Amyloid plaques are composed primarily of amyloid-beta （Aβ） peptides derived from proteolytic
cleavage of amyloid precursor protein （APP）, ａnd are considered to play a pivotal role in Alzheimer＇s
disease （AD） pathogenesis. Presently, AD is diagnosed after the onset of clinical manifestations.
With the arrival of novel therapeutic agents for treatment of AD, there is an urgent need for
biomarkers to detect early stages of AD. Measurement of plasma Aβ has been suggested as an
inexpensive ａnd non-invasive tool to diagnose AD ａnd to monitor Aβ modifying therapies. However,
the majority of cross-sectional studies on plasma Aβlevels in humans have not shown differences
between individuals with AD compared to controls. Similarly, cross-sectional studies of mouse
plasma Aβ have yielded inconsistent trends in different mouse models. However, longitudinal studies
appear to be more promising in humans. Recently, efforts to modify plasma Aβ levels using
modulators have shown some promise. In this review, we will summarize the present data on plasma
Aβ in humans ａnd mouse models of AD. We will discuss the potential of modulators of Aβ levels
in plasma including antibodies ａnd insulin, ａnd the challenges associated with measuring plasma
Aβ. Modulators of plasma Aβ may provide an important tool to optimize plasma Aβ levels, ａnd may
improve the diagnostic potential of this approach.
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