002_trc2_12070 crossref_primary_10_3233_JPD_212596 crossref_primary_10_1002_alz_14059 crossref_primary_10_1016_j_trci_2019_04_006 crossref_primary_10_1016_j_arr_2022_101661 crossref_primary_10_3233_JAD_180232 crossref_primary_10_3389_fnagi_2022_859873 crossref_primary_10_1016_j_neures_2015_04_002 crossref_primary_10_3389_fnins_2022_993767 crossref_primary_10_3389_fnagi_2021_749026 crossref_primary_10_1016_j_celrep_2024_113970 crossref_primary_10_1523_JNEUROSCI_1230_20_2020 crossref_primary_10_1007_s00415_015_7711_x crossref_primary_10_1016_j_ijbiomac_2022_07_158 crossref_primary_10_1016_j_pscychresns_2015_05_014 crossref_primary_10_2139_ssrn_4182791 crossref_primary_10_3389_fnins_2021_781722 crossref_primary_10_1007_s11357_024_01361_3 crossref_primary_10_3233_JAD_231249 crossref_primary_10_1016_j_bbr_2016_05_030 crossref_primary_10_1007_s11682_022_00750_6 crossref_primary_10_1038_nrneurol_2017_111 crossref_primary_10_1002_alz_12958 crossref_primary_10_1002_jnr_23634 crossref_primary_10_1007_s00259_022_05958_8 crossref_primary_10_1016_j_neubiorev_2016_11_023 crossref_primary_10_3233_JAD_201474 crossref_primary_10_1007_s00330_016_4450_z crossref_primary_10_1016_j_neurobiolaging_2024_11_008 crossref_primary_10_1017_S0007114521002567 crossref_primary_10_3389_fneur_2018_00618 crossref_primary_10_1016_j_neurobiolaging_2019_06_003 crossref_primary_10_1016_j_neurobiolaging_2021_02_003 crossref_primary_10_1161_JAHA_123_029797 crossref_primary_10_3233_BPL_220146 crossref_primary_10_1016_j_neuroimage_2019_05_033 crossref_primary_10_3389_fgene_2022_942203 crossref_primary_10_3233_JAD_150487 crossref_primary_10_1016_j_neurobiolaging_2021_04_009 crossref_primary_10_1016_j_neurobiolaging_2017_03_029 crossref_primary_10_3233_JAD_200034 crossref_primary_10_1177_0271678X17722436 crossref_primary_10_1016_j_nicl_2017_12_003 crossref_primary_10_1186_s13063_021_05336_z crossref_primary_10_1002_alz_14310 crossref_primary_10_3233_JAD_160201 crossref_primary_10_3389_fnagi_2024_1345251 crossref_primary_10_1007_s00401_019_01967_4 crossref_primary_10_1177_0271678X20935171 crossref_primary_10_1007_s40263_016_0374_z crossref_primary_10_1016_j_neurobiolaging_2022_12_006 crossref_primary_10_1016_j_nicl_2018_04_016 crossref_primary_10_1002_alz_13461 crossref_primary_10_1016_j_ynirp_2022_100080 crossref_primary_10_1007_s13311_022_01192_0 crossref_primary_10_1016_j_neurobiolaging_2023_06_014 crossref_primary_10_1016_j_athoracsur_2018_07_056 crossref_primary_10_1016_j_jalz_2016_08_010 crossref_primary_10_1021_acsptsci_4c00614 crossref_primary_10_1007_s00401_020_02215_w crossref_primary_10_1212_WNL_0000000000006355 crossref_primary_10_1016_j_nbd_2025_106877 crossref_primary_10_3390_antiox10020143 crossref_primary_10_1177_0271678X16641128 crossref_primary_10_1210_clinem_dgad764 crossref_primary_10_1161_STROKEAHA_120_031073 crossref_primary_10_3390_biom13050830 crossref_primary_10_1002_alz_12666 crossref_primary_10_1017_S1355617722000649 crossref_primary_10_1016_j_ebiom_2024_105355 crossref_primary_10_3892_mmr_2019_9950 crossref_primary_10_1016_j_neurobiolaging_2016_06_006 crossref_primary_10_1002_jnr_24075 crossref_primary_10_1038_jcbfm_2015_157 crossref_primary_10_3389_fendo_2022_1014287 crossref_primary_10_1016_j_mri_2022_12_011 crossref_primary_10_3174_ajnr_A5902 crossref_primary_10_3233_JAD_190645 crossref_primary_10_3171_2015_6_JNS15639 crossref_primary_10_1007_s13311_016_0481_z crossref_primary_10_1177_0271678X20982383 crossref_primary_10_3389_fncel_2015_00017 crossref_primary_10_1177_0271678X15605847 crossref_primary_10_1016_j_jalz_2016_11_007 crossref_primary_10_1161_CIRCULATIONAHA_117_027448 crossref_primary_10_1016_j_neuroimage_2020_117482 crossref_primary_10_1007_s11682_021_00495_8 crossref_primary_10_1186_s13024_025_00798_0 crossref_primary_10_1186_s13195_017_0300_8 crossref_primary_10_1186_s41232_022_00216_8 crossref_primary_10_1016_j_cccb_2020_100001 crossref_primary_10_3233_JAD_180958 crossref_primary_10_3233_JAD_170402 crossref_primary_10_1177_0271678X221141139 crossref_primary_10_3233_JAD_221023 crossref_primary_10_3390_ijms24119272 crossref_primary_10_1177_0271678X211020863 crossref_primary_10_2139_ssrn_4138281 crossref_primary_10_1016_j_ab_2021_114387 crossref_primary_10_1007_s10571_015_0261_z crossref_primary_10_3233_JAD_220601 crossref_primary_10_1016_j_jpsychires_2021_01_053 crossref_primary_10_1007_s13365_020_00859_8 crossref_primary_10_1002_jmri_29462 crossref_primary_10_1038_s41398_021_01374_y crossref_primary_10_3390_jcm8050651 crossref_primary_10_5665_sleep_4658 crossref_primary_10_1002_hbm_23732 crossref_primary_10_3233_JAD_210531 crossref_primary_10_1016_j_cccb_2022_100153 crossref_primary_10_1016_j_neuint_2019_04_005 crossref_primary_10_1515_revneuro_2024_0046 |
| Cites_doi | 10.1001/archneur.1987.00520140035014 10.1523/JNEUROSCI.3669-09.2009 10.3233/JAD-2011-0010 10.1001/jama.286.17.2120 10.1016/S0140-6736(06)69113-7 10.1148/radiol.12120928 10.1126/science.1072994 10.1002/ana.410300410 10.3174/ajnr.A1562 10.1212/WNL.39.11.1427 10.1007/s00406-011-0226-2 10.1002/1531-8249(200001)47:1<93::AID-ANA15>3.0.CO;2-8 10.1007/978-3-642-02498-6_55 10.1097/WAD.0b013e3181b4f736 10.1016/j.neuroimage.2008.06.006 10.1007/s00234-012-1077-x 10.1002/ana.23650 10.1016/j.tics.2011.09.004 10.1016/0022-510X(95)00323-T 10.1212/01.WNL.0000163856.13524.08 10.3174/ajnr.A1955 10.1002/(SICI)1522-2594(199906)41:6<1246::AID-MRM22>3.0.CO;2-N 10.2967/jnumed.108.051946 10.1073/pnas.91.1.33 10.2967/jnumed.106.037218 10.1016/S0197-4580(01)00230-5 10.1016/j.acra.2011.07.015 10.1212/01.wnl.0000296941.06685.22 10.1016/j.jalz.2009.04.1233 10.1002/ana.21955 10.1002/ana.20889 10.1056/NEJMoa1202753 10.3233/JAD-2012-120292 10.3233/JAD-2010-091699 10.1148/radiol.2503080751 10.1097/WAD.0b013e318199ff46 10.1001/archneurol.2011.183 10.1016/j.neurobiolaging.2008.01.012 10.1097/WCO.0b013e328354ff0a 10.1056/NEJM199603213341202 10.1097/00019442-200411000-00002 10.1212/01.WNL.0000055847.17752.E6 10.1016/S1474-4422(12)70291-0 10.1002/mrm.1910230106 10.1002/hbm.22173 10.1016/j.neuroimage.2011.12.077 10.1097/00004728-198308000-00003 10.1148/radiol.2343040197 10.2967/jnumed.107.045385 |
| ContentType | Journal Article |
| Contributor | Jack, Jr, Clifford R Khachaturian, Zaven Vemuri, Prashanthi Figurski, Michal Schuff, Norbert Snyder, Peter Schwartz, Adam Frank, Richard Chen, Kewei Jagust, William Jiminez, Gus Green, Robert C Mesulam, M Marcel Beccera, Mauricio Pawluczyk, Sonia Weiner, Michael Borowski, Bret Hefti, Franz Montine, Tom Dolen, Sara Gunter, Jeff Thompson, Paul DeCArli, Charles Trojanowki, John Q Fox, Nick Thal, Lean Faber, Kelley Lind, Betty Korecka, Magdalena Walter, Sarah Quinn, Joseph Fillit, Howard Neu, Scott Sather, Tamie Jones, David Landau, Susan Paul, Steven Kantarci, Kejal Aisen, Paul Morris, John Holtzman, Davie Reiman, Eric M Buckholtz, Neil Morris, John C Foster, Norm Mathis, Chet Foroud, Tatiana M Kaye, Jeffrey Saykin, Andrew J Harvey, Danielle Koeppe, Robert A Weiner, Michael W Nho, Kwangsik Potkin, Steven Potter, William Gessert, Devon Petersen, Ronald Shaw, Leslie M Donohue, Michael Schneider, Lon S Sorensen, Greg Thomas, Ronald G Raichle, Marc Davies, Peter Ward, Chad Hsiao, John Shen, Li Senjem, Matt Albert, Marylyn Kim, Sungeun Carter, Raina Carrillo, Mar |
| Contributor_xml | – sequence: 1 givenname: Michael W surname: Weiner fullname: Weiner, Michael W – sequence: 2 givenname: Paul surname: Aisen fullname: Aisen, Paul – sequence: 3 givenname: Michael surname: Weiner fullname: Weiner, Michael – sequence: 4 givenname: Ronald surname: Petersen fullname: Petersen, Ronald – sequence: 5 givenname: Clifford R surname: Jack, Jr fullname: Jack, Jr, Clifford R – sequence: 6 givenname: William surname: Jagust fullname: Jagust, William – sequence: 7 givenname: John Q surname: Trojanowki fullname: Trojanowki, John Q – sequence: 8 givenname: Arthur W surname: Toga fullname: Toga, Arthur W – sequence: 9 givenname: Laurel surname: Beckett fullname: Beckett, Laurel – sequence: 10 givenname: Robert C surname: Green fullname: Green, Robert C – sequence: 11 givenname: Andrew J surname: Saykin fullname: Saykin, Andrew J – sequence: 12 givenname: John surname: Morris fullname: Morris, John – sequence: 13 givenname: Leslie M surname: Shaw fullname: Shaw, Leslie M – sequence: 14 givenname: Zaven surname: Khachaturian fullname: Khachaturian, Zaven – sequence: 15 givenname: Greg surname: Sorensen fullname: Sorensen, Greg – sequence: 16 givenname: Maria surname: Carrillo fullname: Carrillo, Maria – sequence: 17 givenname: Lew surname: Kuller fullname: Kuller, Lew – sequence: 18 givenname: Marc surname: Raichle fullname: Raichle, Marc – sequence: 19 givenname: Steven surname: Paul fullname: Paul, Steven – sequence: 20 givenname: Peter surname: Davies fullname: Davies, Peter – sequence: 21 givenname: Howard surname: Fillit fullname: Fillit, Howard – sequence: 22 givenname: Franz surname: Hefti fullname: Hefti, Franz – sequence: 23 givenname: Davie surname: Holtzman fullname: Holtzman, Davie – sequence: 24 givenname: M Marcel surname: Mesulam fullname: Mesulam, M Marcel – sequence: 25 givenname: William surname: Potter fullname: Potter, William – sequence: 26 givenname: Peter surname: Snyder fullname: Snyder, Peter – sequence: 27 givenname: Adam surname: Schwartz fullname: Schwartz, Adam – sequence: 28 givenname: Tom surname: Montine fullname: Montine, Tom – sequence: 29 givenname: Ronald G surname: Thomas fullname: Thomas, Ronald G – sequence: 30 givenname: Michael surname: Donohue fullname: Donohue, Michael – sequence: 31 givenname: Sarah surname: Walter fullname: Walter, Sarah – sequence: 32 givenname: Devon surname: Gessert fullname: Gessert, Devon – sequence: 33 givenname: Tamie surname: Sather fullname: Sather, Tamie – sequence: 34 givenname: Gus surname: Jiminez fullname: Jiminez, Gus – sequence: 35 givenname: Danielle surname: Harvey fullname: Harvey, Danielle – sequence: 36 givenname: Matthew surname: Bernstein fullname: Bernstein, Matthew – sequence: 37 givenname: Nick surname: Fox fullname: Fox, Nick – sequence: 38 givenname: Paul surname: Thompson fullname: Thompson, Paul – sequence: 39 givenname: Norbert surname: Schuff fullname: Schuff, Norbert – sequence: 40 givenname: Charles surname: DeCArli fullname: DeCArli, Charles – sequence: 41 givenname: Bret surname: Borowski fullname: Borowski, Bret – sequence: 42 givenname: Jeff surname: Gunter fullname: Gunter, Jeff – sequence: 43 givenname: Matt surname: Senjem fullname: Senjem, Matt – sequence: 44 givenname: Prashanthi surname: Vemuri fullname: Vemuri, Prashanthi – sequence: 45 givenname: David surname: Jones fullname: Jones, David – sequence: 46 givenname: Kejal surname: Kantarci fullname: Kantarci, Kejal – sequence: 47 givenname: Chad surname: Ward fullname: Ward, Chad – sequence: 48 givenname: Robert A surname: Koeppe fullname: Koeppe, Robert A – sequence: 49 givenname: Norm surname: Foster fullname: Foster, Norm – sequence: 50 givenname: Eric M surname: Reiman fullname: Reiman, Eric M – sequence: 51 givenname: Kewei surname: Chen fullname: Chen, Kewei – sequence: 52 givenname: Chet surname: Mathis fullname: Mathis, Chet – sequence: 53 givenname: Susan surname: Landau fullname: Landau, Susan – sequence: 54 givenname: John C surname: Morris fullname: Morris, John C – sequence: 55 givenname: Nigel J surname: Cairns fullname: Cairns, Nigel J – sequence: 56 givenname: Lisa surname: Taylor-Reinwald fullname: Taylor-Reinwald, Lisa – sequence: 57 givenname: Virginia surname: Lee fullname: Lee, Virginia – sequence: 58 givenname: Magdalena surname: Korecka fullname: Korecka, Magdalena – sequence: 59 givenname: Michal surname: Figurski fullname: Figurski, Michal – sequence: 60 givenname: Karen surname: Crawford fullname: Crawford, Karen – sequence: 61 givenname: Scott surname: Neu fullname: Neu, Scott – sequence: 62 givenname: Tatiana M surname: Foroud fullname: Foroud, Tatiana M – sequence: 63 givenname: Steven surname: Potkin fullname: Potkin, Steven – sequence: 64 givenname: Li surname: Shen fullname: Shen, Li – sequence: 65 givenname: Kelley surname: Faber fullname: Faber, Kelley – sequence: 66 givenname: Sungeun surname: Kim fullname: Kim, Sungeun – sequence: 67 givenname: Kwangsik surname: Nho fullname: Nho, Kwangsik – sequence: 68 givenname: Lean surname: Thal fullname: Thal, Lean – sequence: 69 givenname: Leon surname: Thal fullname: Thal, Leon – sequence: 70 givenname: Neil surname: Buckholtz fullname: Buckholtz, Neil – sequence: 71 givenname: Peter J surname: Snyder fullname: Snyder, Peter J – sequence: 72 givenname: Marylyn surname: Albert fullname: Albert, Marylyn – sequence: 73 givenname: Richard surname: Frank fullname: Frank, Richard – sequence: 74 givenname: John surname: Hsiao fullname: Hsiao, John – sequence: 75 givenname: Jeffrey surname: Kaye fullname: Kaye, Jeffrey – sequence: 76 givenname: Joseph surname: Quinn fullname: Quinn, Joseph – sequence: 77 givenname: Betty surname: Lind fullname: Lind, Betty – sequence: 78 givenname: Raina surname: Carter fullname: Carter, Raina – sequence: 79 givenname: Sara surname: Dolen fullname: Dolen, Sara – sequence: 80 givenname: Lon S surname: Schneider fullname: Schneider, Lon S – sequence: 81 givenname: Sonia surname: Pawluczyk fullname: Pawluczyk, Sonia – sequence: 82 givenname: Mauricio surname: Beccera fullname: Beccera, Mauricio |
| Copyright | The Author (2014). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oup.com 2014 2015 INIST-CNRS |
| Copyright_xml | – notice: The Author (2014). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oup.com 2014 – notice: 2015 INIST-CNRS |
| CorporateAuthor | Alzheimer's Disease Neuroimaging Initiative |
| CorporateAuthor_xml | – name: Alzheimer's Disease Neuroimaging Initiative |
| DBID | AAYXX CITATION IQODW CGR CUY CVF ECM EIF NPM 7X8 7TK 5PM ADTPV AOWAS F1U |
| DOI | 10.1093/brain/awu043 |
| DatabaseName | CrossRef Pascal-Francis Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed MEDLINE - Academic Neurosciences Abstracts PubMed Central (Full Participant titles) SwePub SwePub Articles SWEPUB Göteborgs universitet |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) MEDLINE - Academic Neurosciences Abstracts |
| DatabaseTitleList | Neurosciences Abstracts MEDLINE MEDLINE - Academic |
| Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Medicine |
| EISSN | 1460-2156 |
| EndPage | 1561 |
| ExternalDocumentID | oai_gup_ub_gu_se_199611 PMC3999717 24625697 28440742 10_1093_brain_awu043 10.1093/brain/awu043 |
| Genre | Multicenter Study Research Support, Non-U.S. Gov't Journal Article Research Support, N.I.H., Extramural |
| GrantInformation_xml | – fundername: Canadian Institutes of Health Research – fundername: NCATS NIH HHS grantid: UL1 TR001108 – fundername: NIA NIH HHS grantid: U24 AG021886 – fundername: NIA NIH HHS grantid: P30 AG013846 – fundername: NIA NIH HHS grantid: P30 AG010129 – fundername: NIBIB NIH HHS grantid: P41 EB015922 – fundername: NIA NIH HHS grantid: U01 AG024904 – fundername: NCATS NIH HHS grantid: UL1 TR002529 – fundername: NIA NIH HHS grantid: K01 AG030514 |
| GroupedDBID | --- -E4 -~X .2P .55 .GJ .I3 .XZ .ZR 0R~ 1CY 1TH 23N 2WC 354 3O- 4.4 41~ 482 48X 53G 5GY 5RE 5VS 5WA 5WD 6.Y 6PF 70D AABZA AACZT AAGKA AAIMJ AAJKP AAJQQ AAMDB AAMVS AAOGV AAPGJ AAPNW AAPQZ AAPXW AAQQT AARHZ AASNB AAUAY AAUQX AAVAP AAVLN AAWDT AAWTL AAYJJ ABEUO ABIVO ABIXL ABJNI ABKDP ABLJU ABMNT ABNHQ ABNKS ABPTD ABQLI ABQNK ABQTQ ABSAR ABSMQ ABWST ABXVV ABZBJ ACBNA ACFRR ACGFS ACIWK ACPQN ACPRK ACUFI ACUTJ ACUTO ACYHN ACZBC ADBBV ADEYI ADEZT ADGKP ADGZP ADHKW ADHZD ADIPN ADJQC ADOCK ADQBN ADRIX ADRTK ADVEK ADYVW ADZXQ AEGPL AEJOX AEKPW AEKSI AELWJ AEMDU AENEX AENZO AEPUE AETBJ AEWNT AFFNX AFFZL AFGWE AFIYH AFOFC AFSHK AFXAL AFXEN AFYAG AGINJ AGKEF AGKRT AGMDO AGQXC AGSYK AGUTN AHMBA AHXPO AI. AIJHB AJEEA AKWXX ALMA_UNASSIGNED_HOLDINGS ALUQC ANFBD APIBT APJGH APWMN AQDSO AQKUS ARIXL ASAOO ASPBG ATDFG ATGXG ATTQO AVNTJ AVWKF AXUDD AYOIW AZFZN BAWUL BAYMD BCRHZ BEYMZ BHONS BQDIO BR6 BSWAC BTRTY BVRKM BZKNY C1A C45 CAG CDBKE COF CS3 CXTWN CZ4 DAKXR DFGAJ DIK DILTD DU5 D~K E3Z EBS EE~ EIHJH EJD ELUNK EMOBN ENERS F20 F5P F9B FECEO FEDTE FHSFR FLUFQ FOEOM FOTVD FQBLK G8K GAUVT GJXCC GX1 H13 H5~ HAR HVGLF HW0 HZ~ IOX J21 J5H JXSIZ KAQDR KBUDW KC5 KOP KQ8 KSI KSN L7B M-Z M49 MBLQV MBTAY MHKGH ML0 MVM N4W N9A NGC NLBLG NOMLY NOYVH NTWIH NU- NVLIB O0~ O9- OAUYM OAWHX OBOKY OCZFY ODMLO OHH OHT OJQWA OJZSN OK1 OPAEJ OVD OWPYF O~Y P2P PAFKI PB- PEELM PQQKQ Q1. Q5Y QBD R44 RD5 RIG RNI ROL ROX ROZ RUSNO RW1 RXO RZF RZO TCN TCURE TEORI TJX TLC TMA TR2 VH1 VVN W8F WH7 WOQ X7H X7M XJT XOL YAYTL YKOAZ YQJ YSK YXANX ZCG ZGI ZKB ZKX ZXP ~91 AAYXX ABDFA ABDPE ABEJV ABGNP ABIME ABNGD ABPIB ABPQP ABVGC ABXZS ABZEO ACUKT ACVCV ADMTO ADNBA AEHUL AEMQT AFFQV AGORE AGQPQ AHGBF AHMMS AJBYB AJDVS AJNCP ALXQX CITATION OBFPC 08R AABJS AABMN AAESY AAIYJ AANRK AAPBV ABFLS ABPTK ACIMA ADEIU ADGIM ADORX ADQLU AELNO AGVJH AHGVY AIKOY AIMBJ ASMCH AWCFO AZQFJ B4K BGYMP BYORX DPORF DPPUQ IPNFZ IQODW K78 PQEST UMP ZA5 CGR CUY CVF ECM EIF NPM 7X8 7TK 5PM ADTPV AOWAS F1U |
| ID | FETCH-LOGICAL-c517t-85cf3ff509b35795daa86b83a7d6718901cc8722564f264813831b2c489bcbbd3 |
| ISSN | 0006-8950 1460-2156 |
| IngestDate | Thu Aug 21 07:15:28 EDT 2025 Thu Aug 21 18:26:06 EDT 2025 Fri Jul 11 11:18:36 EDT 2025 Fri Jul 11 08:09:22 EDT 2025 Thu Apr 03 07:05:24 EDT 2025 Thu Nov 24 18:35:09 EST 2022 Tue Jul 01 00:46:06 EDT 2025 Thu Apr 24 23:02:47 EDT 2025 Wed Aug 28 03:22:51 EDT 2024 |
| IsDoiOpenAccess | false |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 5 |
| Keywords | beta-amyloid perfusion imaging magnetic resonance imaging Alzheimer’s disease PET imaging Radionuclide study Nervous system diseases Cognitive disorder Alzheimer disease Central nervous system Nuclear magnetic resonance imaging Cerebral disorder Encephalon Perfusion imaging Central nervous system disease Medical imagery Degenerative disease Amyloid mild cognitive impairment Positron emission tomography Alzheimer's disease |
| Language | English |
| License | CC BY 4.0 |
| LinkModel | OpenURL |
| MergedId | FETCHMERGED-LOGICAL-c517t-85cf3ff509b35795daa86b83a7d6718901cc8722564f264813831b2c489bcbbd3 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 ObjectType-Article-2 ObjectType-Feature-1 For details see Appendix 1 |
| OpenAccessLink | https://academic.oup.com/brain/article-pdf/137/5/1550/13797305/awu043.pdf |
| PMID | 24625697 |
| PQID | 1519839751 |
| PQPubID | 23479 |
| PageCount | 12 |
| ParticipantIDs | swepub_primary_oai_gup_ub_gu_se_199611 pubmedcentral_primary_oai_pubmedcentral_nih_gov_3999717 proquest_miscellaneous_1534854330 proquest_miscellaneous_1519839751 pubmed_primary_24625697 pascalfrancis_primary_28440742 crossref_citationtrail_10_1093_brain_awu043 crossref_primary_10_1093_brain_awu043 oup_primary_10_1093_brain_awu043 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | 2014-05-01 |
| PublicationDateYYYYMMDD | 2014-05-01 |
| PublicationDate_xml | – month: 05 year: 2014 text: 2014-05-01 day: 01 |
| PublicationDecade | 2010 |
| PublicationPlace | Oxford |
| PublicationPlace_xml | – name: Oxford – name: England |
| PublicationTitle | Brain (London, England : 1878) |
| PublicationTitleAlternate | Brain |
| PublicationYear | 2014 |
| Publisher | Oxford University Press |
| Publisher_xml | – name: Oxford University Press |
| References | Bateman ( key 20170425182013_awu043-B8) 2012; 367 Jack ( key 20170425182013_awu043-B27) 2011; 68 Reiman ( key 20170425182013_awu043-B41) 1996; 334 Xu ( key 20170425182013_awu043-B50) 2007; 69 Fleisher ( key 20170425182013_awu043-B21) 2009; 30 Tao ( key 20170425182013_awu043-B47) 2009; 21 Archer ( key 20170425182013_awu043-B5) 2006; 60 Roberts ( key 20170425182013_awu043-B42) 1994; 91 key 20170425182013_awu043-B52 Yoshiura ( key 20170425182013_awu043-B51) 2009; 30 Johnson ( key 20170425182013_awu043-B29) 1987; 44 Dai ( key 20170425182013_awu043-B16) 2009; 250 Jagust ( key 20170425182013_awu043-B28) 2011; 15 Mosconi ( key 20170425182013_awu043-B37) 2008; 49 Alsop ( key 20170425182013_awu043-B2) 2000; 47 Mosconi ( key 20170425182013_awu043-B36) 2005; 64 Terry ( key 20170425182013_awu043-B48) 1991; 30 Chételat ( key 20170425182013_awu043-B13) 2003; 60 Hardy ( key 20170425182013_awu043-B24) 2002; 297 Johnson ( key 20170425182013_awu043-B30) 2005; 234 Raji ( key 20170425182013_awu043-B40) 2010; 31 Chételat ( key 20170425182013_awu043-B14) 2010; 67 Chao ( key 20170425182013_awu043-B11) 2009; 23 Alexopoulos ( key 20170425182013_awu043-B1) 2012; 262 Cohen ( key 20170425182013_awu043-B15) 2009; 29 Oh ( key 20170425182013_awu043-B38) 2014; 35 Chao ( key 20170425182013_awu043-B12) 2010; 24 Silverman ( key 20170425182013_awu043-B45) 2001; 286 Binnewijzend ( key 20170425182013_awu043-B9) 2013; 267 Landau ( key 20170425182013_awu043-B32) 2012; 72 Sojkova ( key 20170425182013_awu043-B46) 2008; 49 Alsop ( key 20170425182013_awu043-B4) 2010; 20 Schuff ( key 20170425182013_awu043-B44) 2009; 5 Wolk ( key 20170425182013_awu043-B49) 2012; 25 Detre ( key 20170425182013_awu043-B18) 1992; 23 Luh ( key 20170425182013_awu043-B34) 1999; 41 Alsop ( key 20170425182013_awu043-B3) 2008; 42 Dougall ( key 20170425182013_awu043-B19) 2004; 12 Ishii ( key 20170425182013_awu043-B25) 1997; 24 Bangen ( key 20170425182013_awu043-B7) 2012; 31 Kim ( key 20170425182013_awu043-B31) 2013; 55 Blennow ( key 20170425182013_awu043-B10) 2006; 368 Fink ( key 20170425182013_awu043-B20) 1996; 137 Matsuda ( key 20170425182013_awu043-B35) 2007; 48 Dashjamts ( key 20170425182013_awu043-B17) 2011; 18 Jack ( key 20170425182013_awu043-B26) 2013; 12 Austin ( key 20170425182013_awu043-B6) 2011; 26 Friedland ( key 20170425182013_awu043-B23) 1989; 39 Li ( key 20170425182013_awu043-B33) 2012; 60 Ossenkoppele ( key 20170425182013_awu043-B39) 2013 De Santi ( key 20170425182013_awu043-B43) 2001; 22 Friedland ( key 20170425182013_awu043-B22) 1983; 7 |
| References_xml | – volume: 44 start-page: 165 year: 1987 ident: key 20170425182013_awu043-B29 article-title: Cerebral perfusion imaging in Alzheimer’s disease. Use of single photon emission computed tomography and iofetamine hydrochloride I 123 publication-title: Arch Neurol doi: 10.1001/archneur.1987.00520140035014 – volume: 29 start-page: 14770 year: 2009 ident: key 20170425182013_awu043-B15 article-title: Basal cerebral metabolism may modulate the cognitive effects of Abeta in mild cognitive impairment: an example of brain reserve publication-title: J Neurosci doi: 10.1523/JNEUROSCI.3669-09.2009 – volume: 26 start-page: 123 year: 2011 ident: key 20170425182013_awu043-B6 article-title: Effects of hypoperfusion in Alzheimer’s disease publication-title: J Alzheimers Dis doi: 10.3233/JAD-2011-0010 – volume: 286 start-page: 2120 year: 2001 ident: key 20170425182013_awu043-B45 article-title: Positron emission tomography in evaluation of dementia: regional brain metabolism and long-term outcome publication-title: JAMA doi: 10.1001/jama.286.17.2120 – volume: 368 start-page: 387 year: 2006 ident: key 20170425182013_awu043-B10 article-title: Alzheimer’s disease publication-title: Lancet doi: 10.1016/S0140-6736(06)69113-7 – volume: 267 start-page: 221 year: 2013 ident: key 20170425182013_awu043-B9 article-title: Cerebral blood flow measured with 3D pseudocontinuous arterial spin-labeling MR imaging in Alzheimer disease and mild cognitive impairment: a marker for disease severity publication-title: Radiology doi: 10.1148/radiol.12120928 – volume: 297 start-page: 353 year: 2002 ident: key 20170425182013_awu043-B24 article-title: The amyloid hypothesis of Alzheimer’s disease: progress and problems on the road to therapeutics publication-title: Science doi: 10.1126/science.1072994 – volume: 30 start-page: 572 year: 1991 ident: key 20170425182013_awu043-B48 article-title: Physical basis of cognitive alterations in Alzheimer’s disease: synapse loss is the major correlate of cognitive impairment publication-title: Ann Neurol doi: 10.1002/ana.410300410 – volume: 30 start-page: 1388 year: 2009 ident: key 20170425182013_awu043-B51 article-title: Simultaneous measurement of arterial transit time, arterial bloodvolume, and cerebral blood flow using arterial spin-labeling in patients with Alzheimer disease publication-title: AJNR Am J Neuroradiol doi: 10.3174/ajnr.A1562 – year: 2013 ident: key 20170425182013_awu043-B39 article-title: Is verbal episodic memory in elderly with amyloid deposits preserved through altered neuronal function? publication-title: Cereb Cortex – volume: 39 start-page: 1427 year: 1989 ident: key 20170425182013_awu043-B23 article-title: Regional cerebral glucose transport and utilization in Alzheimer’s disease publication-title: Neurology doi: 10.1212/WNL.39.11.1427 – volume: 262 start-page: 69 year: 2012 ident: key 20170425182013_awu043-B1 article-title: Perfusion abnormalities in mild cognitive impairment and mild dementia in Alzheimer’s disease measured by pulsed arterial spin labeling MRI publication-title: Eur Arch Psychiatry Clin Neurosci doi: 10.1007/s00406-011-0226-2 – volume: 47 start-page: 93 year: 2000 ident: key 20170425182013_awu043-B2 article-title: Assessment of cerebral blood flow in Alzheimer’s disease by spin-labeled magnetic resonance imaging publication-title: Ann Neurol doi: 10.1002/1531-8249(200001)47:1<93::AID-ANA15>3.0.CO;2-8 – volume: 21 start-page: 664 year: 2009 ident: key 20170425182013_awu043-B47 article-title: A variational image-based approach to the correction of susceptibility artifacts in the alignment of diffusion weighted and structural MRI publication-title: Inf Process Med Imaging doi: 10.1007/978-3-642-02498-6_55 – volume: 24 start-page: 19 year: 2010 ident: key 20170425182013_awu043-B12 article-title: ASL perfusion MRI predicts cognitive decline and conversion from MCI to dementia publication-title: Alzheimer Dis Assoc Disord doi: 10.1097/WAD.0b013e3181b4f736 – volume: 42 start-page: 1267 year: 2008 ident: key 20170425182013_awu043-B3 article-title: Hippocampal hyperperfusion in Alzheimer’s disease publication-title: Neuroimage doi: 10.1016/j.neuroimage.2008.06.006 – volume: 24 start-page: 670 year: 1997 ident: key 20170425182013_awu043-B25 article-title: Demonstration of decreased posterior cingulate perfusion in mild Alzheimer’s disease by means of H215O positron emission tomography publication-title: Eur J Nucleic Med – volume: 55 start-page: 25 year: 2013 ident: key 20170425182013_awu043-B31 article-title: Regional cerebral perfusion in patients with Alzheimer’s disease and mild cognitive impairment: effect of APOE epsilon4 allele publication-title: Neuroradiology doi: 10.1007/s00234-012-1077-x – volume: 72 start-page: 578 year: 2012 ident: key 20170425182013_awu043-B32 article-title: Amyloid deposition, hypometabolism, and longitudinal cognitive decline publication-title: Ann Neurol doi: 10.1002/ana.23650 – volume: 15 start-page: 520 year: 2011 ident: key 20170425182013_awu043-B28 article-title: Lifespan brain activity, β-amyloid, and Alzheimer’s disease publication-title: Trends Cogn Sci doi: 10.1016/j.tics.2011.09.004 – volume: 137 start-page: 28 year: 1996 ident: key 20170425182013_awu043-B20 article-title: Temporal lobe epilepsy: evidence for interictal uncoupling of blood flow and glucose metabolism in temporomesial structures publication-title: J Neurol Sci doi: 10.1016/0022-510X(95)00323-T – volume: 64 start-page: 1860 year: 2005 ident: key 20170425182013_awu043-B36 article-title: Reduced hippocampal metabolism in MCI and AD: automated FDG-PET image analysis publication-title: Neurology doi: 10.1212/01.WNL.0000163856.13524.08 – volume: 31 start-page: 847 year: 2010 ident: key 20170425182013_awu043-B40 article-title: Initial experience in using continuous arterial spin-labeled MR imaging for early detection of Alzheimer disease publication-title: AJNR Am J Neuroradiol doi: 10.3174/ajnr.A1955 – volume: 41 start-page: 1246 year: 1999 ident: key 20170425182013_awu043-B34 article-title: QUIPSS II with thin-slice TI1 periodic saturation: a method for improving accuracy of quantitative perfusion imaging using pulsed arterial spin labeling publication-title: Magn Reson Med doi: 10.1002/(SICI)1522-2594(199906)41:6<1246::AID-MRM22>3.0.CO;2-N – volume: 49 start-page: 1465 year: 2008 ident: key 20170425182013_awu043-B46 article-title: Longitudinal cerebral blood flow and amyloid deposition: an emerging pattern? publication-title: J Nucleic Med doi: 10.2967/jnumed.108.051946 – volume: 91 start-page: 33 year: 1994 ident: key 20170425182013_awu043-B42 article-title: Quantitative magnetic resonance imaging of human brain perfusion at 1.5 T using steady-state inversion of arterial water publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.91.1.33 – volume: 48 start-page: 1289 year: 2007 ident: key 20170425182013_awu043-B35 article-title: Role of Neuroimaging in Alzheimer’s Disease, with Emphasis on Brain Perfusion SPECT publication-title: J Nucleic Med doi: 10.2967/jnumed.106.037218 – ident: key 20170425182013_awu043-B52 – volume: 22 start-page: 529 year: 2001 ident: key 20170425182013_awu043-B43 article-title: Hippocampal formation glucose metabolism and volume losses in MCI and AD publication-title: Neurobiol Aging doi: 10.1016/S0197-4580(01)00230-5 – volume: 18 start-page: 1492 year: 2011 ident: key 20170425182013_awu043-B17 article-title: Simultaneous arterial spin labeling cerebral blood flow and morphological assessments for detection of Alzheimer’s disease publication-title: Acad Radiol doi: 10.1016/j.acra.2011.07.015 – volume: 69 start-page: 1650 year: 2007 ident: key 20170425182013_awu043-B50 article-title: Perfusion fMRI detects deficits in regional CBF during memory-encoding tasks in MCI subjects publication-title: Neurology doi: 10.1212/01.wnl.0000296941.06685.22 – volume: 5 start-page: 454 year: 2009 ident: key 20170425182013_awu043-B44 article-title: Cerebral blood flow in ischemic vascular dementia and Alzheimer’s disease, measured by arterial spin-labeling magnetic resonance imaging publication-title: Alzheimers Dement doi: 10.1016/j.jalz.2009.04.1233 – volume: 67 start-page: 317 year: 2010 ident: key 20170425182013_awu043-B14 article-title: Relationship between atrophy and β-amyloid deposition in Alzheimer disease publication-title: Ann Neurol doi: 10.1002/ana.21955 – volume: 60 start-page: 145 year: 2006 ident: key 20170425182013_awu043-B5 article-title: Amyloid load and cerebral atrophy in Alzheimer’s disease: an 11C-PIB positron emission tomography study publication-title: Ann Neurol doi: 10.1002/ana.20889 – volume: 367 start-page: 795 year: 2012 ident: key 20170425182013_awu043-B8 article-title: Clinical and biomarker changes in dominantly inherited Alzheimer’s disease publication-title: N Engl J Med doi: 10.1056/NEJMoa1202753 – volume: 31 start-page: S59 year: 2012 ident: key 20170425182013_awu043-B7 article-title: Assessment of Alzheimer’s disease risk with functional magnetic resonance imaging: an arterial spin labeling study publication-title: J Alzheimers Dis doi: 10.3233/JAD-2012-120292 – volume: 20 start-page: 871 year: 2010 ident: key 20170425182013_awu043-B4 article-title: Arterial spin labeling blood flow MRI: its role in the early characterization of Alzheimer’s disease publication-title: J Alzheimers Dis doi: 10.3233/JAD-2010-091699 – volume: 250 start-page: 856 year: 2009 ident: key 20170425182013_awu043-B16 article-title: Mild cognitive impairment and alzheimer disease: patterns of altered cerebral blood flow at MR imaging publication-title: Radiology doi: 10.1148/radiol.2503080751 – volume: 23 start-page: 245 year: 2009 ident: key 20170425182013_awu043-B11 article-title: Patterns of cerebral hypoperfusion in amnestic and dysexecutive MCI publication-title: Alzheimer Dis Assoc Disord doi: 10.1097/WAD.0b013e318199ff46 – volume: 68 start-page: 1526 year: 2011 ident: key 20170425182013_awu043-B27 article-title: Evidence for ordering of Alzheimer disease biomarkers publication-title: Arch Neurol doi: 10.1001/archneurol.2011.183 – volume: 30 start-page: 1737 year: 2009 ident: key 20170425182013_awu043-B21 article-title: Cerebral perfusion and oxygenation differences in Alzheimer’s disease risk publication-title: Neurobiol Aging doi: 10.1016/j.neurobiolaging.2008.01.012 – volume: 25 start-page: 421 year: 2012 ident: key 20170425182013_awu043-B49 article-title: Arterial spin labeling MRI: an emerging biomarker for Alzheimer’s disease and other neurodegenerative conditions publication-title: Curr Opin Neurol doi: 10.1097/WCO.0b013e328354ff0a – volume: 334 start-page: 752 year: 1996 ident: key 20170425182013_awu043-B41 article-title: Preclinical evidence of Alzheimer’s disease in persons homozygous for the epsilon 4 allele for apolipoprotein E publication-title: N Engl J Med doi: 10.1056/NEJM199603213341202 – volume: 12 start-page: 554 year: 2004 ident: key 20170425182013_awu043-B19 article-title: Systematic review of the diagnostic accuracy of 99mTc-HMPAO-SPECT in dementia publication-title: Am J Geriatr Psychiatry doi: 10.1097/00019442-200411000-00002 – volume: 60 start-page: 1374 year: 2003 ident: key 20170425182013_awu043-B13 article-title: Mild cognitive impairment: Can FDG-PET predict who is to rapidly convert to Alzheimer’s disease? publication-title: Neurology doi: 10.1212/01.WNL.0000055847.17752.E6 – volume: 12 start-page: 207 year: 2013 ident: key 20170425182013_awu043-B26 article-title: Tracking pathophysiological processes in Alzheimer’s disease: an updated hypothetical model of dynamic biomarkers publication-title: Lancet Neurol doi: 10.1016/S1474-4422(12)70291-0 – volume: 23 start-page: 37 year: 1992 ident: key 20170425182013_awu043-B18 article-title: Perfusion imaging publication-title: Magn Reson Med doi: 10.1002/mrm.1910230106 – volume: 35 start-page: 297 year: 2014 ident: key 20170425182013_awu043-B38 article-title: Covarying alterations in Aβ deposition, glucose metabolism, and gray matter volume in cognitively normal elderly publication-title: Hum Brain Mapp doi: 10.1002/hbm.22173 – volume: 60 start-page: 1083 year: 2012 ident: key 20170425182013_awu043-B33 article-title: Changes in regional cerebral blood flow and functional connectivity in the cholinergic pathway associated with cognitive performance in subjects with mild Alzheimer’s disease after 12-week donepezil treatment publication-title: Neuroimage doi: 10.1016/j.neuroimage.2011.12.077 – volume: 7 start-page: 590 year: 1983 ident: key 20170425182013_awu043-B22 article-title: Regional cerebral metabolic alterations in dementia of the Alzheimer type: positron emission tomography with [18F]fluorodeoxyglucose publication-title: J Comput Assist Tomogr doi: 10.1097/00004728-198308000-00003 – volume: 234 start-page: 851 year: 2005 ident: key 20170425182013_awu043-B30 article-title: Pattern of cerebral hypoperfusion in Alzheimer disease and mild cognitive impairment measured with arterial spin-labeling MR imaging: initial experience publication-title: Radiology doi: 10.1148/radiol.2343040197 – volume: 49 start-page: 390 year: 2008 ident: key 20170425182013_awu043-B37 article-title: Multicenter standardized 18F-FDG PET diagnosis of mild cognitive impairment, Alzheimer’s disease, and other dementias publication-title: J Nucleic Med doi: 10.2967/jnumed.107.045385 |
| SSID | ssj0014326 |
| Score | 2.5280821 |
| Snippet | Patients with Alzheimer’s disease show reduced cerebral blood flow, but it is unclear how this relates to β-amyloid pathology. By comparing patients with... Patients with Alzheimer's disease have reduced cerebral blood flow measured by arterial spin labelling magnetic resonance imaging, but it is unclear how this... Patients with Alzheimer's disease show reduced cerebral blood flow, but it is unclear how this relates to beta -amyloid pathology. By comparing patients with... |
| SourceID | swepub pubmedcentral proquest pubmed pascalfrancis crossref oup |
| SourceType | Open Access Repository Aggregation Database Index Database Enrichment Source Publisher |
| StartPage | 1550 |
| SubjectTerms | Adult and adolescent clinical studies Aged Aged, 80 and over Alzheimer Disease - diagnostic imaging Alzheimer Disease - pathology Amyloid beta-Peptides - metabolism Aniline Compounds Biological and medical sciences Brain - diagnostic imaging Brain - metabolism Canada Cerebrovascular Circulation - physiology Cognitive Dysfunction - diagnostic imaging Cognitive Dysfunction - pathology Databases, Factual - statistics & numerical data Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Ethylene Glycols Female Geriatrics Humans Male Medical sciences Mental Status Schedule Middle Aged Neurologi Neurology Organic mental disorders. Neuropsychology Original Positron-Emission Tomography Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Regional Blood Flow Spin Labels United States Vascular diseases and vascular malformations of the nervous system |
| Title | Association of brain amyloid-β with cerebral perfusion and structure in Alzheimer’s disease and mild cognitive impairment |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/24625697 https://www.proquest.com/docview/1519839751 https://www.proquest.com/docview/1534854330 https://pubmed.ncbi.nlm.nih.gov/PMC3999717 https://gup.ub.gu.se/publication/199611 |
| Volume | 137 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV3rb9MwELfKkBASQjxHeUxG4vFhylbXzuvjBJsGbOMDrdRvUezEXUTWTksjYBL_CX8sd3HiJKLA4EtVpWcn9f18uTvfg5AXOk6TUCTodAf1TcB2cgKVKMcfg7KttI4Vw0Th4xPvcCrez9zZYPCjE7VUruSOulybV_I_XIVrwFfMkv0HztpJ4QJ8B_7CJ3AYPq_E487aotInsd3DdnwGNniWOBiCFdeh5ekFng_nWKRYl0UTgWxqx-IJAjo98svTNKt6qfhFc25TkZ1lOaa-NWFGmFeZXdiAGVscCe-9rj-IcToEftBxOmCX8aLJ9co-57HV7CfLojSCsPw2Ly1wMW--9f-0_tpPALUmfW0vz752nRhMtCGDVjB7ThCaGrQ7qZHFwhs5oJF4PWFtSsTUqHQ7ohdtrc5rHMaxta8IUz6r4gi-B7-UI1Mnql-L--RjdDA9Ooom-7PJNXJ9DEYI9sd4--6DPaMSvGrmZx-9TquA-Xer2XfN3D2FxyRR3jqPC9iB2rROWWfb_Bqi2ytkWyk_kzvkdm210D0DwbtkkC7ukRvHdVzGffK9g0S61LR6MtogkSISKSKRNkikFokUIEItEikMs0h8XdAahxUR4pBaHNIWhw_I9GB_8ubQqRt7OMpl_soJQApwrUFXldz1QzeJ48CTAY_9xANdCVRUpQJYcNcTGiMwGQ84k2MlglAqKRP-kGwslov0EaFjJpXPmBYuV2KsORiMmgNz9DiRgYzTIdluVj9SddV7bL6SRyb6gkfVikSGV0Py0lKfm2ovv6GjwMi_kGz1uGyJQR8U6JAakucN2yMQ6XhOFy_SZVlEoISHYLf4LvsTDReBKzgfDcmmgUp7BwFy1gv9IfF7ILIEWFK-_8siO61Ky4O5EvoMRr4ycOsNmcNfhkvzMirSCLMXGHt8hQd8Qm62W_4p2QBEpc9Ak1_JrWpD_QSvlPyf |
| linkProvider | Flying Publisher |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Association+of+brain+amyloid-+beta+with+cerebral+perfusion+and+structure+in+Alzheimer%27s+disease+and+mild+cognitive+impairment&rft.jtitle=Brain+%28London%2C+England+%3A+1878%29&rft.au=Mattsson%2C+Niklas&rft.au=Tosun%2C+Duygu&rft.au=Insel%2C+Philip+S&rft.au=Simonson%2C+Alix&rft.date=2014-05-01&rft.issn=0006-8950&rft.eissn=1460-2156&rft.volume=137&rft.issue=5&rft.spage=1550&rft.epage=1561&rft_id=info:doi/10.1093%2Fbrain%2Fawu043&rft.externalDBID=NO_FULL_TEXT |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0006-8950&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0006-8950&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0006-8950&client=summon |