Abnormalities of cortical sources of resting state alpha electroencephalographic rhythms are related to education attainment in cognitively unimpaired seniors and patients with alzheimer's disease and amnesic mild cognitive impairment
AuthorBabiloni, Claudio C.
Nobili, Flavio Mariano
Yener, Görsev G.
Frisoni, Glovannl B.
del Percio, Claudio
MetadataShow full item record
CitationBabiloni, C. C., Ferri, R., Noce, G., Lizio, R., Lopez, S., Lorenzo, I. ... del Percio, C. (2021). Abnormalities of cortical sources of resting state alpha electroencephalographic rhythms are related to education attainment in cognitively unimpaired seniors and patients with alzheimer's disease and amnesic mild cognitive impairment. Cerebral Cortex, 31(4), 2220-2237. https://dx.doi.org/10.1093/cercor/bhaa356
In normal old (Nold) and Alzheimer's disease (AD) persons, a high cognitive reserve (CR) makes them more resistant and resilient to brain neuropathology and neurodegeneration. Here, we tested whether these effects may affect neurophysiological oscillatory mechanisms generating dominant resting state electroencephalographic (rsEEG) alpha rhythms in Nold and patients with mild cognitive impairment (MCI) due to AD (ADMCI). Data in 60 Nold and 70 ADMCI participants, stratified in higher (Edu+) and lower (Edu-) educational attainment subgroups, were available in an Italian-Turkish archive. The subgroups were matched for age, gender, and education. RsEEG cortical sources were estimated by eLORETA freeware. As compared to the Nold-Edu- subgroup, the Nold-Edu+ subgroup showed greater alpha source activations topographically widespread. On the contrary, in relation to the ADMCI-Edu- subgroup, the ADMCI-Edu+ subgroup displayed lower alpha source activations topographically widespread. Furthermore, the 2 ADMCI subgroups had matched cerebrospinal AD diagnostic biomarkers, brain gray-white matter measures, and neuropsychological scores. The current findings suggest that a high CR may be related to changes in rsEEG alpha rhythms in Nold and ADMCI persons. These changes may underlie neuroprotective effects in Nold seniors and subtend functional compensatory mechanisms unrelated to brain structure alterations in ADMCI patients.