PET imaging of amyloid deposition in patients with mild cognitive impairment

Forsberg, Anton; Engler, Henry; Almkvist, Ove; Blomquist, Gunnar; Hagman, Göran; Wall, Anders; Ringheim, Anna; Långström, Bengt; Nordberg, Agneta

doi:10.1016/j.neurobiolaging.2007.03.029

« Previous Next »Neurobiology of Aging
Volume 29, Issue 10 , Pages 1456-1465, October 2008

PET imaging of amyloid deposition in patients with mild cognitive impairment

Anton Forsberg
- Karolinska Institute, Department of Neurobiology, Care Sciences and Society, Stockholm, Sweden
Henry Engler
- Department of Nuclear Medicine, Uppsala University Hospital, Uppsala, Sweden
Ove Almkvist
- Karolinska Institute, Department of Neurobiology, Care Sciences and Society, Stockholm, Sweden
- Department of Geriatric Medicine, Karolinska University Hospital Huddinge, Stockholm, Sweden
- Department of Psychology, Stockholm University, Stockholm, Sweden
Gunnar Blomquist
- Department of Oncology, Radiology and Clinical Immunology, Uppsala University, Uppsala, Sweden
Göran Hagman
- Department of Geriatric Medicine, Karolinska University Hospital Huddinge, Stockholm, Sweden
Anders Wall
- Uppsala Imanet AB, Imanet, GE Healthcare, Sweden
Anna Ringheim
- Uppsala Imanet AB, Imanet, GE Healthcare, Sweden
Bengt Långström
- Uppsala Imanet AB, Imanet, GE Healthcare, Sweden
- Department of Biochemistry and Organic Chemistry, Uppsala University, Uppsala, Sweden
Agneta Nordberg
- Karolinska Institute, Department of Neurobiology, Care Sciences and Society, Stockholm, Sweden
- Department of Geriatric Medicine, Karolinska University Hospital Huddinge, Stockholm, Sweden
- Corresponding author at: Karolinska Institutet, Department of Neurobiology, Care Sciences and Society, Division of Molecular Neuropharmacology, Karolinska University Hospital Huddinge, Novum 5th Floor, S-141 86 Stockholm, Sweden. Tel.: +46 8 58585467; fax: +46 8 58585470.

Received 8 January 2007; received in revised form 25 March 2007; accepted 30 March 2007. published online 11 May 2007.

Abstract

It is of great clinical value to identify subjects at a high risk of developing AD. We previously found that the amyloid positron emission tomography (PET) tracer PIB showed a robust difference in retention in the brain between AD patients and healthy controls (HC). Twenty-one patients diagnosed with MCI (mean age 63.3±7.8 (S.D.) years) underwent PET studies with ¹¹C-PIB, and ¹⁸F-fluoro-deoxy-glucose (FDG) to measure cerebral glucose metabolism, as well as assessment of cognitive function and CSF sampling. Reference group data from 27 AD patients and 6 healthy controls, respectively, were used for comparison. The mean cortical PIB retention for the MCI patients was intermediate compared to HC and AD. Seven MCI patients that later at clinical follow-up converted to AD (8.1±6.0 (S.D.) months) showed significant higher PIB retention compared to non-converting MCI patients and HC, respectively (ps<0.01). The PIB retention in MCI converters was comparable to AD patients (p>0.01). Correlations were observed in the MCI patients between PIB retention and CSF Aβ_1-42, total Tau and episodic memory, respectively.