A new method to build multiplex networks using canonical correlation analysis for the characterization of the Alzheimer's disease continuum.

ABSTRACT

Objective. The aim of this study was to solve one of the current limitations for the characterization of the brain network in the Alzheimer's disease (AD) continuum. Nowadays, frequency-dependent approaches have reached contradictory results depending on the frequency band under study, tangling the possible clinical interpretations.Approach. To overcome this issue, we proposed a new method to build multiplex networks based on canonical correlation analysis (CCA). Our method determines two basis vectors using the source and electrode-level frequency-specific network parameters for a reference group, and then project the results for the rest of the groups into these hyperplanes to make them comparable. It was applied to (i) synthetic signals generated with a Kuramoto-based model; and (ii) a resting-state electroencephalography (EEG) database formed by recordings from 51 cognitively healthy controls, 51 mild cognitive impairment subjects, 51 mild AD patients, 50 moderate AD patients, and 50 severe AD patients.Main results. Our results using synthetic signals showed that the interpretation of the proposed CCA-based multiplex parameters (multiplex strength, multiplex characteristic path length and multiplex clustering coefficient) can be analogous to their frequency-specific counterparts, as they displayed similar behaviors in terms of average connectivity, integration, and segregation. Findings using real EEG recordings revealed that dementia due to AD is characterized by a significant increase in average connectivity, and by a loss of integration and segregation.Significance. We can conclude that CCA can be used to build multiplex networks based from frequency-specific results, summarizing all the available information and avoiding the limitations of possible frequency-specific conflicts. Additionally, our method supposes a novel approach for the construction and analysis of multiplex networks during AD continuum.