In Alzheimer disease (AD), which is the most common cause of dementia, the underlying disease pathology most probably precedes the onset of cognitive symptoms by many years. Thus, efforts are underway to find early diagnostic markers as well as disease-modifying treatments for this disorder. PET enables various brain systems to be monitored in living individuals. In patients with AD, PET can be used to investigate changes in cerebral glucose metabolism, various neurotransmitter systems, neuroinflammation, and the protein aggregates that are characteristic of the disease, notably the amyloid deposits. These investigations are helping to further our understanding of the complex pathophysiological mechanisms that underlie AD, as well as aiding the early and differential diagnosis of the disease in the clinic. In the future, PET studies will also be useful for identifying new therapeutic targets and monitoring treatment outcomes. Amyloid imaging could be useful as early diagnostic marker of AD and for selecting patients for anti-amyloid-β therapy, while cerebral glucose metabolism could be a suitable PET marker for monitoring disease progression. For the near future, multitracer PET studies are unlikely to be used routinely in the clinic for AD, being both burdensome and expensive; however, such studies are very informative in a research context.
PET studies facilitate the clinical differentiation between Alzheimer disease (AD) and other types of dementia
Monitoring cerebral glucose metabolism or amyloid deposition by PET could provide diagnostic accuracy in early cognitive impairment
PET amyloid imaging permits the early detection of patients with amnestic mild cognitive impairment—individuals who have a high risk of developing AD
The glucose analog 2-[18F]-fluoro-2-deoxy-D-glucose can be used in PET studies to monitor the clinical progression of AD
PET amyloid imaging has the potential to be used for selecting appropriate patients for future anti-amyloid-β therapies
Multitracer PET studies further our understanding of the underlying pathological disease processes in AD and the relationship between such pathology and the cognitive impairment exhibited by patients
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A. Nordberg gratefully acknowledges the financial support provided by the following: the Swedish Research Council (project 05817), Stockholm County Council–Karolinska Institute (ALF grant), the Foundation for Old Servants, the Stohne's Foundation, the KI Foundations, the Alzheimer Foundation in Sweden, Swedish Brain Power, the EC-FP6 project DiMI (LSHB-CT-2005-512146 and QLK6-CT-2000-00502), and the Swedish Brain Foundation. Anton Forsberg, Michael Schöll (both Karolinska Institute) and Anders Wall (GE Healthcare, Uppsala, Sweden) are thanked for their help in preparing the figures.
The authors declare no competing financial interests.
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Nordberg, A., Rinne, J., Kadir, A. et al. The use of PET in Alzheimer disease. Nat Rev Neurol 6, 78–87 (2010). https://doi.org/10.1038/nrneurol.2009.217
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