Increased synchronization and decreased neural complexity underlie thalamocortical oscillatory dynamics in mild cognitive impairment.

Abnormal patterns of electroencephalographic (EEG) alpha oscillations in preclinical stages of dementia reveal a selective vulnerability of thalamocortical circuits to the cascade of neurodegenerative events heralding Alzheimer's disease (AD). EEG-alpha slowing characterizes both mild cognitive impairment (MCI) and healthy aging, but it remains ambiguous whether different neural mechanisms underlie this oscillatory behavior in normal and pathological senescence. In this study, we show that the strength of phase coupling and the level of phase predictability between thalamocortical and cortico-cortical EEG sources of low alpha frequency are abnormally facilitated in MCI patients when compared to healthy elderly subjects. Additionally, we found a loss of neural complexity intrinsic to both thalamic and cortical generators of lower alpha in MCI patients, which likely influenced the aberrant phase synchronization behavior between EEG-alpha sources in this high risk group of AD. Taken together, these results suggest that different neural mechanisms account for the well known slowing of alpha rhythm present in normal aging and MCI patients. Whether these anomalous neural coding mechanisms of lower alpha generation in MCI patients represent a potential electrophysiological marker of mild AD is a topic for future research.