Carbon 11-labeled Pittsburgh Compound B positron emission tomographic amyloid imaging in patients with APP locus duplication

被引：56

作者：

Remes, Anne M. ^{[1
,3
]}

Laru, Lauri ^{[1
,3
]}

Tuominen, Hannu ^{[2
]}

Aalto, Sargo ^{[4
,5
]}

Kemppainen, Nina ^{[5
,6
]}

Mononen, Helina ^{[1
]}

Nagren, Kjell ^{[5
]}

Parkkola, Riitta ^{[7
]}

Rinne, Juha O. ^{[5
]}

机构：

[1] Univ Oulu, Dept Neurol, FIN-90014 Oulu, Finland

[2] Univ Oulu, Dept Pathol, Oulu, Finland

[3] Oulu Univ Hosp, Clin Res Ctr, Oulu, Finland

[4] Abo Akad Univ, Dept Psychol, Turku, Finland

[5] Univ Turku, Turku PET Ctr, Turku, Finland

[6] Turku Univ Hosp, Dept Neurol, Turku, Finland

[7] Turku Univ Hosp, Dept Radiol, Turku, Finland

来源：

ARCHIVES OF NEUROLOGY | 2008年 / 65卷 / 04期

关键词：

D O I：

10.1001/archneur.65.4.540

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Objective: To investigate amyloid accumulation by carbon 11-labeled Pittsburgh Compound B (C-11-PiB) in hereditary cerebral amyloid angiopathy and APP locus duplication. Design, Setting, and Patients: Positron emission tomography with C-11-PiB and magnetic resonance imaging were performed for 2 patients, 49-year-old and 60-year-old siblings with APP locus duplication, with hereditary Alzheimer disease and cerebral amyloid angiopathy. Main Outcome Measure: Change in C-11-PiB uptake. Results: Uptake of C-11-PiB was increased especially in the striatum (caudate nucleus to 225% and 280% of the control mean and putamen to 166% and 185% of the control mean) and in the posterior cingulate (to 168% and 198% of the control mean), and it was marginally increased in other cortical brain areas. The pattern of increased C-11-PiB uptake was different from that seen in sporadic Alzheimer disease. Conclusions: Amyloid imaging with C-11-PiB positron emission tomography is a useful tool for detecting in vivo amyloid accumulation in patients with hereditary cerebral amyloid angiopathy. However, the pattern of (11)CPiB accumulation differs between patients with typical AD and patients with APP locus duplication.

引用

页码：540 / 544

页数：5

共 14 条

[1] Molecular imaging with Pittsburgh compound B confirmed at autopsy - A case report [J].

Bacskai, Brian J. ;

Frosch, Matthew P. ;

Freeman, Stefanie H. ;

Raymond, Scott B. ;

Augustinack, Jean C. ;

Johnson, Keith A. ;

Irizarry, Michael C. ;

Klunk, William E. ;

Mathis, Chester A. ;

DeKosky, Steven T. ;

Greenberg, Steven M. ;

Hyman, Bradley T. ;

Growdon, John H. .

ARCHIVES OF NEUROLOGY, 2007, 64 (03) :431-434

[2] Phenotype associated with APP duplication in five families [J].

Cabrejo, Lucie ;

Guyant-Marechal, Lucie ;

Laquerriere, Annie ;

Vercelletto, Martine ;

De la Fourniere, Francois ;

Thomas-Anterion, Catherine ;

Verny, Christophe ;

Letournel, Franck ;

Pasquier, Florence ;

Vital, Anne ;

Checler, Frederic ;

Frebourg, Thierry ;

Campion, Dominique ;

Hannequin, Didier .

BRAIN, 2006, 129 :2966-2976

[3] Novel amyloid precursor protein mutation in an Iowa family with dementia and severe cerebral amyloid angiopathy [J].

Grabowski, TJ ;

Cho, HS ;

Vonsattel, JPG ;

Rebeck, GW ;

Greenberg, SM .

ANNALS OF NEUROLOGY, 2001, 49 (06) :697-705

[4] MRI detection of new hemorrhages: Potential marker of progression in cerebral amyloid angiopathy [J].

Greenberg, SM ;

O'Donnell, HC ;

Schaefer, PW ;

Kraft, E .

NEUROLOGY, 1999, 53 (05) :1135-1138

[5] PET amyloid ligand [11C]PIB uptake is increased in mild cognitive impairment [J].

Kemppainen, N. M. ;

Aalto, S. ;

Wilson, I. A. ;

Nagren, K. ;

Helin, S. ;

Bruck, A. ;

Oikonen, V. ;

Kailajarvi, M. ;

Scheinin, M. ;

Viitanen, M. ;

Parkkola, R. ;

Rinne, J. O. .

NEUROLOGY, 2007, 68 (19) :1603-1606

[6] Voxel-based analysis of PET amyloid ligand [11C]PIB uptake in Alzheimer disease [J].

Kemppainen, N. M. ;

Aalto, S. ;

Wilson, I. A. ;

Nagren, K. ;

Helin, S. ;

Bruck, A. ;

Oikonen, V. ;

Kailajarvi, M. ;

Scheinin, M. ;

Viitanen, M. ;

Parkkola, R. ;

Rinne, J. O. .

NEUROLOGY, 2006, 67 (09) :1575-1580

[7] Imaging brain amyloid in Alzheimer's disease with Pittsburgh Compound-B [J].

Klunk, WE ;

Engler, H ;

Nordberg, A ;

Wang, YM ;

Blomqvist, G ;

Holt, DP ;

Bergström, M ;

Savitcheva, I ;

Huang, GF ;

Estrada, S ;

Ausén, B ;

Debnath, ML ;

Barletta, J ;

Price, JC ;

Sandell, J ;

Lopresti, BJ ;

Wall, A ;

Koivisto, P ;

Antoni, G ;

Mathis, CA ;

Långström, B .

ANNALS OF NEUROLOGY, 2004, 55 (03) :306-319

[8] Amyloid deposition begins in the striatum of presenilin-1 mutation carriers from two unrelated pedigrees [J].

Klunk, William E. ;

Price, Julie C. ;

Mathis, Chester A. ;

Tsopelas, Nicholas D. ;

Lopresti, Brian J. ;

Ziolko, Scott K. ;

Bi, Wenzhu ;

Hoge, Jessica A. ;

Cohen, Ann D. ;

Ikonomovic, Milos D. ;

Saxton, Judith A. ;

Snitz, Beth E. ;

Pollen, Daniel A. ;

Moonis, Majaz ;

Lippa, Carol F. ;

Swearer, Joan M. ;

Johnson, Keith A. ;

Rentz, Dorene M. ;

Fischman, Alan J. ;

Aizenstein, Howard J. ;

DeKosky, Steven T. .

JOURNAL OF NEUROSCIENCE, 2007, 27 (23) :6174-6184

[9] Dementia in hereditary cerebral hemorrhage with amyloidosis-Dutch type is associated with cerebral amyloid angiopathy but is independent of plaques and neurofibrillary tangles [J].

Natté, R ;

Maat-Schieman, MLC ;

Haan, J ;

Bornebroek, M ;

Roos, RAC ;

van Duinen, SG .

ANNALS OF NEUROLOGY, 2001, 50 (06) :765-772

[10] Hereditary dementia with intracerebral hemorrhages and cerebral amyloid angiopathy [J].

Remes, AM ;

Finnilä, S ;

Mononen, H ;

Tuominen, H ;

Takalo, R ;

Herva, R ;

Majamaa, K .

NEUROLOGY, 2004, 63 (02) :234-240

← 1 2 →