**4.2 FDG PET for imaging frontotemporal dementia**

Reduced glucose metabolism in the frontal (mostly the frontal cortex) and anterior temporal regions is the characteristic hallmark observed in FDG PET scans of FTD patients. Such impairment is not always symmetric, and thought to be related to the aphasia and semantic memory deficits common in such patients. This (mostly) frontal impairment allows distinction of FTD from AD. For example, Foster and co-workers were recently able to distinguish FTD from AD with 86% specificity and 97.6% sensitivity, beyond clinical features alone (Foster, et al., 2007). Frontal metabolic decline, however, is not limited to FTD and can be apparent in certain cases of AD. In such cases where there is FTD / AD overlap in the FDG PET scans, it is recommended to conduct additional scans exploring microglial activation or amyloid deposits (see Section 2). For example, microglial activation characteristic of FTD has been investigated (A. Cagnin, et al., 2004). Alternatively, an amyloid positive scan would strongly suggest AD, whilst an amyloid negative scan would indicate FTD (Figure 5) (Kadir and Nordberg, 2010).

Fig. 5. High PIB retention was observed in patient with AD (A) and patient with DLB (B). In contrast, low PIB retention was observed in patient with PD (not demented) (C) and in patient with FTD (D). *(Parts A and B reprinted with permission from Ahmadul K and Nordberg A, Targetspecific PET probes for neurodegenerative disorders related to dementia. J Nucl Med. 2010;51:1418- 1430; Part C reprinted with permission from A. Johansson, et al. [11C]-PIB imaging in patients with Parkinson's disease: preliminary results. Parkinsonism Relat. Disord. 2008;14:345-347; Part D courtesy of Professor Henry Engler, Uppsala PET Center, Academical Hospital, Uppsala, Sweden).*

Other diseases (e.g. progressive supranuclear palsy, spino-cerebellar atrophy) or lifestyle choices (e.g. cocaine abuse) can also lead to frontal metabolic impairment. Consequently, other areas of reduced cerebral glucose metabolism should be considered when making a diagnosis as, despite its name, there are more widespread hemispheric defects in glucose metabolism that occur in FTD. For example, reduced glucose metabolism in the orbital gyrus, anterior cingulate gyrus, frontal cortices, anterior temporal cortices, hippocampus, subcortical structures, parietal region, sensorimotor cortex, and the cerebellar cortex, discussed by Ishii (Ishii, 2002), are consistent with the pathological features and *post-mortem* findings of FTD.
