Abstract
Alzheimer's disease (AD) is the most common cause of dementia worldwide. As advancing age is the greatest risk factor for developing AD, the number of those afflicted is expected to increase markedly with the aging of the world's population. The inability to definitively diagnose AD until autopsy remains an impediment to establishing effective targeted treatments. Neuroimaging has enabled in vivo visualization of pathological changes in the brain associated with the disease, providing a greater understanding of its pathophysiological development and progression. However, neuroimaging biomarkers do not yet offer clear advantages over current clinical diagnostic criteria for them to be accepted into routine clinical use. Nonetheless, current insights from neuroimaging combined with the elucidation of biochemical and molecular processes in AD are informing the ongoing development of new imaging techniques and their application. Much of this research has been greatly assisted by the availability of transgenic mouse models of AD. In this review we summarize the main efforts of neuroimaging in AD in humans and in mouse models, with a specific focus on β-amyloid, and discuss the potential of new applications and novel approaches.
Highlights
Alzheimer’s disease (AD) is the most common cause of dementia worldwide, accounting for 65–75% of all cases of dementia (Bianchetti and Trabucch, 2001; Brookmeyer et al, 2011)
In this review we summarize the main efforts of neuroimaging in AD in humans and in mouse models, with a specific focus on β-amyloid, and discuss the potential of new applications and novel approaches
spin echo (SE) has superior resolution, accurately reflects plaque size, T2* gradient echo (GRE) reflects plaque iron content, overestimates plaque size 20 μm plaques seen at 3 months ex vivo, 35 μm plaques at 9 months in vivo; plaques staining for amyloid typically stained for Fe; not all plaques seen on magnetic resonance imaging (MRI) seen due to size
Summary
Alzheimer’s disease (AD) is the most common cause of dementia worldwide, accounting for 65–75% of all cases of dementia (Bianchetti and Trabucch, 2001; Brookmeyer et al, 2011). Synaptic dysfunction leads to alterations in brain activity and connectivity, evident as regional alterations in activity on functional studies (Bokde et al, 2009) These data support a primary role for Aβ in the pathogenesis of AD ( clearly there are other aspects that are very important). A recent study demonstrated, for the first time, that there was an association between the rate of Aβ deposition and memory decline in a cohort of AD patients (Villemagne et al, 2013) These findings arose out of the Australian Imaging, Biomarkers and Lifestyle study, which is a multi-year prospective study of 1112 individuals with either AD, MCI or no pathology (age-matched healthy controls), and perhaps demonstrates the need for such large, well-controlled studies in order to discern correlations between Aβ burden and cognitive function. The potential of imaging biomarkers draws closer to realization
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
