Atrophy of amygdala and abnormal memory-related alpha oscillations over posterior cingulate predict conversion to
Laura Prieto Del Val1, Jose L Cantero1, Mercedes Atienza1
1Laboratory of Functional Neuroscience, CIBERNED, Network Center for Biomedical Research in Neurodegenerative Diseases, Pablo de Olavide University, Seville, Spain.
Abstract:
Synaptic dysfunction, a key pathophysiological hallmark of Alzheimer's disease (AD), may account for abnormal memory-related EEG patterns in prodromal AD. Here, we investigate to what extent oscillatory EEG changes during memory encoding and/or retrieval enhance the accuracy of medial temporal lobe (MTL) atrophy in predicting conversion from amnestic mild cognitive impairment (aMCI) to AD. As expected, aMCI individuals that, within a 2-year follow-up period, developed dementia (N = 16) compared to healthy older (HO) (N = 26) and stable aMCI (N = 18) showed poorer associative memory, greater MTL atrophy, and lower capacity to recruit alpha oscillatory cortical networks. Interestingly, encoding-induced abnormal alpha desynchronized activity over the posterior cingulate cortex (PCC) at baseline showed significantly higher accuracy in predicting AD than the magnitude of amygdala atrophy. Nevertheless, the best accuracy was obtained when the two markers were fitted into the model (sensitivity = 78%, specificity = 82%). These results support the idea that synaptic integrity/function in the PCC is affected during prodromal AD and has the potential of improving early detection when combined with MRI biomarkers.
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