Since A?? pathology is required for a diagnosis of AD, the early demonstration of the absence of A?? may lead instead to further evaluation of potentially treatable causes towards of impairment (for example, depression) in these patients. When, and in what population of patients, should amyloid PET imaging be used? It is easy enough to identify and rule out the extremes. On the one extreme, a well characterized patient whose disease has progressed beyond the point where a scan would influence medical management would likely derive little benefit from a PET scan. On the other extreme the evidence to date is not sufficient to support routine use in screening cognitively normal subjects, even in the presence of risk factors.

Although the results discussed above (for example, [55,61]) suggest that subjects who are amyloid-positive on PET scan may perform worse on cognitive tests, the results have not been entirely consistent across trials, and the effects are subtle and of uncertain clinical relevance. Most important, too few amyloid-positive subjects have been identified and followed longitudinally to give guidance to the patient regarding likelihood and time course of future cognitive deterioration. Current estimates of 10 years or more between the first signs of excess A?? accumulation and onset of dementia suggest that many amyloid-positive elderly patients might pass on before experiencing significant cognitive decline. In between these extremes lie a large number of patients that could potentially benefit from PET amyloid scans.

With three 18F-labeled amyloid targeted ligands having entered or already completed phase III trials, it is likely that amyloid PET scans will be broadly available within the next few years. Additional studies and consensus evaluations are needed to determine the best use for these agents. Despite the positive results described above, it is clear that an amyloid PET scan is not sufficient to confer a diagnosis of AD. A?? can Dacomitinib be present in association with other disease conditions, including DLB, Parkinson’s disease and cerebrovascular disease. nearly It remains unclear whether this reflects the coincidence of two or more disease entities (for example, AD independently in addition to DLB) or whether A?? (and tau) pathology can be found independently in multiple disease entities. In either case, the advent of PET amyloid imaging techniques does not obviate the need for clinical/cognitive evaluation. Moreover, the information obtained from amyloid PET imaging may be enhanced by additional biomarker studies, including, for example, functional imaging [72], or molecular imaging aimed at dopamine systems [73-75].

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