Different β-amyloid binding patterns in Alzheimer and Parkinson diseases: It's the network!

Neurology. 2013 Jul 3. [Epub ahead of print]

Eidelberg D, Martin W.

Source

From the Center for Neurosciences (D.E.), The Feinstein Institute for Medical Research, Manhasset, NY; and the Department of Medicine (Neurology) (W.M.), University of Alberta, Edmonton, Canada.

Abstract

11C-Pittsburgh compound B (PiB) PET is a sensitive and increasingly popular imaging tool for assessing the deposition of fibrillar β-amyloid aggregates in the brains of living patients with Alzheimer disease (AD). Increased cortical PiB binding also occurs in dementia with Lewy bodies, but rarely in cognitively impaired individuals with Parkinson disease (PD).1,2 To date, most PiB PET studies have focused on identifying significant group differences in radiotracer binding in single brain regions or in the cortex overall. However, recent evidence suggests that the deposition of protein aggregates in neurodegenerative disorders evolves at the systems level, with involvement of discrete sets of interconnected brain regions.3,4 In this regard, techniques of pattern analysis based upon principal component analysis (PCA) and other multivariate procedures are increasingly used to quantify disease-related circuit changes in functional brain images.5.