![Representative images of Fluorodeoxyglucose PET ([18F]FDG-PET) images in a control subject (left) and a patient with advanced Alzheimer’s Disease (AD) (right).](https://neurotorium.org/cdn-cgi/image/format=auto,quality=85,metadata=none/wp-content/uploads/figure-4.png)
Representative images of Fluorodeoxyglucose PET ([18F]FDG-PET) images in a control subject (left) and a patient with advanced Alzheimer’s Disease (AD) (right). [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. Areas of abnormal metabolism include posterior regions such as the posterior cingulate cortex and lateral parietal cortices. Also, there is decreased metabolism in lateral temporal cortices. Note how all these regions are normal in the control subject. Furthermore, note that primary sensory areas, such as the visual cortex and sensory-motor strip, are relatively spared in patients with AD. This helps nuclear medicine physicians identify the FDG-PET pattern.
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.
Related content
Social and physical exposome factors—like poverty, pollution, and inequality—accumulate over time, shaping biological aging and cognitive decline. Through inflammation and cellular stress, these exposures drive neurodegeneration, highlighting the need for longitudinal, integrative research.
The exposome reframes dementia as the product of cumulative physical and social exposures-like pollution, nutrition, and inequality-across life. These factors shape brain aging through inflammation and epigenetic change. Lifespan, global studies are key to equitable dementia prevention.
