Mapping brain β-amyloid

Purpose of review This article reviews recent developments in the field of amyloid imaging using PET, specifically the ability to quantify the amount and distribution of brain beta-amyloid, the protein that occupies a central position in leading theories of the pathogenesis of Alzheimer's disease. Recent findings Several imaging-disorder correlations place the technique itself on a stronger footing by showing good agreement between in-vivo and histological measures of beta-amyloid deposition. Correlations between beta-amyloid and other measures of dementia cognition, brain atrophy, and glucose metabolism - appear to support a view that beta-amyloid triggers a host of downstream alterations that are closely related to dementia severity and progression. However, associations between PET measures of beta-amyloid and cognition are generally fairly weak. The implications for clinical use are still uncertain. It seems likely that amyloid imaging will be useful for differentiating dementias associated with beta-amyloid from those that are not, but the utility of this approach will depend on the availability of effective beta-amyloid-directed treatments. Similarly, amyloid imaging offers the potential for predicting which nondemented individuals will eventually develop Alzheimer's disease, although here again the measurement of downstream beta-amyloid effects may be important. Summary The ability to quantify the onset and progression of beta-amyloid disorder in the brain offers the potential for investigating a host of questions concerning individual and neural vulnerability and the amyloid hypothesis of Alzheimer's disease itself. These findings will have important basic and clinical implications.