Unidirectional Influx and Net Accumulation of PIB

Gunnar Blomquist*, 1, Henry Engler2, Agneta Nordberg3, 4, Anna Ringheim5, Anders Wall5, Anton Forsberg3, Sergio Estrada5, Pernilla Frändberg5, Gunnar Antoni5, Bengt Långström5, 6
1 Department of Oncology, Radiology and Clinical Immunology, Uppsala University, Uppsala, Sweden
2 Department of Nuclear Medicine, Uppsala University Hospital, Uppsala, Sweden
3 Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden
4 Geriatric Clinic, Karolinska University Hospital Huddinge, Stockholm, Sweden
5 Uppsala Imanet AB, GE Health Care, Uppsala, Sweden
6 Department of Biochemistry and Organic Chemistry, Uppsala University, Uppsala, Sweden

Article Metrics

CrossRef Citations:
Total Statistics:

Full-Text HTML Views: 1294
Abstract HTML Views: 1025
PDF Downloads: 403
Total Views/Downloads: 2722
Unique Statistics:

Full-Text HTML Views: 653
Abstract HTML Views: 545
PDF Downloads: 299
Total Views/Downloads: 1497

Creative Commons License
© Blomquist et al; Licensee Bentham Open

open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

* Address correspondence to this author at the Department of Oncology, Radiology and Clinical Immunology, Section of Biomedical Radiation Sciences, Uppsala University, S- Uppsala Sweden; Tel: 46 18 666900; Fax: 46 18 666819; E-mail:


The compound {N-methyl-[11C]}2-(4’-methylaminophenyl)-6-hydroxybenzothiazole, “PIB”, measured by positron emission tomography, has been demonstrated to image brain β-amyloid deposition in Alzheimer’s disease (AD). In the present study the benefit of measuring the PIB accumulation rate together with the unidirectional influx of PIB into the brain was investigated in healthy control subjects and patients with AD. In a monkey changes in the influx rate constant K1 of PIB closely followed changes in CBF, caused by alteration of PaCO2. In addition, K1 was high both in the monkey and in humans, suggesting that this parameter reflects CBF. Most AD patients studied showed clearly higher accumulation rate for PIB than the controls in cortical brain areas, while a few patients showed as low accumulation as the controls. K1 did not correlate with the accumulation rate, indicating that K1 for PIB provides extra information besides the accumulation rate.

Keywords: Alzheimer´s disease, beta amyloid, cerebral blood flow, kinetic modeling, PET.