Figure: PET imaging of brain metabolism in Alzheimer’s disease: Representative images of Fluorodeoxyglucose PET ([18F]FDG-PET) images in a control patient (left) and a patient with advanced AD (right).3 [18F]FDG-PET measures glucose metabolism from neurons and astrocytes and decreased cerebral [18F]FDG-PET signal is often interpreted as a sign of neurodegeneration.3 Areas of abnormal metabolism include posterior regions such as the posterior cingulate cortex and lateral parietal cortices.3 Also, there is decreased metabolism in lateral temporal cortices.3 Note how all these regions are normal in the control patient. Furthermore, note that primary sensory areas, such as the visual cortex and sensory-motor strip, are relatively spared in patients with AD.3 This helps nuclear medicine physicians identify the FDG-PET pattern.3 More information on FDG-PET visual reads can be found in Nobili F, Arbizu J, Bouwman F, et al. Eur J Neurol. 2018;25(10):1201-1217.3
[18F]FDG-PET allows the investigation of the extent and location of hypometabolism, which reflects neuronal dysfunction.2 It measures glucose metabolism from neurons and astrocytes, with a decreased cerebral signal interpreted as a sign of neurodegeneration.3 This method is particularly useful for early diagnosis, as it can identify characteristic patterns of neurodegeneration in AD earlier than MRI, in patients with MCI on the path to developing AD. 2,4,5 [18F]FDG-PET is also useful for staging of the disease and for differential diagnosis.2 This is because patterns of brain hypometabolism are closely associated with type and severity of cognitive deficits, and tend to be fairly distinct in different neurodegenerative diseases and their variants.2 In AD, areas of abnormal metabolism include posterior regions such as the posterior cingulate cortex and lateral parietal cortices.3 Additionally, there is decreased metabolism in lateral temporal cortices.3 Primary sensory areas, such as the visual cortex and sensory-motor strip, are relatively spared in patients with AD, allowing physicians to identify the FDG-PET pattern.3 While [18F]FDG-PET is included in the diagnostic criteria of several neurodegenerative diseases associated with brain hypometabolism, the use of [18F]FDG-PET is limited due to its inability to provide information about the neuropathology underlying the detected patterns of hypometabolism.2 As of 2020, amyloid imaging alone, was considered insufficient to predict time to clinical conversion in prodromal and asymptomatic stages.2
References:
1.Gauthier S, Rosa-Neto P, Morais JA, Webster C. World Alzheimer Report 2021: Journey through the diagnosis of dementia. Available at: https://www.alzint.org/u/World-Alzheimer-Report-2021.pdf. Accessed 15 November 2023.
2.Chételat G, Arbizu J, Barthel H, et al. Amyloid-PET and 18F-FDG-PET in the diagnostic investigation of Alzheimer’s disease and other dementias. Lancet Neurol 2020; 19 (11): 951–962.
3.Therriault J. Biomarkers for the in vivo diagnosis of Alzheimer’s disease. Available at: https://neurotorium.org/biomarkers-for-the-in-vivo-diagnosis-of-alzheimers-disease/. Accessed 15 November 2023.