Temporo-Parietal Brain Network Impairment Is Related To EEG ALPHA3/ALPHA2 Power Ration in Prodormal Alzheimer’s Disease

The identification and validation of biomarkers for diagnosing, monitoring progression and predicting onset of Alzheimer's disesae (AD) has been a main focus of AD research in the past 10 years. In line with recently published research criteria. , it is becoming clear that the integration of different biomarkers is a milestone for a correct and early diagnosis of midl cognitive impairment due to AD [1,2]. To date, the most studied and validated biomarkers are Abeta42 and tau in the cerebrospinal fluid (CSF), glucose hypometabolism on fluorodeoxyglucose positron emission tomography (18F-FDG PET), atrophy of hippocampal volume (HV) on magnetic resonance (MR), and brain amyloid deposition on amyloid imaging with PET [3,4]. Anyway, some controversies remane to debate. The latter biomarkers have a good sensibility in identifying subjects with a neurodegenerative disorders at high risk to convert in dementia, but they lack a reliable specificity that allow a clear-cut diagnosis of the different subtypes of dementias. Of note, in neurodegenerative disorders, like AD or other dementias, the brain networks modifies many years before clinical manifestations. Recent MRI studies have demonstrated that a large neural network is altered in subjects with prodromal AD, including precuneus, medial temporal, parietal ad frontal cortices [5-9]. In particular, subjects with cognitive decline have shown early atrophy and loss of grey matter in cortical specific brain areas [10,11], including hippocampal, medial temporal and parietal lobes. In the conceptual frame of the integration of biomarkers for an early and highly predictive diagnosis, the EEG could be a reliable tool [12]. Indeed, it is widely accepted that the cerebral EEG rhythms reflect the underlying brain network activity [13]. As a consequence, modifications in EEG rhythms could be an early sign of disease associated with AD-related structural and functional networks. Recently, it has been demonstrated that the increase of high alpha relative to low alpha power is a reliable EEG marker of hippocampal atrophy and amigdalo-hippocampal complex atrophy [14,15]. Furthermore, the increase in alpha3/ alpha2 power ratio has been demonstrated predictive of conversion of patients with MCI in AD, but not in non-AD dementia [16]. The same increase of alpha3/alpha2 power ratio was found to be correlated with hippocampal atrophy in subjects with AD [12]. Finally, a recent study have shown that MCI subjects with highest alpha3/alpha2 power ratio present a peculiar pattern of basal ganglia and thalamic atrophy, detected with voxel-based-morphometry (VBM) tecnique, as compared to MCI groups with middle and low alpha3/alpha 2 power ratio [12]. The present explorative study shares the same theoretical background. The aim of the study is to extend the relationship of the alpha3/alpha2 EEG power ratio to the study of cerebral cortex atrophy in subjects with MCI. Two principal reasons supports this aim: 1) the hippocampal complex is strongly connected with temporo-parietal cortex; 2) in AD due to MCI there is the presence of both hippocampal and brain cortical atrophy. The cortical thickness analysis may provide a more sensitive measure of pathology by computing the distance between the white matter surface and GM/CSF boundary over the Abstract