Positron emission tomography (PET) with 2-[fluorine-18]fluoro-2-deoxy-D-glucose (FDG) is a highly useful imaging modality for the diagnosis of neurodegenerative disorders (1–6). FDG is an analog of glucose, the main energy substrate of the brain. After uptake and phosphorylation by hexokinase, FDG becomes trapped in neurons, allowing imaging and measurement of the cerebral metabolic rate for glucose. This is closely related to neuronal and synaptic function in numerous human resting and functional activation studies (1–3). Characteristic patterns of altered metabolism seen at FDG PET can markedly improve the clinical diagnosis for specific types of dementia such as FTD, Alzheimer disease, and DLB, each of which has characteristic metabolic signatures, although there is some overlap. An essentially normal or preserved cerebral uptake pattern can also help distinguish reversible pseudodementia due to depression from a primary neurodegenerative syndrome (12,13). Recognition of the common patterns of altered cortical metabolism seen in these various entities is crucial for identifying the cause of cognitive impairment. With use of proper technique, and with the increasing availability of computer-assisted diagnostic (CAD) statistical mapping tools, the neuroimager can play a key role in the workup of patients with cognitive impairment.
