Conclusion The ability to image brain A?? in vivo is advancing our understanding of the neurobiology of cognitive impairment and holds promise as a tool that will contribute to the detection of early pathological changes and prediction of who selleckbio will ultimately develop AD and who will maintain cognitive health. From a number of studies, it is clear that PET amyloid imaging shows robust differences in A?? levels among groups of AD, MCI and CN individuals. When groups are combined, associations between higher A?? and lower cognitive performance, especially episodic memory, emerge consistently across studies. Within diagnostic groups, correlations between A?? burden and cognitive performance are less clear in cross-sectional investigations (summarized in Tables ?Tables11 and ?and2).2).

The few longitudinal studies to date that included measures of change in cognitive performance over time provide more convincing evidence that increased A?? correlates with greater decline in verbal memory, and perhaps other cognitive measures, such as executive function and mental status. The potential utility of A?? imaging as a clinical tool for early diagnosis of preclinical AD remains limited by its lower specificity due to the high proportion of PiB-positive CN individuals [3,5,28,31,35]. Additional challenges in interpreting a positive amyloid scan are the presence of amyloid plaques in other forms of dementia, for example, Lewy body disease [28], and the fact that A?? also binds to intravascular amyloid, as is the case with cerebral amyloid angiopathogy [46].

Further, current radiotracers for A?? imaging label predominantly fibrillar A?? and do not measure soluble forms, providing only a partial quantification of A?? burden. Despite these limitations, A?? imaging in combination with information on cognitive function can help inform early detection and diagnosis of AD. The ways in which joint consideration of A?? imaging and cognitive function may help inform prediction of AD and cognitive health are illustrated in Table ?Table4.4. This simplified table shows that, in the presence of cognitive impairment, A?? imaging will help distinguish between A??-positive individuals with MCI who are likely to progress to AD versus A??-negative individuals with MCI who have a much lower risk of progression.

A??-negative individuals with apparent cognitive Brefeldin_A impairment may be misdiagnosed as MCI and convert back to normal, may have a different neurodegenerative disorder or other condition, or may selleck chemical be false negative A?? cases due to a different isoform [30]. Similarly, A?? imaging may help distinguish between CN individuals with longitudinal decline in memory who are likely to develop AD versus those whose memory decline may be associated with other factors, such as other medical conditions or medications.