Early manifestation of amyloid-beta toxicity can be detected in cognitively normal subjects with brain amyloid deposition, according to a study published in the March issue of Biological Psychiatry.
Important functional connections within the default mode network are disrupted in Alzheimer's disease, and are likely from amyloid-beta plaque-associated neuronal toxicity, according to Yvette I. Sheline, MD, the director of the center for neuroimaging and depression at the School of Medicine, Washington University in St. Louis, Mo.
Sheline and her group determined if pathological effects of amyloid-beta plaques could be seen, even in the absence of a task, by examining functional connectivity in cognitively normal participants with and without preclinical amyloid deposition.
The researchers compared 35 participants with Alzheimer's disease and 68 cognitively normal participants who were further subdivided by PET Pittsburgh Compound B (PIB) imaging into those without evidence of brain amyloid (PIB) and those with brain amyloid (PIB+) deposition.
Resting state functional MRI (fMRI) demonstrated that, compared with the PIB group, the PIB+ group differed significantly in functional connectivity of the brain and was in the same direction as differences found in the AD group, according to Sheline and colleagues.
Thus, before any manifestations of cognitive or behavioral changes, there were differences in resting state connectivity in cognitively normal subjects with brain amyloid deposition, suggesting that early manifestation of amyloid-beta plaque toxicity can be detected using resting state fMRI, concluded the authors.